Does a reduction in stem cells mean possible earlier death? The basis of this question relies on my understanding of these 2 facts:

1) A person has a certain number of stem cells from birth
2) Stem cells are the basis of all cells and are used to repair and replenish

I read an article about stem cells being found in fat removed by lipsuction and that the trials that has been done on using these stem cells for repair elsewhere in the body.

My question is, if stem cells are used for repair in the body and you have a certain amount of them, if you "lose" some via liposuction, does this then mean you have less stem cells and therefore less chance of repair and could then theoretically die sooner?

It's more than likely my lack of knowledge on the subject but I would like to understand why.

Stem cells persist because they have the capacity to self-renew.  At birth you will have a finite number of each stem cell type (e.g. hematopoietic stem cells that make blood, gut epithelium stem cells that make gut lining etc).  The general picture is that as tissues require replenishment, a stem cell divides. One daughter cell starts to differentiate (and divide) into mature cells required by the tissue, whereas the other daughter cell retains stem cell function.

So a stem cell is typically defined as a cell with the capacity to: (i) self-renew and  (ii) to give rise to one or more cell types in a tissue. A hematopoietic stem cell can give rise to T-cells, B-cells, neutrophils, red blood cells, platelets etc.  The ability to self-renew means that, in general, stem cells don't 'run out' during a lifetime.

[ Its important to note that to define a cell as a stem cell, scientists use strange hybrid of: in vitro or animal assays + cell surface markers + location in the tissue + measures of 'having the capacity to make continued contribution to new cells'.  So lets just say that stem cells are only ever as well defined as our choice of assays combined with the interpretation of those results. ]

I mention the challenge of defining stem cells because, in recent years as assays and technologies improved, cells such a oocytes (eggs) or adult neurons, which were once thought to be finite, have been shown to have be replaced/renewed, presumably by some 'stem cell like' cell(s).

As noted above, stem cells are usually involved in the replenishment of a particular tissue type.  So liposuction, which will remove fat cells, should not affect the numbers of hematopoietic or neural stem cells and so on.

Any claim of clinical benefit of a 'stem cell treatment' using liposuction should be backed by clear data.

A longer answer would get into:
(i) the concept of 'plasticity' where the classical view - a fixed pathway between a stem cell giving rise to one daughter cell that  gives rise to mature cells and the other returns to a stem cell state - is open for debate, and
(ii) the idea that since stem cell definitions are only as good as our assays, there may be potential plasticity even among stem cells that we cannot 'detect' yet.

Theoretically, yes. Although, to my knowledge it has not been proven. As far as I'm aware there is no known link between liposuction and leukemia, liposuction would most likely not remove enough stem cells to produce such an effect. I've been doing a lot of research into stem cells lately and from what I have found there have not been many, if any, in depth studies on the impact of stem cell removal as the implantation of stem cells is usually the main focus.


How does noradrenaline result in rise of systolic blood pressure even when the cardiac output is decreasing? Systolic blood pressure[SBP] depends on the cardiac output. When Nor adrenaline is given there is vasoconstriction due to alpha-1 action on blood vessel, vasoconstriction results in increased total peripheral resistance and thus increases the diastolic blood pressure. The beta-1 action [increase in cardiac output] on heart by Nor adrenaline is counteracted by the reflex bradycardia  resulting in decreased cardiac output. Given the fact that SBP depends on cardiac output and the cardiac output is decreasing, why is there a rise in SBP on administering nor adrenaline?

Your question involves comparing an observed response to administration of noradrenaline/norepinephrine, which causes vasoconstriction thereby increasing the BP (during both systole & diastole,) to the hemodynamic/pharmacodynamic response of the cardiovascular system as a whole, which is decreased cardiac output & decreased cardiac work.  This is similar to asking why opening a finite water tank eventually slows down even though the pressure increases when you turn on the faucet.


