text:
How does steroid dependence occur?
I have seen on the internet that prolonged steriod treatment can result in the development of steroid drug tolerance leading to decreased hormone secretion. In turn this may lead to drug dependence, as you need to keep taking that drug to keep your body to function normally.
Can steroid treatment lead to drug dependency, and if yes, how?

I have made an edit to specify your question as your original question was unfortunately too broad for Biology SE to be acceptable as a valid question. Feel free to roll back if these edits are inappropriate

Your question on probiotic dependence, although unlikely to happen, could make a new separate question.

All classes of drugs react differently in the body. Some bind to receptors, some clean receptors, some drugs cause re-uptake inhibition in the brain, and others destroy viral and bacterial infections. Classifying drugs and how the human body would develop a tolerance to them in a post on this website would take pages upon pages to answer. When you say steroids, i'm assuming you are talking about anabolic steroids. That is the male sex hormone testosterone and its multitudes of derivatives. (DHT and non-DHT). Your body does not in fact develop a "dependance" on the drugs, rather it is a checks and balances system that your endocrine system establishes. Lets say you take a dosage of Testosterone Cypionate at 200mg a week for a 20 week interval from your G.P (common treatment for andropause). In laymans terms, your body senses the increase of testosterone and tells your Leydig Cells in the testes to stop signaling LH (responsible for testosterone production). Because it sees that there is already an abundance of the hormone. Now, once treatment stops, there are a series of protocols one could take to stimulate the natural production of testosterone again. Other forms of AAS are much harder on the HPTA than others however. (Trenbolone Acetate)

I edited and specified the question and it still fits your answer I think (it's not my area of expertise). Please check. If the OP doesn't roll back you could adapt your answer since the first part ("...would take pages to answer") is pretty much redundant then - thanks!

Yea it was definitely a needed edit. The title of his original question didn't really fit the breadth of what he was actually asking. Your edits are completely necessary in my opinion. As answering distinct drug dependencies would be outlandish here.

Steroid treatment with glucocorticoid drugs such as dexamethasone, prednisolone, hydrocortisone, etc. can lead to drug dependence, that is, an adaptive state formed after long-term administration. Drug dependence may cause withdrawal syndrome after stopping the drug abruptly.
Glucocorticoids are used to treat inflammatory, allergic, immune and malignant diseases. In the insufficiency of the adrenal cortex, the dose of glucocorticoid should mimic the physiological concentration and circadian rhythm of cortisol secretion to compensate for the inadequate production of natural cortisol. Even in the case of relatively low exposure to glucocorticoid therapy, long-term excessive replacement can lead to weight gain, glucose intolerance and abnormal bone metabolism, which can lead to osteoporosis.
In various conditions such as congenital adrenal hyperplasia, polycystic ovary syndrome and certain types of tumors, the body may produce too much androgens, male hormones. Such patients may not show signs of glucocorticoid deficiency. Women may experience symptoms such as hirsutism, oligomenorrhea, acne, infertility, and male pattern baldness. Men are usually asymptomatic, but acne, early baldness, and testicular adrenal gland resting tumors may occur. In this case, the use of glucocorticoids is prescribed to suppress excessive androgen production, rather than to compensate for the lack of cortisol. Here, the prescribed glucocorticoid acts in the following way through the hypothalamic-pituitary-adrenal (HPA) axis feedback loop: increased glucocorticoids suppress the release of adrenocorticotropic hormone (ACTH), thereby inhibiting the biosynthesis of pregnenolone from cholesterol. Pregnenolone is a steroid and the precursor of all other steroids, including glucocorticoids, mineralocorticoids, androgens and estrogens. Therefore, glucocorticoid drugs suppress excessive androgen production, but at a cost of suppressing all other steroid hormones as well.
The type of glucocorticoid drug prescribed depends on whether the goal is to compensate cortisol insufficiency or to suppress excessive androgen production. Hydrocortisone suppresses HPA least and dexamethasone most, with prednisolone in the middle.
When glucocorticoids are used in doses exceeding equivalent physiological production by a healthy organism, and the glucocorticoid treatment is suddenly stopped, HPA suppression prevents the adrenal glands from producing enough cortisol. Even lower but close to physiological doses of glucocorticoid drugs for long time may cause problems. Over a period of several weeks to several months or years, this may result in the gradual atrophy of cortisol producing cells in the adrenal glands, unable to respond to ACTH stimulation the HPA axis, leading to secondary adrenal insufficiency, i.e. the inability to produce normal levels of cortisol. Therefore, glucocorticoid withdrawal must not happen suddenly. Generally, patients taking glucocorticoid doses for less than two weeks are less likely to develop HPA axis suppression, and can stop treatment suddenly without gradual reduction, except patients receiving frequent "short-term" steroid therapy, such as in asthma.
In the case of chronic treatment that has been carried out for months or years, the goal is to gradually reduce the therapeutic dose to a physiological level, such as by reducing the dose step-by-step every 3-4 days for a few weeks, and then slowly withdrawing the drug for several months, to restore the HPA axis. Importantly, the adrenal suppression effect may last for a period of time, so after stopping glucocorticoid treatment, it may take more than a year for the HPA axis to fully recover.
Further reading:

Paragliola RM, Papi G, Pontecorvi A, Corsello SM. Treatment with
Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal
Axis. Int J Mol Sci. 2017 Oct 20;18(10):2201. doi:
10.3390/ijms18102201. PMID: 29053578; PMCID: PMC5666882
Nicolaides NC, Pavlaki AN, Maria Alexandra MA, Chrousos GP. Glucocorticoid Therapy and Adrenal Suppression. 2018 Oct 19. In: Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K, Grossman A, Hershman JM, Hofland HJ, Kaltsas G, Koch C, Kopp P, Korbonits M, McLachlan R, Morley JE, New M, Purnell J, Singer F, Stratakis CA, Trence DL, Wilson DP, editors. Endotext Internet. South Dartmouth (MA): MDText.com, Inc.; 2000–. PMID: 25905379


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Persistent HPV and CVD in Women?
Cardiovascular disease is the number one morbidity factor of women.
I am studying the relationship between persistent HPV infection and CVD (Cardiovascular Disease) in inadequate immune responses.
There are some statistical evidences but pathways are unknown:

HPV linked to cardiovascular disease in women in women; excludes obesity, smoking and diabetes.
Troubles With Heart Are Linked to HPV which highlights benefits of HPV vaccination only in HPV infection
No reliable method to clear the HPV virus. HPV vaccination prevents cervix cancer indirectly by preventing infections (prevent oncogene activation, its early form formation and developing into cancer). (Duodecim, Infection diseases, HPV-vaccines [Finnish])
No support for the statement that HPV vaccination may reduce CVD later in women's lives. 3 But vaccines should create herd immunity (neutralizing antibodies mediates active protection), also in males and other sites than cervix. Some cross protective effects against non-targeted HPV types [VCS].
Nearly 20 percent of individuals with CVD do not show any risk factors, indicating that other 'nontraditional' causes may be involved in the development of the disease, here.

Compare HPV-Cervical Cancer and HPV-CVD.
The former seems to have much more local effects because of cellular pathways (DynaMed Plus hpv and cervical cancer).
The latter is probably associated by broader pathways involving tissue-organ level, without any analysis in Op. cit.
Mechanism of HPV-CVD (systematic) which includes local and systematic pathways

Local. HPV's role in inactivating two tumor suppressor genes, p53 and retinoblastoma protein (pRb) -- the same process by which HPV causes cancer. p53 has been shown to be essential in regulating the process of atherosclerosis; the retinoblastoma gene plays a pivotal role in regulating cell proliferation. Here. Stable infection - dysplasia or undetectable in some genotypes. [Meijer] about the gradual development of cell-mediated immune response presumed mechanism.
Inadequate immune response and persistent HPV infection (E6, E7).
Systematic?

Sources

Human Papillomavirus and Cardiovascular Disease Among U.S. Women in the National Health and Nutrition Examination Survey, 2003 to 2006. Journal of the American College of Cardiology, 2011; 58: 2001-2006 DOI: 10.1016/j.jacc.2011.07.038
Cardiovascular disease prevention for women attending breast and cervical cancer screening programs: the WISEWOMAN projects. The WISEWOMAN Workgroup.
Meijer CJLM, Helmerhorst TJM, Rozendaal L, van der Linden JC, Voorhorst FJ, Walboomers JMM. Histopathology. 1998;33-83-86. 2. Schiffman M, Kjaer SK. J Natl Cancer Inst Monogr. 2003;31:14-19. 3. Ho GYF, Bierman R, Beardley L, Chang CJ, Burk RD. N Engl J Med. 1998;338:423-428.

Pathway organ level

HPV-cervix cancer
HPV-lung cancer (here put research pressure in some universities instead of HPV-CVD)
HPV-CVD

[conjuncture] Tissue-Organ level mechanism
Preventing infection of cervix does not prevent the manifestation spreading to CVD by vaccines Cervarix/Gardasil.
I propose a tissue-organ level mechanism because I cannot explain the relationship only by the cellular level mechanism.
Assume skin has a visual-processing pathway of peripheral neurons, as described here i.e. it preprocesess some events of the geometrical data before going to the target organ (here the heart).
Missing of such an unit can cause alterations in the balance of sympaticus-parasympaticus firing, thus causing alterations of the pacemaking and conduction system.
Unknown

How is CVD formed in HVP infection in women? Compare incidence of non-HPV and HVP cases where CVD has been formed
HPV 16, 18, 31, 33 and 45 most common agents in cervical cancer. HPV is associated with many conditions: vaginal cancer, vulvar cancer, VIN, VaIN, CIN, AIS, genital warts, ... I think we cannot assume that those types causing the cervical cancer are mostly associated with CVD.
High-risk HPV and anogenital cancer. Can we assume that these agents are associated with CVD?