Where do mushrooms get their energy from? I'm wondering where field mushrooms get their energy from.
I've heard that they can easily grow on soil in a dark room. So, it seems to me that there wouldn't be any photosynthesizing plants from which they could get energy. Also, as far as I know, they don't have seeds from which they could directly get energy initially.

So, I have two questions:

Where do mushrooms get their initial energy from? (The spores, if that is the right term)
Where do they get their energy from in later stages? (If there is a difference at all)

Mushrooms are the fruiting bodies of fungi. Fungi get their energy by decomposing dead or decaying organic material, such as fallen leaves or dung.

Some background: spores of fungi germinate forming mycelia consisting of threadlike hyphae. When the hyphae of different fungi meet, they may have sex and form mushrooms. The mushrooms produce the spores. See https://en.wikipedia.org/wiki/Fungus.

So, each of these stages get their energy ultimately from decomposition, although the mushrooms get their energy from the mycelium. Spores rely on their internal energy storage to germinate and start decomposing. Even though spores are tiny, the have energy stored, like all cells do.

Research mushroom " metabolism/enzymes/catabolism/respiration/glycolysis" to read nice texts of concise info for that topic.

Mushrooms use enzymes to break down cellulose and substrates into smaller substances and eventually they use CO2 for respiration, glycolysis, and ATP production.
https://books.google.fr/books?id=xmB_DYPp9LIC&pg=PA49&lpg=PA49&dq=mushroom+metabolism&source=bl&ots=mEkG_WGfaY&sig=9XAXzpPgSMHkRg_8kPjE1LIYatQ&hl=en&sa=X&ved=2ahUKEwjfwJvjmLLdAhXjx4UKHUiiA_UQ6AEwA3oECAkQAQ#v=onepage&q=mushroom%20metabolism&f=false

Cellulose is not that different from sugar and mushrooms get sugar from it using cellulase and lignase enzymes, although some mushrooms dont have cellulase. https://www.google.fr/url?sa=t&source=web&rct=j&url=https://www.researchgate.net/post/What_are_the_nutrients_required_for_the_growth_of_mushrooms_like_oyster_and_shiitake/amp&ved=2ahUKEwj4pLC3m7LdAhWRyIUKHf27DD0QFjACegQICBAB&usg=AOvVaw2b-TTVDZHQBcS8l-TMYmz0&ampcf=1

Its the digestion process is probably a complex physical absorption by the hyphae, so research hyphae structrures, they must be cool.
https://www.ck12.org/biology/fungi-nutrition/lesson/How-Fungi-Eat-BIO/


Why do women mature (physically) earlier than men? All sources I've read (the first page) states that the fact that women mature (in the sense of physical maturing) earlier than man is caused by the earlier selective prunning in brain. Though, this is an explanation just for the mechanism, not for the cause.

So what is the real evolutionary reason women mature earlier (though, probably slower) than men?

This is a question about Neoteny and Heterochrony.

The closest field of study which will have specialists of this kind of topic is the study of the late maturation of humans compared to other species, which has had some research: 5-7 years ago there were some papers measuring the different bone growth rates of humans compared to chimpanzees and exploring the notion of natural selection through preference of immature traits: being attracted to girls with child like faces, smaller nose, large eyes, small voice, babyish, with various causes for example allowing for later brain pruning and longer brain development.

If you research in google publications you can find some research on the topic, for example:

Heterochrony in human evolution: the case for neoteny reconsidered

Sexual selection, physical attractiveness, and facial neoteny: cross-cultural evidence and implications (1995)

The origins of sex differences in human behavior: Evolved dispositions versus social roles.

It's all about evolutionary selection due to survival fitness. A complex age dynamic is at work in human evolution due to our extended lifetime, memory and brain size, amidst heavily variable social patterns (mate selection, monogamy, tribe size, bride rights, patriarchal/matriarchal systems) in paleolithic humans.

Bonobos mature at roughly the same time: 9 years, and female bonobos have a baby at 11 to 13 years. I think that illustrates the flexibility of maturation age according to the role of the adults.