How can you hypothesize the relationship between HPV and CVD?
Which HVP genotypes can cause CVD?

This is an impressively referenced question, but I don't think it's reliably answerable for several reasons:

it's POB
the association is merely theoretical at this point
the study 'results' were based on a very small number of women.

While the percentage of woman with HPV is high, those with no other risk factors for CVD who have experienced MIs is much lower.
The idea is interesting enough to warrant further study perhaps, but certainly not enough to answer your questions, "How can you hypothesize the relationship between HPV and CVD? Which HVP genotypes can cause CVD?" I mean, if you want good, referenced answers, there isn't an answer yet.

What is POB? Pelvic Ovarian ... ?

Not sure what POB stands for either... Though searching for it I came up with Victoria Beckham's hairstyle... Posh (Spice) + bob = POB... :-)

@Masi - POB = Primarily Opinion Based (not evidence-based). Makes a reliable answer not possible.

@anongoodnurse I do not think so. The question is about how you can reach the evidence based answer, not how you are there.

CVD is the leading cause of death in the developed world and HPV is the most common STD in the developed world. When dealing with something that common alot would need to be ruled out before any causative relationship was hypothesized for example the first link did not consider that oral Contraceptive use is higher in women (obviously) would increase atherosclerosis / CVD related causes of death in the absence of other CVD associated factors such as obesity

Yes, this is a valid point. You have to rule out the 1) contraception use in this question and its relation to atherosclerosis > CVD, ... 2) obesity when you are getting away. There is a net of those factors where the causalities need to be defined.

source: Stack Exchange

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sort: votes


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To determine no beating cardiomyocytes from ECG or video recording
I am trying to find data and some method by which I can see and say that there are some cardiomyocytes not working.
I have reviewed many arrythmia data where I think I can see much cardiomyocetes there and there which are not beating at all.
Is there any method with available data for the recognisition of cardiomyocytes without beating?
I am particularly interested in the paediatric data.
I am using at the moment ECG data after cardiac infarction.
What is the name of this video record?
Picture from House season 3 episode 2:

A number of cardiomyocytes is lost during an infarction. Instead, fibrous tissue forms, but it only preserves structural integrity, having no contractile function [1]. Myocardial infarction is an uncommon condition in pediatrics, happening very rare, when embolization occurs due to blood coagulation affections or heart congenital defects [2].
The fibrous tissue has different properties, thus modifying:

MDE-MRI images [3]
ECG: deep Q wave [4]
echocardiography: hypoechoic and hyperdense echoes inside the fibrotic material (the latter compatible with calcium) [5]

That video record is probably about 3D Echocardiography (look here at Video 2 and figure 2).
References:

Yao Sun, Myocardial repair/remodelling following infarction: roles of local factors
Nicola Carano et al., Acute Myocardial Infarction in a Child: Possible Pathogenic Role of Patent Foramen Ovale Associated With Heritable Thrombophilia
Harikrishna Tandri et al., Noninvasive detection of myocardial fibrosis in arrhythmogenic right ventricular cardiomyopathy using delayed-enhancement magnetic resonance imaging
ECGpedia - Pathologic Q Waves
Berenzstein CS et al., Usefulness of echocardiography and doppler echocardiography in endomyocardial fibrosis

The video in House series is probably fake. I cannot understand from which angle you can get so circular picture. Those real-life pictures are much more challenging than the one in House.

@Masi I could't understand that either.

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Why do spinner dolphins spin?
Spinner dolphins have a behavior where they jump out of the water and spin a bunch of times in the air. Wikipedia's article on this just states

These spins may serve several functions

and doesn't anything. Are there any known reasons for their extreme spinning behavior?

No single factor is considered to be the reason for the aerial spinning behavior (Hester et al., 1963; Norris and Dohl, 1980; Norris et al., 1994). The various factors include leadership or dominance, alertness, acoustic communication, courtship display, defining positions of members in the school, and dislodging ectoparasites. The most notable ectoparasites are remoras and whalesuckers (order Perciformes, family Echeneidae). ... Hester et al. (1963) suggested that the aerial maneuvers executed by spinner dolphins are involved in the removal of remoras. ... While aerial spinning maneuvers may not have developed specifically to remove ectoparasites like remoras, dynamically it is plausible that this proves to be an added benefit.

--Dynamics of the aerial maneuvers of spinner dolphins

From Lammers - Spinner dolphins of islands and atolls, Ethology and Behavioural Ecology of Odontocetes, 2019 (https://link.springer.com/content/pdf/10.1007/978-3-030-16663-2.pdf) :

Invariably, the question arises: Why do they do it? Probably the most
common answer is to rid themselves of parasites, including remoras
(Hester et al. 1963; Norris and Dohl 1980; Norris et al. 1994b).
However, this answer alone is rather unsatisfying, as most odontocetes
face the problem of parasites yet do not display the acrobatic
aptitude of spinner dolphins. Thus, additional explanations are
necessary that account for the spinner dolphin’s distinct behavioral
ecology. Norris et al. (1994b) proposed that the bubble plume produced
underwater by reentering spinning dolphins would offer a strong target
for echolocating pod-mates and therefore serve as a beacon of sorts to
help define the envelope of the pod or perhaps act as a target to more
distant subgroups.
Similarly, the reentry sound produced by a leaping dolphin could serve
as an Fig. 17.3 A collated sequence of a spinner dolphin, Stenella
longirostris, performing a spinning leap. This sequence was taken from
Twitter, with permission by the Wyland Foundation. In this compilation
of a video sequence, the leap begins on the right side, and the
dolphin turns on its axis two times, until it lands to the left. Leaps
can be in this vertical stance, but also horizontally to the water,
and can incorporate over three turns of the body axis while in-air 380
M. O. Lammers omnidirectional cue to nearby animals. Still, these
explanations probably cannot reconcile the large variety of aerial
behaviors in the spinner dolphin repertoire. Perhaps an additional
clue lies in the fact that behavioral state can be inferred from the
pod’s aerial displays. Thus, it may be that spinners use aerial
displays to regulate the pod’s state in their perpetual effort to
achieve and maintain group cohesion. These acrobatic leaps are perhaps
designed as a signal of group social cohesion for entering or leaving
a bay, or for signaling an after-feeding “party mood” as has been
suggested for dusky dolphins (Würsig and Würsig 1980).

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Why do I only breathe out of one nostril?
I was just sitting with my hand next to my nose and I realized that air was only coming out of the right nostril. Why is that? I would think I would use both, it seems much more efficient. Have I always only been breathing out of my right nostril?

Excellent question :) I've wanted to know this for along time. You will find that if you check on your nostrils for a long time that you alternate, after some time you breath mostly out of your left nostril instead, and then after some time it will switch back again.

I wonder how many people are sticking their fingers up their nose to test this out now.

This can also be caused by Nasal septum deviation

Related: https://skeptics.stackexchange.com/questions/19596/

This topic was covered on the British comedy panel show Qi: http://www.youtube.com/watch?v=E1jvRJV91co

This is a natural phenomenon called the nasal cycle. It is discussed in this paper by Telles et al. (1994), among many others. The nostrils are used on an alternating cycle of about 2-3 hours, controlled by the autonomic nervous system. If you notice alternating congestion, that also seems to be coupled to the nasal cycle (Hasegawa and Kern 1977, 1978).
Normally, the direct cause is blockage caused by alternating engorgement of erectile tissues on each side of the nose.

Below, I explain that the nasal cycle may be an artifact of the way the autonomous system works in humans (and some other organisms) or it may provide a first barrier against invasion of infective organisms via the nose. The full answer requires some background information.
Wikipedia and the nasal cycle
The Wikipedia article on the nasal cycle, nicely paraphrased in the answer by George Daccache, offers hints but not real answers.  For example, the Wiki section called Research on the effects states,

In 1994, breathing through alternate nostrils showed effects on brain hemisphere symmetry on EEG topography.

suggesting that perhaps natural nasal cycling relates somehow to communication or coordination between the two brain hemispheres. However, the cited study (Stancak and Kuna 1994) is based on forced alternate nostril breathing (FANB). The Wiki section then states,

D.S. Shannahoff-Khalsa published in 2007 on the effect of this cycle and manipulation through forced nostril breathing on one side on the endogenous ultradian rhythms of the autonomic and central nervous system.

All this sentence ultimately says is that a 2007 paper looked at the effects of FANB on ultradian rhythms. The Wiki section doesn't actually include results from the study so it provides no useful information.$^1$ I will try to explain with more depth.
What is Forced Air Nostril Breathing?
Forced Air Nostril Breathing (FANB) requires a person to close one nostril, breath in, close the second nostril and open the first nostril, and breath out. The person repeats this process several times in a 10-15 minute period. In fact, FANB is a yoga technique called Nadi Shodhan Pranayama. The Telles et al. paper mentioned above used FANB, as has nearly every study on the effects of the nasal cycle.
None of these studies actually explain the natural nasal cycle.  FANB is not natural. It changes natural breathing rhythms and requires the person to focus on the physical movements of the fingers to close the alternating nostrils. FANB occurs for a 10-15 minute period of time and is finished. This is not the same as the 2-3 hour natural nasal cycle. In my opinion, any conclusions drawn from studies using FANB apply only to FANB but not to the natural nasal cycle.
Then why does the nasal cycle occur?
The nasal cycle is a natural ultradian cycle (see here and here. Not only is it present in humans, but the nasal cycle has also been observed in rats, rabbits, domestic pigs, cats and dogs (see references in Eccles 1996]). Thus, the nasal cycle may at least be a feature of mammals but it may be a feature of other bilateral animals that use nostrils for respiration. In addition, the nasal cycle may be an artifact of the evolution of bilateral symmetry in animals, and how the autonomic nervous system operates between the two sides.
The autonomic nervous system controls the nasal cycle. The autonomic nervous system has two divisions, the sympathetic nervous system and the parasympathetic nervous system. Interestingly, these two divisions show a lateralized ultradian rhythm (Shannahoff-Khalsa 2007).  This means that the parasympathetic nervous system dominates one side of the body and the sympathetic nervous system dominates the other side of the body. The two systems later switch dominate sides. This dominance switching back and forth between the parasympathetic and sympathetic happens with a regular rhythmic cycle every few hours. As it happens, this switching between sides correlates very well with the nasal cycle (Shannahoff-Khalsa 1991).  When the parasympathetic-sympathetic systems switch sides, so do the nostrils. This is also associated with a switch in EEG activity between the two brain hemispheres (Werntz et al. 1983).
Therefore, the nasal cycle may not have a specific function, adaptive or otherwise. Instead, it could result from dominance of the parasympathetic system. Whichever side is dominated by the parasympathetic system will have the primary nostril in use for respiration. However, others have argued that the nasal cycle does provide a function. For example, Eccles (1996) argued that the nasal cycle may function as a respiratory defense mechanism. They found that the rate of cycling increases when nasal infection is present in the nose. They argue that the congestion-decongestion helps generate "plasma exudate" (nasal fluids derived from blood plasma) which may help remove bacteria and viruses.
The nasal cycle is an interesting phenomenon but whether it evolved as an adaptation (such as a mechanism proposed by Eccles et al. (1996) or is simply an artifact of the operation of the autonomic nervous system may never be known for sure.
Footnote

One of many reasons why you should always interpret Wikipedia entries very cautiously, even skeptically.

Citations
Eccles, R. 1996. A role for the nasal cycle in respiratory defense. European Respiratory Journal 9: 371-376.
Hasegawa, M. and E.B. Kern. 1977. The human nasal cycle. Mayo Clinic Proceedings 52: 28-34.
Hasegawa, M. and E.B. Kern. 1978. Variations in nasal resistance in man: a rhinomanometric study of the nasal cycle in 50 human subjects. Rhinology 16: 19-29.
Stancak, A. and M. Kuna. 1994. EEG changes during forced alternate nostril breathing. International Journal of Psychophysiology 16: 75-79.
Telles, S. et al. 1994. Breathing through a particular nostril can alter metabolism and autonomic activities.
Werntz, D.A. et al. 1983. Alternating cerebral hemispheric activity and the lateralization of autonomic nervous function. Human Neurobiology 2: 39-43.

I find it sad that this well-referenced answer is out-voted by a more recent answer, that is incomplete and only contains web/wikipedia references.

Interesting, I wonder do other mammals have a cycle of this kind?

As others have said, this phenomena is called the nasal cycle, a process controlled by the autonomic nervous system that alternants congestion between your nostrils. Mentalfloss of all places has an article about this that explains:

...it makes our sense of smell more complete. Different scent
  molecules degrade at different rates, and our scent receptors pick up
  on them accordingly. Some smells are easier to detect and process in a
  fast-moving airstream like the decongested nostril, while others are
  better detected in the slower airstream of the congested nostril.
  Nasal cycling also seems to keep the nose maintained for its function
  as an air filter and humidifier. The alternating congestion gives the
  mucous and cilia (the tiny hairs up in your nose) in each nostril a
  well-deserved break from the onslaught of air and prevents the insides
  of your nostrils from drying out, cracking and bleeding.

link: http://mentalfloss.com/article/30363/why-does-your-nose-get-stuffy-one-nostril-time

hmmmm.... I don't really buy the smell part. The nasal cycle lasts 2-3 hour, which seems to long to account for desensitization to smell...

The article doesn't mention anything about desensitization to smell, though; it only suggests that the nasal cycle keeps either nostril from drying out.  As for whether the difference in airflow allows the two nostrils to each sense certain smells better, a better source would be Stanford University, which published an article about this in Nature.  http://news.stanford.edu/pr/99/991103smell.html http://www.nature.com/nature/journal/v402/n6757/abs/402035a0.html

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Is this a large bee? (species identification)
While hiking in some low hills near Taipei in the late afternoon in July an hour after it rained, I saw this large flying insect visiting flowers the way bees do.
I'm curious, is it a bee (if so, what kind), does it come from a hive or live on its own, and does it sting?
I'm estimating its body to be about 5 cm long. While not captured in photos, I'm pretty sure I remember it sticking its head into flowerers. It was moving flying from place to place fairly quickly and difficult to get any photos at all, this is the best I could do.
edit: Since further clarification of the size was asked for in comments, I'll add here also that the length of "about 5cm" that I mentioned wold be for nose to tail when stretched straight, (rather than in it's current somewhat curled position) and it could certainly be 4.5 cm. But I'm fairly sure it's closer to 5 cm (2 inches) than to 4 cm. I've added a few more images of the flower sans insect. I've cropped my friend on the left out of the images.

Five centimeters long?? As in, would cover the palm of your hand?

@Dubukay I've seen giant hornets in Japan about that long, so a 5 cm bee isn't impossible. But without knowing the size of that flower in OPs image we can't be certain of their estimate for the bee.

@user137 Yeah, I’m aware that it’s possible, but with those petunia-looking flowers that the bee is sitting on I figured it’d be worth checking

@Dubukay If the bee is 5 cm long, the flower must be at least 20 cm long. I also suspect OP's estimate is too large, but I'm no expert on Taiwanese flowers.

@Dubukay "Five centimeters long?? As in, would cover the palm of your hand?" As my palm is 9.5 cm wide (3 and 3/4 inches), no. 5cm is but 2 inches. When it straightens out, this insect is about 5 cm from nose to tail. I'll go to 4.5 cm, but I'm fairly sure it's closer to 5cm than to 4cm when measured end-to-end rather than in the somewhat curled position shown. Yes it sounds large, doesn't it! Thus the title; "Is this a large bee?"

@user137 I've added an edit to the question which reflects the comment above.

Good question, thank you for providing images and a good description!
The bee is not Bombus dahlbomii but rather a Red-headed Carpenter (Xylocopa ruficeps) a surprisingly rare bee with few records and the lack of a Wikipedia page (as of May 14, 2024).
How to Identify
The bee is either in the carpenter bee group or the bumblebee group, the two main groups of large bees. The bee can be narrowed down to a carpenter bee, due to the shiny abdomen

Non-professionals commonly confuse carpenter bees with bumblebees; the simplest rule of thumb for telling them apart is that most carpenter bees have a shiny abdomen, whereas bumblebee abdomens are completely covered with dense hair. Males of some species of carpenter bees have a white or yellow face, unlike bumblebees, while females lack the bare corbicula of bumblebees; the hind leg is entirely hairy.  Source: https://en.wikipedia.org/wiki/Carpenter_bee

After clarifying that it is a carpenter bee, the genus can be easily found due to the large size of the bee pictured as the genus Xylocopa (Large Carpenter Bees).
The exact species can be found by going through the range maps of each species in the genus Xylocopa. The species ID is simple as there is only one bee of the genus Xylocopa that is in the Taiwan range. https://www.inaturalist.org/taxa/570760-Xylocopa-ruficeps/map#5/20.756/106.743
Here is an example:

https://www.inaturalist.org/photos/219358554, Photo 219358554, (c) Janus Olajuan Boediman, all rights reserved, uploaded by Janus Olajuan Boediman

2 comments: 1) please provide a source/citation for your first quote. 2) I'm not sure i'd trust inaturalist as any sort of authority of all possible species in any given area (as you've done in this post and a handful of others). It's good that you add this explicit info, but I just personally would not rely on it as the definitive stopping point of what species are/are not present in any given area. It's probably better for ruling in favor of the presence of something somewhere vs using as evidence that only 1 species' range is in any given area

@theforestecologist 1) Thanks, fixed. 2) That's ridiculous, INat has been used in hundreds of research projects. INt is one of the largest mass data collection systems in the world and has been used as a reputable source. In fact INat is the leading source of information on all living things and has been used to document animal movements via the range map system. INat is very scientific, all of the IDs required for data (range maps, etc) are verified by a 2/3s majority identification system. Obviously you haven't contributed to INat. It is a pretty neat system and I encourage you to try it out

I will redirect you here: https://forum.inaturalist.org/t/research-credibility/43603

I'm not discounting it's utility. I'm suggesting that just because some organism is NOT on there at some location doesn't mean that that organism is not found in that location. Again, it's the statement that "the only species found in x on inat is y, so no other species exists there" that I question -- I'm not sure I would use such a statement supported by inat as definitive proof that other species don't also live there. Not everything is on inat.

@theforestecologist Inat has more records than any other scientific data collection. Range is indicated on Inat when some species observations are few and far between. If, for example a species is discovered on an Island that has never been reported on that Island via Inat. The Inat team will color the island a light green, indicating that this is the range of that species even though no one has found that specific species there: https://www.inaturalist.org/pages/taxon_ranges

Note: My mistake. I did not notice the location is Taiwan. There are giant honey bees in China, such as Apis dorsata Fabricius, however their size is only 17-20mm.
========
I suggest  Bombus dahlbomii. It can grow up to 40 mm long, 1.6 inch

Picture
Wiki

OP says they found the bee outside Taipei, but Bombus Dahlbomii is South American. The wikipedia link you give doesn't say if this bee is found outside South America.

Ops. My mistake. I cannot find a anything about a  40-50mm bees native to china. There are large enough wasp but the color and presence of hairs do not match.

Thanks, it certainly looks similar. Taiwan being an island active in shipping, there's certainly a possibility of movement from South America. Though I don't know how to read these 1, 2, 3 but if dahlbomii could be anywhere in South Neotropical Region then that would include here as well. Would this necessarily be a queen, and could it sting?