Human females can have babies in between 9 and 15 years for the most part, some of them at 7, so maturation age is an evolutionary trait rapidly changeable according to fitness of the resulting offspring, so it is entirely fine tuned by survival performance.

EDIT: I wrote this answer to be helpful, but apparently my lack of sources and "errors?" deserve a mark down. so here is an additional text:

"They found that Paleolithic girls arrived at menarche - the first occurrence of menstruation - between seven and 13 years. This is a similar age to modern girls, which suggests that this is the evolutionarily determined age of puberty in girls.

'This would have matched the degree of psychosocial maturation necessary to function as an adult in Paleolithic society based on small groups of hunter-gatherers,' they write.

Disease and poor nutrition became more common as humans settled, causing puberty to be delayed. Modern hygiene, nutrition and medicine have allowed the age of menarche to fall to its original range.

However, today there is a mismatch between sexual maturity and psychosocial maturity, with sexual maturity occurring much earlier. This mismatch is a result of society becoming vastly more complex, with psychosocial maturity therefore taking longer to reach."

Note that they are talking about female adult paleolithic maturity and tasks at that age. Females compete for mates by attractiveness and fitness, and some research suggests that males compete for females by other mechanisms, even force or threat.(ref)

There is clearly a reason for which men are available to make and care for their offspring later than females. Females prefer older males by at least a couple of years with moderate adult muscle mass(ref), and in our species males of 17 to 35 years are biologically the strongest and wisest. Nature would have it that 11 /13 year old fathers clearly are counter productive to the survival of their partner and child in an ordinary setting of hunter gatherers, because of the very long gestation and complexity of human survival tasks.

The human mental maturation range has a wide variety of deviation, and between the age of 8 and 25, we are pre-programmed to be in an intense task of learning and physical adventure. Physical coordination of the male can reach an optimal level as late as the age of 22, 3/4 years after his bones have finished growing and his muscles and reflexes have had time to increase and adapt to his new frame, which is why athletes are at their physical peak between the ages of 18-27, and the "mental pruning" article suggests that their mind continues to re-organize itself well beyond the age of 30. During that stage, a human male is programmed to learn a wide array of advanced skills: flint knapping, tool making, botanic knowledge, hunting skills, clothes making, landscape exploration, orientation, memorization of food places, wells, tree climbing, metal work, net weaving, pottery, pigments, weapons, blow darts, wild animal experience (game, lions, rhinos, birds, rodents, traps, stalking, poisons, frogs) etc... All that time based survival experience reinforces the notion that a male reaches his functional optimum as a provider and protector of his family well after his sexual maturation age.

Females have a less physically intensive role to play in human society. While they can learn all the hunting/survival skills of the male, their central role is to be nourished and provide for the child(ref). Their parenting tasks rely less on individual memory because they stay socially at home more (papua new gineans, africans, aborigines, yanomami). Their task can be less intense physically, require less physical training, and can be less intensive on memory and adventure (being nourished, childcare, craftwork, leadership of the group at home and less in exploration and precarious tasks). Both the human male and female memory has a very important role for guiding the group. A female can provide guidance up till the age of 50-90 in a natural setting.

Females are generally less expendable and adventurous than males, because a male can potentially have 3 offspring every day, he is limited by the number of females, and she can only have 1 offspring every 9 months, she is more precious to the multiplication of the group.

Add to that the function of memory, hunter gatherer fitness, and social acumen, absorption of mental and survival skills

Other great apes have gestation periods arount 8.5 months compared to our 9.

Because of the difficulty to assess the paleolithic social and environmental pressures that caused the sex age maturation difference, it's a question that theorists would be unwise to wade into to any great depth, in an academically competetive field. A good anthropologist should be able to list all the predominant selection factors.


Why don't we see life form again and over again? If life formed on earth by natural laws, why can't we observe the formation of life from matter today? Is it because this is a rare phenomenon? It seems just after formation of earth life formed on earth and around 2-3 billion years has passed. It must be enough time for life to form several times from scratch.