My bee's abdomen is dark/black and appears smooth, your bee's abdomen is bright orange and fuzzy. My bee's hind legs are orange and fuzzy, your bee's hind legs are black and smooth. Not knowing much about bees, I don't know if that is a big difference or not. There is also of course also the geography thing still...


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Is this a hawk, or an eagle?
I saw this large bird gliding fairly low over the trees while hiking in the late afternoon in some hills near Taipei recently. It seemed quite large compared to what I normally see here. It's quite difficult to gauge, but I'd guess the wing span was one meter or so.
It made that shrill, descending, single "peeeew" sound that I associate with birds of prey (probably mostly from old movies or TV commercials).
Is it at all possible to guess if this is a hawk or an eagle from these cell phone snapshots? These are cropped out of the full resolution originals. A half-size original for scale is also included.

This is indeed in the Family Accipitridae also known as the Hawks, Eagles, and Kites Family.
But it is neither a eagle or hawk! This bird in the photo you provided is actually in the goshawk and sparrowhawk family (Genus Accipiter)
Further identification features and range provide the exact species of Crested Goshawk (Accipiter trivirgatus)

Powerfully built hawk of forests, especially hilly woods. Namesake crest is usually held low and not very visible. Adult has a gray head, brown wings, whitish underparts with thick orange-brown stripes in belly and streaks in breast, and white throat with black borders. Juvenile similar but with brown head, sparingly marked underparts, and very short crest. Appears stockier and relatively shorter-tailed in flight than other accipiters. Flying adults may also show a fluffy white clump of feathers on both sides of the tail. Source: https://ebird.org

Image ref: https://www.inaturalist.org/photos/250380634, Photo 250380634, (c) Max Hsieh(雁子), some rights reserved (CC BY-NC), uploaded by Max Hsieh(雁子)

 Image ref: https://www.inaturalist.org/photos/333485461, Photo 333485461, (c) krishy, some rights reserved (CC BY-NC)

Excellent, thanks again! One of the nice things about Taipei is that because of the terrain and the culture, the city is interspersed with a lot of natural areas, which means one can photograph an Accipiter trivirgatus ssp. formosae from Da An park and post it in inaturalist.org

It's great when a new user stops by and solves a six year old mystery, and writes a wells-sourced, informative answer.

@uhoh Haha, thank you so much! You are very welcoming. I am going to go and answer all of your unanswered questions when I get the time. At least the ones that are in my range :) Thank you so much for your support! I have never been welcomed to a stack exchange site this kindly before


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Is gut bacteria Succinivibrionaceae's low methanogenesis understood well enough for GM of cattle gut bacteria to be considered?
After watching the Periodic Table of Videos episode linked in this question I watched the episode Wallabies and Methane where Sir Poliakoff says (a bit after 02:00):

So the point of this paper was that Wallabies have different bacteria in their stomachs, which instead of producing methane, produced succinic acid, which is the diacid of butane.

 Succinic acid, Source
The paper he references seems to be Isolation of Succinivibrionaceae Implicated in Low Methane Emissions from Tammar Wallabies Pope, P. B. et al. Science 29 Jul 2011: Vol. 333, Issue 6042, pp. 646-648 DOI: 10.1126/science.1205760
Question: I can not understand the abstract, and the paper is paywalled. Presumably much more work has been done since its publication in 2011. How well is  Succinivibrionaceae's low methanogenesis understood; well enough for the genetic modification of cattle gut bacteria to be considered?

Abstract
The Tammar wallaby (Macropus eugenii) harbors unique gut bacteria and produces only one-fifth the amount of methane produced by ruminants per unit of digestible energy intake. We have isolated a dominant bacterial species (WG-1) from the wallaby microbiota affiliated with the family Succinivibrionaceae and implicated in lower methane emissions from starch-containing diets. This was achieved by using a partial reconstruction of the bacterium’s metabolism from binned metagenomic data (nitrogen and carbohydrate utilization pathways and antibiotic resistance) to devise cultivation-based strategies that produced axenic WG-1 cultures. Pure-culture studies confirm that the bacterium is capnophilic and produces succinate, further explaining a microbiological basis for lower methane emissions from macropodids. This knowledge also provides new strategic targets for redirecting fermentation and reducing methane production in livestock.

I may need help with tags; I didn't see genetic-engineering or genetic-modification. I can not think of a shorter but still accurate and descriptive title, help is appreciated there as well, thanks!

Old question, but: it's worth noting that there is substantial variation in methane emissions even among ruminants such as cattle. And indeed, even among cattle, Succinovibrionaceae are associated with lower methane emissions. So quite possibly you don't need to do any engineering, though there are apparently a large number of (then) poorly described metabolic genes that might be relevant:

Lower emissions were accompanied by higher Succinovibrionaceae abundance and changes in acetate and hydrogen production leading to less methanogenesis, as similarly postulated for Australian macropods. Large numbers of predicted protein sequences differed between high- and low-methane-emitting cattle. Ninety-nine percent were unknown, indicating a fertile area for future exploitation.

Instead of sorting through all those proteins (which might be fun but would probably take a lot of work), it might be more effective and easier to simply make cattle rumens better places for low-methane bugs to live, if your goal is to reduce methane. Possibly unrelated to these bugs, but for example feeding seaweed to cattle lowers their methane production by affecting their microbiome through antimicrobial activity.
The old adage in microbial ecology is often wrong but always helpful to remember: "everything is everywhere, and the environment selects". So set up an environment that selects for the kind of bug you want!

This is probably a better answer than an answer to the question as-asked, +1!

The question — which I would regard as off-topic as not being about a problem in biology — was about whether science had progressed sufficiently for some unspecified genetic manipulation (I assume GM does not stand for General Motors) to be performed. Your information is not without interest, but provides a non-answer to a non-question.


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What is biological dark matter?
I recently stumbled upon the Biological Dark Matter wiki page. Its pretty light on details, but it appears to be genetic material found in humans that doesn't fall into currently classifications.
But what do we know about it? Is it really a big black box that we know nothing about? The article claims that it can make 40% of the genetic material in our gut, and I find it hard to believe that we really know nothing about it.

Interesting, I've never heard the term before. First, that Wikipedia page does not cite any peer reviewed research so it's not really informative at all. That said, the term seems to refer simply to the presence of genetic material that does not belong to known organisms. This article may interest you: http://www.nature.com/nature/journal/v499/n7459/full/nature12352.html

There are multiple answers to this question depending on who you ask (meaning, what their field of expertise is).
The biological dark matter from the wikipedia article in question seems to mean sequence from metagenomic samples which was not assigned to any of our commonly known domains of life. That might not necessarily mean that it does not belong to them. Sometimes it is hard to decide where a small particle of sequence informations belongs to, because it does not match anything we know. Still, it might be from a perfectly "normal" bacterium. Or it might be a result of sequencing errors.
Additionally, depending on how you assign a taxonomy to the sequence, there might be cases where there are so many different possibilities for where this sequence came from (because it is very conserved in a lot of different organisms, even from different domains of life), that this sequence will not get any taxonomy assigned. Not because there is none, but because we cannot safely decide which it is.
Some people also speak of this information as "dark matter".
There is for example this project which specifically is designed to study the dark matter we can (or at least for some reason do) assign to be microbes, but not more specifically.
Basically, any decision of where to place potential dark matter sequence is guided by our previous knowledge about the domains of life and the genomes of all those organisms. This knowledge is very incomplete.
I am sorry this answer lacks some more nice sources. Most of the information is based on my knowledge as a person working with datasets that might include "dark matter", if I would call it that. (I call it "not assigned sequence".) I don't have the time right now to add more sources, but if needed I can maybe add some later.
Edit:
As a fast add-on after re-reading your question: How much of the sequence is unassigned for example if one would study your gut depends a lot on what is actually there in you gut that we know, how diverse the community in your gut is, what database is used for comparison and how old this database is, how the data is preprocessed and analysed, and so much more. But yes, there is still a lot of genomic information in nature that has not made it into any database.

Take a look at this article: http://phys.org/news/2014-01-scientists-biological-dark.html
Is this the same "biological dark matter" you're asking about? If so, it sounds like what used to be called "junk DNA" or "non-coding DNA", which is what it was referred to as up until a few years ago when scientists discovered it is actually regulatory DNA, very interesting stuff, but basically it regulates gene expression, thus why it is usually in the form of RNA instead of a protein.
I hope this answers your question, I would strongly urge you to do some research on regulatory DNA, it's very intriguing.


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Effect of extremely hard water on marine life?
When researching water quality standards, I found that a minimum and maximum was set for water hardness. Several sources also state that water can in fact be too hard. The question is how does hard water harm marine life? I understand that it is required to reduce the toxicity of Hydrogen ions and other trace metals, but cannot find anything concerning the effect of water that is too hard.

I don't have any direct adverse effects of extremely hard water but marine organisms have quiet specific ranges of hardness according to http://www.cichlid-forum.com/articles/hardness.php

Wiki Found relatively easily on wikipedia. Affects cystein residues in proteins, binds to DNA backbone, affects prostetic groups, etcetc.

You should define hardness in your question. There a few types of hardness defined. In general, increasing hardness is a result of increasing pH and vice versa; which means hardness (increasing from another reason) may also lead to a n increase in pH. marine water is not just a simple composition of salts... edit for dummies added.

Water hardness refers to the concentration of calcium and magnesium ions in fresh water. Has nothing to do with pH. In salt water, these ions are at much higher concentrations and thus water hardness makes no sense in salt water.

Hard water helps in direct and indirect ways.
Indirectly, hard water plays an important role in regulation of pH. Respiration and other physiological activities release substances into water that change the water pH and the ions that cause hardness act as buffers and help maintain pH.
Directly, they determine the ease with which osmoregulation occurs. The harder the water, the lesser the influx of water. So the fishes act like an open system and are influenced by the surrounding water.
There are very few fish who absolutely need soft water to survive.
Since your pH and hardness are pretty low, it allows you to raise multiple fish from South America. You could do tetras, dwarf cichlids and New World cichlids, Plecos as well.
Potentially discus and altum angelfish as well if you're up to the huge challenge.
However, livebearers will not tolerate this type of water. That goes the same for African cichlids.
Otherwise hard water is completely fine for marine life and other aquatic species.
Link
Link
Hope this information helped!
-Sartoaster

If you look at the Wiki text on Hard Water, Marine hard water is not mentioned once. That's because it's a term used mostly to qualify freshwater.
Sea water doesn't vary alot in the oceans, only in inland seas and near estuaries and glacial melt, it's called brackish water, brine, not soft seawater.
Sea water which undiluted is called salty, highly saline, high salinity, water, not Hard Seawater.
Marine life isn't affected by the stone type mineral content of the seawater as much as by the highly reactive salts, both sodium and chloride are very harmful to life compared to most stones a the less soluble mineral salts.
Seawater contains a lot more calcium generally than most river water, even though some river water can be completely saturated in calcium and have very high PH. Some fish can adapt to a wide range of soft water hardness, and some fish can adapt to very salty water, but most fish are specialists who don't live in wildly varying ecosystems, only in the sea and in constant softness freshwater.
Read some aquarium chemistry experiments. they are aquariumabulous and will give you a lot of knowledge about marine biogeochemistry. It's pretty interesting to look at any pond and river and plant and know what chemistry it has, what it needs, and the processes changing it, it's quite simple to learn too, just learn some basic experiments and guides on water and pedology organic and mineral reactions and biology.


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Is intron removal coordinated?
Are the introns present in a nascent rna molecule removed simultaneously or are they removed in some sort of sequential fashion or is removal completely random?

There are two different ways to interpret this question:

Does the spliceosome splice all introns of an mRNA simultaneously or sequentially?

Can a spliced mRNA be re-spliced?

How does a spliceosome proceed along the mRNA?
According to this review:

splicing generally proceeds in a 5′ to 3′ direction, although neighboring introns are not always excised in this order, nor are all introns completely removed during synthesis (36).

Splicing tends to happen immediately following transcription of introns, so it is to some extent necessarily sequential (same review):

Time course measurements by RT-PCR of multiple pre-RNA species synthesized after reversing 3 hours of DRB inhibition have shown that intron excision occurs within 5 – 10 minutes of synthesis of the downstream neighboring exon, irrespective of the length of the intron, the length of the gene or whether the intron is excised by the major or minor spliceosome (42).

Thus, it is not physically possible in many cases to splice all the introns of a RNA simultaneously, because splicing begins before pre-mRNA synthesis is even complete.
Re-splicing mature/spliced mRNA
There are a few different mechanisms by which RNA can be spliced at more than one point. For example, ribozyme splicing occurs in a spliceosome-independent fashion, so an mRNA with a ribozyme in it and also non-ribozyme introns will necessarily have multiple rounds of splicing.
There is additionally so-called recursive splicing of very long genes/introns. This is when a spliced intron must be handled in multiple rounds due to its length/complexity; it's a bit involved so I won't go into it here.


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Why do physicians try to match HLA complexes for organ transplant?
My understanding of acute transplant rejection is that donor dendritic cells present donor antigens on MHC1 to host naive CD8+ T-cells resulting in an immune response against the graft. If you match MHC1 complexes between donor and host, wouldn't t-cell activation actually be more likely than the case where MHC1 complexes between donor and host are different?
Reasoning: I imagine in the case where MHC1 complexes between donor and host are different that the  t-cell receptor is unable to bind the MHC1 complex in the first place..making the transplant essentially invisible. In the case where MHC1 complex between donor and host are the same, the t-cell receptor would bind the MHC1 complex, and increase the likelihood of an immune response. Given that HLA mismatch is a major cause of transplant rejection, something is wrong with my reasoning. Thoughts?

There are no T cells in a host that attack foreign MHC1?

Cells with low MHC1 or non-recognizable MHC1 are destroyed by NK cells, so e.g. viral infections, intracellular bacterial infections and cancer cells cannot hide with their "abnormal" proteins...

I seem to remember from my (far behind) immunology that such is also the case with T CD8+ cells. Is that not the case?

@Raoul I don't think so, but I am not sure. Afaik TCR-MHC1 connection is required to activate CD8+ T-cells, and TCR does not necessary connect to non matching MHC1. Afaik anergy happens when it is connected to the MHC1, it recognizes the oligopeptide pattern with the TCR, but it does not have enough stimulus for activation. It needs costimulation e.g. B7 protein from an APC or cytokin from a CD4+ T-cell to lower the activation threshold. If it does not get it, it will die after a while. I'll check what happens when a CD8+ T-cell meets with a non MHC1 cell.

@Raoul It seems like much more complicated than we both thought. I'll edit my answer later.

@Raoul Still reading articles in the topic. ;-) Just a short report: it seems like there are multiple cell types with NK ability, e.g. NK cells, NKT cells (subgroup of T-lymphocites), etc... (possibly more). These cells can kill other cells if they don't recognize the MHC1 (MHC1 does not exist or not compatible). Regular T-cells (without NK receptor) seems like having the same ability by not compatible MHC1, but I am not sure yet about the mechanism. I think I'll need a weak more to read all articles I opened and come to a conclusion about how the immune response works in this case.

@Raoul Have you finished this work? I've been citing  you at https://biology.stackexchange.com/questions/104879/transplant-rejection-through-direct-allogenic-antigen-detection-where-do-the-t/104976#104976

T-cells are selected against self reactivity so those that react to self-MHC are selected against and die by anergy. That's why they try to match the donor and the recipient's MHC molecules, to diminish the immune response.

On activation of host cells by foreign APC/dendritic cells with non identical MHC1

It cannot be ruled out that there do exist host T cells that do not bind to host MHC1 and have not been sorted out by so called positive or negative selection. They would not be activated by any presentation of antigen on host type MHC1 (conversely, presentation on foreign, non identical MHC1 might acitvate them, and there would be no sorting out of non-tolerant cells). Cp. comment above
inf3rno:  "it seems like there are multiple cell types with NK ability, e.g.  (...) NKT cells (subgroup of T-lymphocites), etc... (possibly more)."
To sum up: assuming that there are T cells that react to foreign, not host MHC, there is no need  for antigens being presented on (identical) host MHC1

On presentation on (identical) host MHC1

a. in case some antigen is presented on host MHC1 that there has been a process of inducing tolerance for
there would be no specific host T cells "left" to mount a reaction, as they would have been sorted out.
Apart from pre-tolerance, your reasoning should apply, as there is no process of tolerization after a certain period of "youth".
"Given that HLA mismatch is a major cause of transplant rejection, something is wrong with my reasoning."  - To sum up, nothing's wrong, as there is rejection with identical MHC1 too, according to my reasoning above (with the exceptio of "tolerance").
However, refering to first part of my answer,  this (rejection with self MHC1) does not imply that there is no rejection with non-identical MHC1. There is no  either/or. Both situations know rejection. From "self MHC1 has rejection" does not follow "foreign MHC1 doesn't".

In short, if a T cell does not find its corresponding MHC 1 complex on a particular cell, its default behavior will be to attack it. Binding to the MHC complex will cause a period of anergy in the bound T cell.

"Binding to the MHC complex will cause a period of anergy in the bound T cell." - I think this refers to T cells that encounter their specific antigen while strolling in the blood without having been primed/immunisized before by APC/dendritic cells, cp. Janeway's.


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Does every wave length of UV kill bacteria?
Will every wave length of UV work for killing bacteria? So will UV A, UV B and UV C all work? Or will only the shortest of the three, UV C, work? Also, will the average UV lamp help against bacterial growth (if it is shone on an object for 3-5 minutes for example)? What about a longer period: a bacterial colony in a petri dish under an average household UV lamp for a day? Would the growth be reduced noticeably? Or would the change be too small to notice when using the average UV lamp? Does the type of UV also matter for this (A/B/C)?

Can you tell us where you want to use UV as an antibacterial measure?

I'm planning on using it on two places: on my hands, and on a bacterial colony in a petri dish with nutrients.

The CDC's disinfection guidelines lists UV radiation between 328 and 210nm as effective for disinfection, with a maximum of bactericidal activity occurring between 240-280nm. At this wavelength DNA damage (Thymine dimers) is induced with a high rate.
Due to practical reasons UV light is mostly used to disinfect water, if used in rooms there is some effectiveness against microorganisms in the air and some on surfaces, but on one hand the effectiveness is reduced  by square with the distance from the UV source and on the other hand you need completely empty surfaces where nothing casts shadows. The other problems are plastic materials which may get damaged by repeated UV exposure.
Have a look at this reference (only available via Google Books): "Principles and practices of disinfection, preservation and sterilization." and this subchapter.

I'm planning on using it both directly on my hands, with the lamp being quite close to my hands (we're talking about a distance of centimeters here). I'm also planning on shining the lamp on a bacterial colony in a petri dish with nutrients, again with quite a small distance (decimeters, this time).

Be very careful with your hands. This will cause sunburns in a very short time (depending on the source this might happen in minutes).

Would 3-5 minutes be harmful? Because that's how long I'm planning on exposing my own skin. The fear of getting sunburns would, however, be quite a strong reason not to.

With the UV sources that I know from the lab this is definitely enough to get a strong sunburn. But why do you want to expose your skin like this?

I would like to know whether the UV light would be able to kill the bacteria on my hands and disinfect them.