The first life was probably so fragile and simple we would likely not even recognise it if it did appear. We don't know exactly how, or where, life first appeared but nearly all theories suggest simple collections of enzymes in protected environments that slowly gather the mechanisms needed for free-living life over time.

This works in the ancient world because there is no competition so even the simplest and most inefficient replicator is able to reproduce, spread, and advance. Today, any new life would have to compete with existing life which has had billions of years to evolve into highly efficient forms. A new abiogenesis event would simply pass unnoticed, a brief flicker quickly snuffed out by modern life.

The answer may be that life did not form on Earth. There is not even the slightest hint of evidence that life formed on Earth. The known facts about early lifeforms on Earth from fossils and everything we know about geology of the early Earth and the Early solar system is at odds with abiogenesis having occurred on Earth. One of the arguments against abiogenesis on Earth is precisely the question asked.

The problem is not just that we don't see life forming in a natural environment, as this can be easily explained away by invoking competition from other life forms. Also one can note that the conditions on Earth today are different from that of the early Earth (oxygen is poisonous to early life forms). A more fundamental problem is that we can't reproduce some of the fundamental chemistry needed for abiogenesis in the lab under conditions that have existed on our planet during the time life could have evolved.

E.g. the synthesis of ribose, which is the backbone of RNA from inorganic chemicals does not seem to be possible under Earthlike conditions. A recent experiment demonstrated that under intense ultraviolet irradiation of water, methanol and ammonia under cryogenic conditions at extremely low pressures one can form ribose in the lab. Similarly, we cannot get amino acids to form under Earth-like conditions, we again need to resort to irradiating interstellar ice analogues in near vacuum conditions.

We also need to consider how can we end up with only left or right handed molecules of each type as found in Nature. It has been demonstrated that replicating systems where both variants are presents, will lead to an end state where only one type will survive. But we then get domain formation where in different disconnected farts the symmetry will be broken in a random way. This may be good enough to explain why we only have left-handed life on Earth today.

An alternative idea is to invoke the fact that the Weak interaction does not respect parity symmetry. Now the Weak interaction is too weak to be relevant for molecular dynamics. But in radioactive beta-decay, this interaction plays a dominant role, beta-radiation consist of only left-handed electrons. One can then postulate that abiogenesis happened in an environment where there was irradiation by cosmic beta radiation, which would lead to an asymmetry in the breakup of chiral molecules, which would then be further amplified by auto-catalytic processes. This is the Vester-Ulbrict hypothesis, which was recently been successfully put to the test in the lab.

Another argument against abiogenesis on Earth is that the required far from thermal equilibrium conditions never existed on Earth, while they do exist in objects like comets and proto-planets. This is more general argument than the examples given above. Basically, what you want is to get to a collection of self replicating molecular machines from their simple building blocks, without there being any machines to build them from scratch.

Molecules in living organisms are synthesized using extremely complex molecular machinery such as the ribosome. Without such machinery, the natural environment has to play the role of the agents involved in the construction. What is needed are both far from thermal equilibrium conditions and places where half build, unstable molecules can be metastable, allowing the complete molecule to appear. This suggest that cryogenic conditions should play a role here.

We can also note here that life on Earth exists in a compartmentalized form, all the chemistry happens inside a lipid membrane (a cell). Many of the essential molecules would not be stable in a hypothetical environment that could have existed in Earth's geological history. Then just like life today exists mainly in conditions that were hostile to early life forms (the oxygen in our atmosphere would kill them), similarly it may well be the case that conditions on Earth have always been hostile to processes that could lead to abiogenesis.

The molecules essential for life as we know it may have evolved without any compartmentalization in the interior of comets or proto-planets (this would qualify as life in the sense of an auto-catalytic process that is capable of evolving), compartmentalized lifeforms could have arisen later there.