No, mo likely not. Or not completely as your hands are not a flat surface. There will be shadows and areas of low exposure. Plus the risk of sunburns (which can also occur in the eye when you look to long into the lightsource with unprotected eyes. Chemical disinfection works better. Even better is wearing gloves and disinfect them.

Forget the sunburns. The UV kills the bacteria because it is applied at wavelengths and for time periods which cause lots of DNA damage. If you do this to your hands regularly, you're practically inviting melanoma.

@RumiP. It will cause immediate damage to your skin and this is important to keep in mind. This can lead (in the longer perspective) to the development of skin cancer (can also be other forms like squamous cell carcinoma or basal cell carcinoma).


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Why are fibroblast used so commonly in cell biology?
Fibroblasts are some of the most commonly used cells in cell biology. What are the properties of those cells which makes them commonly used ?

I'd guess its because the cells are pretty easy to get and they can be preserved and used over time.

agree with @shigeta. Also, they can be differentiated.

@WYSIWYG Why can they be easily differentiated?

This is more a matter of the cells being cooperative and someone getting lucky and finding a protocol to do so.  There could be and probably are cells that differentiate more easily and are easier to maintain, but we haven't really found them yet.  Now we're getting into a real answer - @WYSIWYG do you want to start putting this in an answer?

From the comments by Shigeta and WYSIWYG :-
1.They are easy to get and they can be preserved and used over time.
2.They can be differentiated easily.
3.Due to historic reasons - someone getting lucky and finding a protocol for these cells.


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Function of heparin and dextran sulfate for removing proteins
From this article :

The reaction was terminated and the histones, and most nonhistones,
  were removed by adding the nuclease-treated chromosomes to a solution
  containing dextran sulfate (2 mg/ml) (Pharmacia), heparin (0.2 mg/ml)
  (Sigma), 10 mM Tris (pH 9.0), 10 mM EDTA, 0.1% Nonidet P40, and 1 mM
  phenylmethylsulfonyl fluoride (PMSF) at a ratio of 1 volume of
  chromosomes to 3 volumes of solution.

What is the function of  dextran sulfate and heparin in removing the proteins ?

See here.
Histones are basic proteins (cationic, high pI) because they are required to interact with polyanionic DNA at physiological pH. Heparin and dextran are polyanions which form insoluble salts with the cationic histones.(Dextran is a polymer of glucose. In dextran sulphate it is derivatised with sulphonate groups creating a polyanionic material.)
Immobilised heparin is sometimes used as an affinity matrix for purification of DNA-binding proteins like transcription factors.


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

Amiodarone blocks potassium channels and block alpha and beta channels.

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

Are your notes a good source of reliable information?

hello again masi, my interstitial fluid & pharmacology friend... yes, the adrenergic receptors work via 2nd messenger not as ion channels... also as I understand it a lot of the class III antiarrhythmics have properties of all the other classes and class II are beta-blocker... so this is confirmation of your source... like you I also have no information about alpha blockade as this is irrelevant to it's effects as an antiarrhythmic... my source is my memory from med school, even less reliable than your notes....

Amiodarone inhibits sodium, potassium and calcium currents. Its major antiarrhythmic properties are thought to be related to prolongation of the
action potential duration. Amiodarone also exerts an antiadrenergic
effect by non competitively inhibiting alpha- and beta-receptors (Ghuran & Camm, 2000).
Alpha blockers relax certain muscles and help small blood vessels remain open by antagonizing norepinephrine's tightening effects on the muscles in the walls of smaller arteries and veins, which improves blood flow and lowers blood pressure (Mayo Clinic). Beta blockers decrease the effects of epinephrine (adrenaline), reducing heart rate and reducing its force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow (Mayo Clinic).
Alpha-adrenergic receptors and Beta-adrenergic receptors are G-protein coupled receptors (Wallukat, 2002). Hence, they do not form channels and your notes are incorrect. The ion currents are mediated by channels, though.
References
- Ghuran & Camm, J Clin Basic Cardiol (2000); 3: 206
- Wallukat, Herz (2002); 27(7): 683-90


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Explanation about cytogenetic notation
What is the correct meaning of cytogenetic notation "inv(4)(p13q22)" ?

Inversions at chromosome 4, at the p arm 13 is inverted AND at q
arm 22 is inverted

OR

Inversions at chromosome 4, the p13 is
Swapped with q22

Do you have a source

Those are the break points of the inversion. So chromosome 4 was cut at p13 and q22 and the fragment was reinserted in the reverse direction, giving a pericentric inversion.

So the explanation number 1 is the correct !!!!

@d.putto Actually neither really sound correct to me.


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

You mean having two differently colored eyes?

Here is another that is now marked as a duplicate of this post and that contains answer that already received several upvotes and are therefore eventually worth checking

At the DNA level there are several mechanisms that  might be cited.
A mutation (change in the DNA sequence) of a gene may actually render one or both copies of the gene defective.  In the case of albino-ism, the skin is pink - no melanin pigment is made at all.  This is a case of both copies of a vital gene being defective and an ability lost completely. A "loss of function" recessive trait.
Blue eyes have no retinal pigment - they are a loss of function recessive. Some cases of genetically inherited diabetes (<1%) dwarfism and obesity are examples of this.  There are many others - many genetic diseases are like this.
This can be caused by a single mutation in each copy of the gene, and others an entire segment of the chromosome can be lost or disrupted by a new, often nonsensical sequence dropped into the gene region.
Other changes can affect the way the genes turn on and off. - similar sequence changes in the regulatory sequences next to the gene sequence will make the gene behave differently. Even babies of african descent may be born with blonde hair and blue eyes and get the darker pigmentation later.  this is genetically caused by a change in they timing of the genes for hair and eye color turning on at other times (blonde hair and blue eyes have little or no pigment, so if the genes are off, then this is what you get).  So when genes are active can cause dominant (always on) versus recessive (sometimes off) patterns. which are because one copy of the gene behaves differently than the other copy.
Sometimes a single mutation in one copy of the gene can cause rather interesting effects. A single good gene and a mutated, less effective gene might result in lost of activity because the mixture of the two genes is different between a wholly functional or wholly variant set of genes.
A classic example is the sickle cell Anemia.  two copies of sickle cell hemoglobin causes the red blood cells to be stiff and misshapen which in turn causes a painful condition in the carrier.  a person with a single copy of the sickle cell gene does not have this problem - is nearly asymptomatic. So we say sickle cell anemia is recessive for the HbS mutation.  but in reality there is plenty of the HbS version of hemoglobin (Hb) in the blood cells, just that the mixture of the two does not cause the anemia.
Much rarer is an additive function from a genetic sequence change.  The immune system is where you will most often see this.  Since the sequences that drive immunity vary widely, some immune sequences are rare - such as inborn immunity to HIV.

+1 for the sickle cell example. However, the phenotype of misshapen cells is dependent on the oxygen loading of the hemoglobin - low O2 -> sickle-cell shape (Stryer, Biochemistry, 3rd ed).

One version or allele of the gene for eye color may encode instructions to make the brown pigment, while the blue allele makes no pigment. Alternatively, it is possible, logically speaking, that the blue allele blocks the productions of brown pigment, but this is not the case.
Now, brown vs blue is not a case of one gene and two alleles. After producing pigment, it must be transported, deposited and such. Many processes are involved. So, the pigment deposition process may be functional or not, but as above, it is often found that a non-functional version is simply non-functioning and not actively inhibiting the process. There are numerous cases where an aberrant form of a protein, encoded by a variant allele, acts as an active inhibitor of a given biological or biochemical process.
The key to your question as written is blue eye color is a lack of pigmentation.

If recessive allele is non functioning then how is it possible for that trait to be expressed in case of homozygous recessive condition?

Sorry to blockquote, but this note from wikipedia gets to the heart of the question:

Which trait is dominant?
The terms dominant and recessive refer to the interaction of alleles in producing the phenotype of the heterozygote. If there are two alternative phenotypes, by definition the phenotype exhibited by the heterozygote is called "dominant" and the "hidden" phenotype is called "recessive". The key concept of dominance is that the heterozygote is phenotypically identical to one of the two homozygotes. That trait corresponding to the dominant allele may then be called the "dominant" trait.
Dominance is a genotypic relationship between alleles, as manifested in the phenotype. It is unrelated to the nature of the phenotype itself, e.g., whether it is regarded as normal or abnormal, standard or nonstandard, healthy or diseased, stronger or weaker, or more or less extreme. It is also important to distinguish between the "round" gene locus, the "round" allele at that locus, and the "round" phenotype it produces. It is inaccurate to say that "the round gene dominates the wrinkled gene" or that "round peas dominate wrinkled peas."

Recommended reading for an overview:

http://en.wikipedia.org/wiki/Dominance_relationship
http://en.wikipedia.org/wiki/Dominant_negative

You can also look to "dominant negative" phenotypes to get a good idea of what "dominance" entails (this was the concept that really locked it in for me in college). One example is Marfan syndrome, where the mutant allele of FBN1 (fibrillin-1) produces a version of the protein that is antagonistic to the protein produced by the "healthy" allele.
Dominant negative and semi-dominant alleles can be seen when the protein forms dimers to function. Activin type receptors form dimers to transduce a signal from an extracellular ligand into the cell. A truncated receptor protein that has the dimerization domain but  lacks the intracellular domain necessary for signal transduction will act in a dominant negative fashion over the wildtype allele: Dimers are formed but the signal is not transduced. This has been implicated in hereditary colorectal cancers.