A different argument comes from the conditions in the early solar system and what we know about life on Earth from the geological record. The earliest evidence for life on Earth dates back to 3.7 billion years ago. These are stromatolites, which then shows that 3.7 billion years ago there were very sophisticated life forms on Earth.

Petty much all of the enormously complex molecular machinery found in modern cells had to be present already in the bacteria that formed these stromatolites. Abiogenesis would thus have had to occur quite some time earlier. However, from 4.1 to 3.8 billion years ago, the inner solar system was subject to what is called the Late Heavy Bombardment (LHB). During this period the conditions on Earth were rather inhospitable for life. Whether life could have survived impacts so large that oceans on Earth would have evaporated is a matter of ongoing debate.

One has to note here that the people who argue that life did evolve on Earth during this period, tend to favor LHB scenarios that are one the extreme limits of the geological scenarios, one then assumes that it was not that much of a big deal, e.g. the largest impacts could have been smaller than what most geologist think. However, recent geological evidence points in the opposition direction. It has recently been found that the size of the impactor that formed Mare Imbrium on the moon was enormously larger than was previously estimated. The impactor is now estimated to have had a diameter of 250 km.

Taking into account that the Earth is a much larger target than the Moon, so it would have been hit more frequently than the Moon and the largest objects to hit the Earth would also be larger than the largest ones to hit the Moon, the idea that perhaps the LHB was not so bad for life on Earth becomes quite problematic.

But the main argument against abiogenesis on Earth is simply the lack of evidence in favor of it; it shouldn't be a surprise that that things don't add up when one assumes the truth of a hypothesis that is not supported by any facts.


What is the maximum altitude where humans can survive? What is the highest altitude that a human can survive without being pressurized?  Let's assume that oxygen and heat/insulation are not the limiting factors?
Why I asked.

Short answer
Between 62,000 and 63,500 feet (18,900 and 19,350 meters) blood begins to boil at body temperature. This altitude, referred to as the Armstrong limit, is generally considered to be the absolute limit compatible with life. At this point, humans cannot survive without pressurization measures.

Background
Atmospheric pressure drops at higher altitudes. As you go higher into the atmosphere, gases start to expand due to the lower atmospheric pressure. This is what causes your ears to pop when driving up in the mountains or when an airjet lifts off. At altitudes higher than 10,000 feet (3.5 km) people unaccustomed to the reduced atmospheric pressure may become short of breath or experience dizziness. At altitudes above 20,000 ft (6.1 km) supplemental oxygen is required to support life and at 34,000 ft (10.4 km), 100% oxygen is necessary to equal the partial pressure of oxygen in sea level air. Above 40,000 ft (12.2 km), 100% oxygen must be administered pressurized (NASA).

Altitudes above 50,000 ft (15.2 km) are considered near-space and man requires a pressurized suit to be safe. At 55,000 ft (16.8 km), atmospheric pressure is so low that water vapor in the body starts to boil at ambient temperatures, causing the skin to inflate. At 63,000 ft (19.2 km) blood at normal body temperature (98 F / 37oC) starts to boil. At altitudes above 65,000 ft atmospheric pressure approaches that of space, i.e., a vacuum (NASA).

Between 62,000 and 63,500 ft (18.9 - 19.4 km), blood at body temperature (37oC) begins to boil. This is the point beyond which humans absolutely cannot survive in an unpressurized environment. This point is named the Armstrong limit, after Harry George Armstrong, who founded the U.S. Air Force’s Department of Space Medicine in 1947. On Earth, the Armstrong limit is somewhere between 62,000 and 63,500 feet (18.9 and 19,4 km), or about 12 miles.

As a reference, the highest point on earth is the peak of the Mt. Everest at 29,000 ft (8,8 km).

Above the Armstrong limit, water in the soft tissues of your body vaporizes, causing gross swelling, though the tight seal of your skin would prevent you from actually bursting apart. Your eyes, likewise, would refrain from exploding, but continued escape of gas and water vapor leads to rapid cooling of the mouth and airways (Goslin, 2008).

Water and dissolved gas in the blood forms bubbles in the major veins, which travel throughout the circulatory system and block blood flow. After about one minute circulation effectively stops. The lack of oxygen to the brain renders you unconscious in less than 15 seconds, eventually killing you. When the pressure gets very low there is just not enough oxygen, which is thought to be the first and most important concern (Goslin, 2008).

Note that under conditions of near-vacuum, death is not instantaneous. At one three-hundred-eightieth of atmospheric pressure at sea level, dogs were shown to survive up to 90 seconds. During their exposure they weren't in a great state (the dogs were bloated, ice covered their tongue, and many more horrible facts to be read in (Goslin, 2008)). Monkeys were even shown to cope for 3.5 minutes under these conditions.

Reference
- Goslin, Sci Am February 2008

I thought it was about 5km, pregnant women are unable to function at this height & red blood cells are so thick the heart is pumping soup.


What are some potential consequences for attempting to cure Type one Diabetes? Type one diabetes has been in my family for a few generations. As a carrier and having a mother with the disorder, I've done a lot of research on it. As I am completing my High school Biology course, I've gotte a better understanding of how the disorder may be treated. (Stem cell therapy, gene replacement, etc). Here's a hypothetical scenario: Scientists develop a modified virus that contains a normal person's beta cell genetic makeup, injects it into the pancreas, and reproduces. The virus and beta cells reproduce, and the body detects the virus, but not the beta cells. (or neither, and the virus is not harmful). The beta cells create insulin, and the Diabetes is cured. Would this work, and would this hurt the immune system? Would it be possible for the scientists to blunder and either create too potent a virus or too much of the virus?

High school biology apparently failed to teach you that many conditions, like type I diabetes are not classically Mendelian. The term "carrier" does not apply to you...you are just someone with a predilection who hasn't developed the condition (but who might...I have heard of someone developing type I diabetes in college)

  Scientists develop a modified virus that contains a normal person's
  beta cell genetic makeup,

How much DNA do you think you can cram into a virus?  Not having the right beta cell DNA is almost certainly not the cause of type I diabetes, anyway.

  The virus and beta cells reproduce, and the body detects the virus,
  but not the beta cells.

How do you think the immune system responds when it detects a virus?  Hint, it kills the hosting cell.

A virus that induced a small percentage of pancreatic alpha cells to undifferentiate and redifferentiate beta cells might work...but you would still have the same immune system that went agro on your beta cells the first time.  They might do the same when exposed to new beta cells.  And there is a fine line between undiffernetiated cells and cancerous cells.


Why do sperm have centrioles and do female eggs cells even have centrioles? I was just wondering why it is that sperm have centrioles underneath the acrosome, but that also prompted a thought as to whether eggs have them too?

Oocytes do not have centrioles. During fertilization, the centrioles of the sperm become the centrioles of the zygote. Only one pair is needed, as there is only one cell (i.e. zygote) right after fertilization.

During fertilization the centrosme inter the ooplasm with the sperm nucleus,  if the oocyte still keep its centrosme there will result 2 centrosme in zygote with 4 centriole. Each one will migrate to pole of cell and produce 4 poles not two and the 4 daughter cells of one division will have one centriole in this case through mitosis will shut off.


What is this insect in Southern California? I saw this insect flying around in Southern California, USA during the summer. It is about 1.25 cm in length. When it flies, it opens up its wings like a ladybug's.  What is this?

This is a scarab beetle that belongs to the genus Cyclocephala, and has the nickname of "masked shafer" (gallery). There are over 300 different species within this genus, however, the species most common to southern California is C. hirta and C. pasadenae, with me leaning more towards the former.

C. hirta; San Diego County, CA (source)

C. hirta; San Leandro, CA. (source)

C. pasadenae; Vail, AZ (source)

  When it flies, it opens up its wings like a ladybug's.

Ladybug, left; masked chafer, right.