This is the correct answer here... the others don't really get to the heart of the matter: It's not that there is a dominant vs recessive trait it is - for symplicity sake here - that there are at least 3 versions AA Aa and aa and the first 2 produce the same exact phenotype (albeit they go about it slightly differently possibly) and the third produces a second thing. (didn't read any answer below-so those might be saying the same thing)

A gene is dominant (lets call it B) when its presence in combination with a recessive allele (heterozygotic Bb) leads to the same phenotype as homozygotic BB. A recessive allele leads only to phenotypic expression when it is present twice (homozygotic bb).
To illustrate this rather abstract definition of dominant and recessive alleles let's look at a striking example, namely a gene mutation responsible for albinism.
One of the causes that can lead to albinism is a mutation  in the gene that encodes tyrosinase (TYR). Tyrosinase is used by melanocyte cells to convert the amino acid tyrosine into the pigment melanin that colors the skin, hair, and eyes (Ballantine, 2009). Animals lacking tyrosinase have white skin and hair and red eyes, such as the kangaroo in the picture below (source: Listverse):

One functional gene (B) is enough to allow for pigmentation to occur and hence it is dominant. The other mutated allele (b) produces nonfunctional enzyme, but is recessive as one functional allele produces sufficient enzyme to allow for normal pigmentation in a Bb individual.
In your question you mention blue and brown eyes. AS @Larry_Parnell indicates, in blue eyes the eyes do not contain the pigment melanin and are therefore blue (the blue color is caused by non-pigmented optic effects). Brown eyes are therefore dominant as the melanine colors the eyes such that the blue color is masked (it is still there though). The phenotype of blue eyes is therefore recessive, as one allele for brown eyes is enough to bring pigment into the iris.
Note that other interactions also exist, such as co-dominance (e.g., the ABO blood group system where the genes for A and B antigens are both dominant over O) and incomplete dominance. I refer to the wiki page on dominance here, as the question is not specifically about these interactions.
references
Ballantine. Sci Am February 2009
Wikipedia - Dominance (genetics)

Below are some insights about the evolution of dominance. It does not directly answers your question but understanding how it is thought to evolve also help understand the mechanism governing dominance relationship between alleles.

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright.
Fisher's hypothesis
According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes).
Wright's hypothesis
According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.
Is Fisher's or Wright's hypothesis correct?
Current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. Note also that some other alternative explanations may exist in the literature but Wright and Fisher original hypotheses are by far the most considered hypotheses for the evolution of dominance. During my undergrad, I remember a speaker (but I forgot his name, sorry!) who showed that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be a good explanation as well.

There are 2 main mechanisms.
Case 1: active/inactive product. A gene with 2 alleles: inactive and active, that codes for a cosmetic difference. In the case you gave (brown over blue eye color), the brown coloring is due to melanin.
If you have 1 functioning copy of the gene for melanin in eye color, then this causes melanin to be produced and the brown color overrides whatever would have been there otherwise.
Case 1b: active/inactive paradigm and disease. A common examples are sickle-cell anemia and red-green colorblindness where you need just 1 functioning copy of a gene to avoid negative health effects. These are insidious for inheritance purposes as it can make people asymptomatic carriers of heritable diseases (even worse in the era before genetics and biology as a field of study since there would be families with widespread, unpredictable, unexplainable occurrences of various diseases - often explained as a "curse" by those who didn't know better)
Case 2: the spoiler. This dominance pattern tends to be associated with genetic diseases where a mutation causes a protein to go rogue and damage its host. Having even one copy of such a mutation is a bad thing, and worse because the chance of handing it down to the next generation is roughly a coin flip (if you have 1 copy) and guaranteed (if you have 2 copies).


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What is the name of the condition where no pacemaker cells are active in the heart for a short-time?
Assume that the heart is beating, but no pacemaker cells are working for at least 15 seconds.
This would be a very long compensatory pause if extrasystole started it.
There may be some low frequent cells working at lower frequency (less than 10 Hz) but I do not understand what.
What is the name of condition where main pacemaker cells are not beating?
Main pacemakers are SA-node, AV-node and Purkinje-fibers/His-bundle.
Raoul is correct.
This is called asystole.
It is temporal in the above case.
My definition in research but note the difference to current Clinics so you do not get confused: Asystole is a state of no cardiac electrical activity from pacemaker cells when the conduction system and cardiomyocytes can be still functioning (so the case in my thread). The conduction system and cardiomyocytes of the ventricles are responsible for the bradycardia in my case for short-term.
What do you think about this case?
Some bradycardia?
Can you suspect asystole there between?

Please, do not make diagnoses based on just this picture (which is often the current standard).
Assume case where you see Time-Frequency of the heart perfectly and where you can see exactly the functioning of pacemaker cells at different frequency levels.

Masi I have edited the question title which was confusing, please feel free to roll back

If there are no pacemaker cells active, no muscle contraction will occur. This condition is named asystole. It can be a temporary or definitive condition. Some would call it "extreme bradycardia" in temporary cases, but this is just an euphemism.
Edit:
Ok, so let's try to clear up the confusion a bit. Technically, there is no asystole involved here (not even temporary). This rhythm is regularly irregular (irregular, but has a pattern), while asystole has no pattern by its very nature.
What you are seeing here is not the consequence of low frequency firing from pacemaker cells. The supraventricular extrasystoles (every 3rd QRS complex) are a consequence of early ventricular depolarization not triggered by SA node activity. The P wave that would normally trigger the 3rd complex does in fact occur, but it is synchronous with the abnormal QRS complex, which is why you cannot see it. The compensatory pause is due to lengthening of the hyperpolarized state in pacemaker cells, and is a consequence of the addition of the hidden P wave and the extrasystole in a short time.
In conclusion, this pattern is not the result of delayed pacemaker firing, but of early depolarization of cardiomyocytes by an accessory pacemaker.

I have marked on this strip the maximal time interval of SA node hyperpolarization. Depending on when the P wave hidden in the extrasystole occurs, the real time may be shorter than the above interval.

Thank you for your fast answer! You are right. It is temporal asystole. I added a case picture which I think is little bradycardia and suspect asystole. What do you think?

As you can see, there are 12 QRS complexes on this 14 sec. time interval, which yields a ventricular frequency of 51/min. This is termed bradycardia. Furthermore, every third complex has an altered signal, is not preceded by a P wave, and is followed by a compensatory pause. Those complexes are supraventricular extrasystoles, and the rhythm on this strip is termed "trigeminism".

I think the case is extreme bradycardia and asystole. What can give frequencies of 5 Hz for 10 seconds? Probably something starts to excite when bradycardia reaches its maximum at 3s (first missing P wave).

I suggest that you read a bit on supraventricular arrhythmias, and especially trigeminism.

Let's define extreme bradycardia as the condition which starts asystole for some period of time. I think it is not now blunt.

Thank for the edit! Please, see my updated definition of the asystole. What do you think? I defined it as no cardiac electrical activity from Pacemaker cells.

You are right. There is extrasystole just about at 3 second (early depolarisation), after which no action potential is done from main pacemakers for the rest of the time and bradycardia. So the condition when main pacemakers do not work (like for 10 seconds) is called temporary asystole, right? During this time, I agree with you what you describe, but I am just interested on the condition when main pacemakers do not work for 10 seconds although QRS complexes can be seen but with those conditions you describe.

On the above strip, the inactivation (hyperpolarization) of the main pacemaker (the SA node) starts on the 3rd P wave (hidden in the abnormal QRS complex) and ends on the subsequent P wave, triggering a new (normal) QRS complex. If the pacemaker did not work for 10 seconds, you would have either an escape rhythm than can be junctional (SA node inactivation only), ventricular (SA & AV node inactivation), or a 10 second asystole. This is not apparent on this strip. Here, the inactivation can be estimated to be 1.4 sec. at most.

Yes, I think this is a escape rhythm where a 10 second asystole. You should visit me in some conference such that you could see my research. I know that the temporary asystole is not apparent in the strip. By current guideline, you estimate the inactivation to be 1.4 seconds if you take risks - this is a boundary case!

I accepted this answer because of the phrase Escape rhythm with a 10-second asystole where the last choice of the type is backed by my research.

Bradycardia is a heart rate under 60 beats per minute. Your strip shows a heart rate of ~54 BPM (so, yes, it's bradycardia), and the rhythm is trigeminy. There is no asystole involved.
In the following rhythm strip, initially it shows supraventricular tachycardia (of >150 BPM). After adenosine administration, a short period of asystole occurs, allowing the SA node to resume it's normal pacemaker rhythm., then resumption of sinus rhythm (at just under 100 BPM). Notice there are **no electrical complexes) during the asystole. It's not a matter different guidelines. There is no asystole in your rhythm strip.

How can you say that there is no asystole involved? Do you have evidence?

Ok, I am doing research here. In clinics,only clear asystole  can be detected. I am trying to detect asymptomatic asystoles which occur only short time.

Please read about event-triggered cardiac monitoring.

I know Holter but it is very cumbersome and errorprone, even single important beat can be missed. Current approach in clinics tries to take bigger sample of data - this is ok with current imaging technology, but requires much resources. 48h Holter is now standard. I am researching cardiograms and developing their imaging technologies. I can propose that the case has partial asystole with pacemakers of extremely low frequency active (not even Purkinje/His fibers). And this is confusing me, since I do not understand what can cause so low frequency.

This is what electrophysiology is all about. Event triggered monitoring can be for 30 days, is different from Holter.

Yes, you are right. We are actually doing the same things, just different point of views how to approach these challenges. I am doing algorithms for these devices and trying to use significantly less data to the analysis. It would be nice to have some good Review article about Electrophysiology with right sources. I have an intuition that the problems of missing significant peaks in Holter cannot by completely bypassed by these Event triggered monitoring (just taken longer data - you must have much simpler algorithms). It is probably about particle-swarm-optimization with simpler application.


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Manufacturing toxoids

Toxoids produced by tetanus and diphtheria bacteria are detoxified
  with formaldehyde, yet their antigen properties remain.