I have seen that bug for years, I know its a type of beetle and you are not suppose to smash em. This is just coming from my own research and talking with friends. I think they are called June Bugs.

Heres a descriptor I found.

mahogany-colored beetle of the scarab beetle family, widely distributed in North America and especially abundant in the NE United States and the adjacent parts of Canada. It is also known as June bug, although true bugs belong to a different insect order. The adults, which may swarm in great numbers in early summer and are attracted to lights, feed by night on the foliage of deciduous trees and hide during the day. The eggs are laid in the soil, where the larvae, called white grubs, remain for two or three years, eating the roots and other underground parts of grasses, grains, and trees. The grubs cause great destruction to lawns and fir trees. Many birds and small mammals, such as skunks and pigs, root out the grubs and eat them. The insects pupate underground in the fall and emerge as adults the following spring. June beetles are sometimes called cockchafers, a name used primarily for some of their close relatives in the Old World. They are closely allied to the leaf chafers, including the rose chafer. June beetles are classified in the phylum Arthropoda , class Insecta, order Coleoptera, family Scarabaeidae.


Can people with AIDS/HIV be vaccinated? If there is no immune system,it  seems like vaccines wouldn't do much since there is no adaptive immune system to develop antibodies and memory cells. But can people with AIDS/HIV still be vaccinated? It is expected that a normal person will have antibodies to attack the minimal infection produced by the vaccine and generate memory cells, but without an immune system I expect vaccines to be deadly.

Is that right?

Can people with AIDS/HIV be vaccinated?

Yes. Immunization is an important part of the overall treatment strategy for HIV positive individuals. HIV infection is a risk factor for a number of vaccine preventable infectious diseases. Immunization in these patients is particularly important because of their increased risk of developing disease. (See Cecil Medicine Ch 396)
Can the immune system still mount a response to the vaccine?
Yes. HIV infection does lead to a decreased immune response. Though the primary deficiency is a decrease in both CD4+ (helper) T-cell count and function, there is, perhaps consequently, B-cell dysfunction as well. This would suggest that vaccines are less immunogenic. When this is studied directly, as would be expected, we see that vaccines are less immunogenic, but they are still effective.
Which vaccines are given?
Specific recommendations are based on both the age of the individual and their immune status. As a rule, vaccines are more effective when given early in the natural history of an HIV infection or after immune reconstitution with HAART, but there is some effectiveness and little risk of heat killed or subunit only vaccines even in highly immunosuppressed individuals. While live attenuated vaccines are contraindicated in individuals with a CD4+ cell count below 200, these vaccines are given routinely to other HIV positive patients. Current guidelines are found here. Here is the main figure from those guidelines:

A person with AIDS cannot be vaccinated. The immune system is no longer functional and is unable to mount an immune response to your vaccine.

If the vaccine is a "live vaccine", the person will get a dose of viruses that body can no longer fight against. And the live vaccine would probably give the AIDS patient an infection of what the vaccine was suppose to protect against

However if the vaccine is an attenuated vaccine (which is the case for most vaccines made today), then all your be introducing into the body is parts and pieces of a virus or bacteria. These piece can trigger an immune response in a healthy person but as they just pieces, are not a live cell or a functional virus. So in a person with AIDS, the attenuated vaccine will be harmless.

A person with HIV can be vaccinated. The HIV virus is in the body multiplying. However the immune system while damaged is still functional.


Genetics: pedigree following a rare trait autosomal recessive I have two questions pertaining to this pedigree
I believe it to be an  autosomal recessive trait.

The probability that individuals IV-1 and IV-2 would give rise to an affected individual would be:
A. 1/4 b. 1/2 c. 1/8 d. 1/12 e. 1/24
Suppose individual IV-2 was unaffected. The probability of his marriage giving rise to an affected child would be:
A. 1/4 b. 1/2 c. 1/8 d. 1/12 e. 1/24

I worked on this problem for the last hour or so and figured up question 1 to be 1/2 and question two to be 1/4. I don't feel this is correct. I feel like I am missing something. If you don't mind showing the calculations for how you came about an answer that would be greatly appreciated.