Source : Biological Science by Taylor
What does formaldehyde do ?

The toxins of both Clostridium tetani and Corynebacterium diphtheriae are so toxic that you cannot use them for immunization, since the amount needed for proper antibody production would kill the individuals. For that purpose the toxins are "de-toxified" by reacting them with formaldehyde which takes away the toxicity but the resulting toxoids are still immunogenic.
This happens by the reaction of the formaledehyde with the free aminogroups of the sidechains of the amino acids to form azomethin groups. This changes the protein so much, that it cannot bind to glangliosides any more which renders it untoxic. The immune system can still recognize unmodified parts (for this 8-10 amino acids in one stretch are enough) and make antibodies.


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Immune reaction to "new" protein
I read in Bruce Alberts Molecular Biology of the cell :

Normal mice,for example, cannot make an immune response against one of their own protein components of the complement system called C5.
  Mutant mice, however, lack the gene encoding C5(but are otherwise
  genetically identical to the normal mice) can make a strong immune
  response to this blood protein when immunized with it. Natural
  immunological tolerance for a particular self molecule persists only
  for as long the molecule remains present in the body. If a self
  molecule such as C5 is removed, an animal gains the ability to respond
  to it after a few weeks or months. Thus, the immune system is
  genetically capable of responding to self molecules but learns not to
  do so.

So, why does an immune reaction not happen when a new protein is introduced to patients lacking it ? For example if you give clotting factor to hemophilic patient.

They actually can produce antibodies against the clotting factor (as @Xylo pointed out, many patients do produce the clotting factor that's being replaced, just in insufficient quantity, which lowers a lot the risk of an immune response). The antibodies against the clotting factor are called inhibitors. See here for more info.

Thanks !  In the link you provide, it is written that the reason for this is uncertain. Do you think the reason could be the one I pointed out in the post ?

Yes, and my understanding is that the uncertainty resides in the fact that even some patients which do produce endogenous clotting factor sometimes react, while you'd expect they shouldn't.

Does the endogenous clotting factor reaction classify as autoimmune ?

Sometimes the antibodies are actually the origin of the clotting problem and in that case yes, absolutely. Now when the patient is naturally lacking any production of that factor and the antibodies appear due to therapy, then I guess so but I'm not sure, sorry.

You are absolutely right in that there will be immune reaction against proteins that are not naturally present in the body.
However, hemophilia is not caused by complete lack of protein. It is due to loss of function of the clotting factors due to mutations. The proteins are still present, but they do not have the ability to bind and/or activation of their catalytic function. So, there will be no immune activity against exogenous clotting factors given to hemophiliac patients.

Thanks !   I am not able to recollect any examples but isn't there any disease where a protein is totally not made and then we artificially give that protein ?

When it comes to genetic disorders, you have to remember humans have diploid chromosomes. Most eukaryotes are diploid. So, if there is deletion of a gene on one chromosome its allele would still be present and its gene product will be made in the tissues/cells that they are normally expressed.

ok! SO it is extremely rare that there will be disorder such that no protein is expressed but I think there can be at least one !

I cannot recall any specific disease where both copies are deleted. But, it is possible.  An example of the situation you are describing would be blood determinant antigens, O, A and B. When people with O-type are transfused with A-, B- or AB-donor blood, there will be immune reaction against it.  So, to summarize, if you transfuse with protein  that was not present will definitely generate an immune response.

In hemophilia, it will not as the protein is already present albeit in active state.

This is a concept of the immune system called "Immune tolerance". Basically it makes sure, that you cannot make antibodies against yourself (which would obviously be bad).
New antibodies are "tested" against the body and if there is an autoreactivity, the corresponding B-cells go into apoptosis.
If this self-protection does not work, this leads to autoimmune diseases like SLE.
The Wikipedia article about it is quite nice for the beginning and also has a lot of references for further reading.


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Shine-Dalgarno sequence and expressing proteins

Shine-Dalgarno sequence present in the prokaryotic mRNA plays a role in initiation of translation. In eukaryotes a Shine-Dalgarno like sequence is present but does not play an important role in initiation of translation.
We often try to express a eukaryotic gene in a prokaryote. For example : expressing insulin gene in E.Coli.

My question : If eukaryotes do not have the shine dalgarno sequence , then how can a eukaryotic protein be expressed in a prokaryote ? (I am especially interested in knowing about this in case of cDNA expression)


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SNP genotyping using PCR
I read this wikipedia article on SNP genotyping and wasn't able to understand this part :

In examining the results, if a genomic sample is homozygous, then the
  PCR products that result will be from the primer which matches the SNP
  location to the outer, opposite strand primer as well from the two
  opposite, outer primers. If the genomic sample is heterozygous, then
  products will result from the primer of each allele to their
  respective outer primer counterparts as well as from the two opposite,
  outer primers.

Can anyone explain this ?

Valid XHTML http://nar.oxfordjournals.org/content/29/17/e88/F1.large.jpg.
Figure 1. Schematic presentation of the tetra-primer ARMS-PCR method. The single nucleotide polymorphism used here as an example is a G→A substitution, but the method can be used to type other types of single base substitutions. Two allele-specific amplicons are generated using two pairs of primers, one pair (indicated by pink and red arrows, respectively) producing an amplicon representing the G allele and the other pair (indicated by indigo and blue arrows, respectively) producing an amplicon representing the A allele. Allele specificity is conferred by a mismatch between the 3′-terminal base of an inner primer and the template. To enhance allelic specificity, a second deliberate mismatch (indicated by an asterisk) at position –2 from the 3′-terminus is also incorporated in the inner primers. The primers are 26 nt or longer, so as to minimize the difference in stability of primers annealed to the target and non-target alleles, ensuring that allele specificity results from differences in extension rate, rather than hybridisation rate. By positioning the two outer primers at different distances from the polymorphic nucleotide, the two allele-specific amplicons differ in length, allowing them to be discriminated by gel electrophoresis. (http://nar.oxfordjournals.org/content/29/17/e88/F1.expansion)


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How well do we notice asynchronicity?
I'm stopped at a stoplight and, with nothing to do, my thoughts wander to the timed don't-walk sign that governs any pedestrians who might wish to cross the street I'm driving along.
I can see two such signs, one on my side of the cross street, and one across the way. They are synchronized: each counts down the seconds at exactly the same time as the other, as far as I can tell, lighting up as "5", then a second later as "4", etc. Nothing's wrong with my ocular nerve or brain, as far as I know. Can you fill in the blanks please?
I can be …% sure that the lights are synchronized within … seconds of one another. (Not something trivial like "100" and "1", of course.)

I'm only familiar with human perception of audio-visual asynchronies, but in that case it is highly context-dependent and varies by individual. Under best-case scenarios, humans can detect an audio delay of 100 milliseconds. Under more normal conditions, 200-300 milliseconds is the threshold for perception.  I would imagine we'd be better at detecting asynchrony between two visual stimuli in general, but the fact that you can't look at both lights at once probably makes it harder to detect asynchrony. So it's probably hard to know what the result is on balance without testing it specifically.

Thanks for the info, @seaotternerd. I figured it varies widely by individual, which is why I asked for a confidence interval rather than a straight answer.

The lights are probably working off the same controller, so actually are synchronous to within maybe the few nanoseconds it takes electrical impulses to travel through different length wires.

Can I add something to the question? What about audio delay in audio visual clip?

@DevashishDas - your added question is about intersensory asynchrony; for the answer see the answer on this question: http://biology.stackexchange.com/questions/31505/latency-differences-between-our-senses/31666#31666

@jamesqf Well, assume we don't know that: assume it's not necessarily true.

Short answer
I can be 75% sure that the lights are synchronized within 0.02 - 0.2 seconds of one another.
Background
Interesting question, but hard to answer! Because it has been unanswered for quite a while I will try to formulate an answer that may provide an approximate value for the minimal asynchrony perceivable.
The temporal resolution of the visual system can be quantified in a number of ways. As you are referring to relatively simple stimuli, the critical flicker fusion frequency is probably the most relevant. At a certain critical frequency, a flickering stimulus will appear as a continuous stimulus (Holcomb, 2009). For example, the good old CRT screens can sometimes seem to be flickering. The mains is 50 Hz (US) or 60 Hz (Europe, Australia), and indeed the critical flicker fusion frequency is 5 - 50 Hz, dependent on the lighting conditions (Kalloniatis & Luu). Hence, stimuli separated by 200 ms (low lighting) to 20 ms (high lighting conditions) can be temporally resolved.
I am aware that your question is different, as you ask whether two stimuli on the retina can be perceived as being asycnchronous. Flicker fusion testing is mainly done with flash stimuli, i.e., a single stimulus per image, not two. However, from the various measures of temporal resolution of the visual system that have been used to date, the critical flicker fusion has the most conservative value, in that it provides the top-value of temporal resolution. Higher-level processing is much slower and values of around 4 Hz are obtained. For example, when subjects are tested on a stimulus of dots that are white when moving right and black when moving left, and they change directions/colors at a certain frequency, it becomes hard to tell whether the color change and direction change are synchronized at alteration rates of ~5 Hz and higher (Kalloniatis & Luu).
As to your question what the percentage chance is that stimuli separate by 20 -200 ms are separable, I can say that in general, psychophysical procedures determine the threshold defined as halfway between chance and 100% correct. Assuming a typical yes/no tasK (are the traffic lights synchronous yes/no?), chance would be 50% (guessing), and threshold would thus be defined as halfway between 50% and 100%, i.e., 75% correct.
References
- Holcomb, Trends Cog Sci 2009; 13(5): 216-21
- Kalloniatis & Luu, WebVision, chapter "Temporal Resolution" 2007

authors: محمد الخثيميً