Question 1

Okay, so I'll go through my own process for you here step by step, moving down the tree.  Here's an annotated version of your diagram with my own thoughts (it's been a while since I've done this but should hopefully be accurate):

Generation 2:  As you realised, the trait is autosomal recessive so the female (II:2) has the genotype aa.  The male is considered wild type unless informed otherwise, giving him a genotype of AA.  I think you had worked all this out, but they are shown in red on the diagram.

Generation 3: Using the two genotypes of the parents from II (red), we know that all the progeny in generation III are carriers - i.e. Aa genotypes.  This is indicated for III:6 in orangey-brown.  I think you also worked this out successfully.  However in your original chart, III:7 is noted as Aa.  III:7 is from outside of the affected family and would therefore again be considered to have be wild type and therefore instead have the genotype AA - shown in purple.

Generation 4: In order to work out the potential genotypes of IV:1 we have to do a cross between the two parents III:6 and III:7 - which works out as follows:

        |          Male          |
        |     A            a     |
        |------------------------|
F       |                        |
e     A |    AA            Aa    |
m       |                        |
a       |                        |
l     A |    AA            Aa    |
e       |                        |

As you can see, there is a 50% chance of IV:1 being healthy AA and a 50% chance of being a carrier Aa - shown in green.  As IV:2 is affected, we know his genotype is aa (pink).

Generation V:  Now for answer to your first question.  If IV:1 had the AA genotype then the child could never be affected, reducing the odds to 50% immediately. Of this remaining 50%:

        |          Male          |
        |     a            a     |
        |------------------------|
F       |                        |
e     A |    Aa            Aa    |
m       |                        |
a       |                        |
l     a |    aa            aa    |
e       |                        |

50% of the offspring would be affected.

Therefore the probability of V:I being affected is $\frac{1}{2} \times \frac{1}{2} = \frac{1}{4}$

Question 2

The second question seems very odd to me.  If IV:2 was unaffected in the literal sense of the word they would be wild-type AA.  This would make the probability of them having an affected child as 0.

As this isn't one of your options, I assume they mean that IV:2 is a carrier (Aa).  We are this time therefore crossing either AA or Aa (IV:1) with Aa (IV:2).  Again, if IV:1 is heterozygous dominant (AA) none of her children will be affected.  This means the odds are again reduced by a half.  In the case that she is heterozygous Aa then the cross becomes:

        |          Male          |
        |     A            a     |
        |------------------------|
F       |                        |
e     A |    AA            Aa    |
m       |                        |
a       |                        |
l     a |    Aa            aa    |
e       |                        |

Giving 25% healthy, 50% carrier and 25% affected.

As you're looking for affected children: $\frac{1}{2} \times \frac{1}{4} = \frac{1}{8}$

From my own point of view, I think the answer to no. 1 is a 50% chance i.e. 2 out of 4. My reason is because, IV-1 could be a carrier of the trait and since the IV-2 is affected that means 2 will be affected.
No 2. For the second question, the answer is 1 out of 4, because it's obvious both (IV-1 and IV-2) would be carriers of the trait from their family pedigree, and have 1 in a 4 chance of developing an offspring with the trait.


How accurate is facial reconstruction in forensics? I’ve seen on tv where they reconstruct heads and faces from the remains of ancient people and I was wondering if anyone had a source that has pictures of maybe side by side of a facial reconstruction Vs. a picture of the actual person being reconstructed. I know it takes a long time to fully decompose but surely there’s been a reconstruction done of a recent person who’s been photographed

okkkk. I did a big project on this... and here's some of my research... let's hope it answers your question

Facial reconstruction (also known as craniofacial identification) is a method used in the forensic field.  Many people view facial reconstruction as an art instead of science.  Art is commonly portrayed as the expression or application of human creative skill and imagination, typically in a visual form such as painting or sculpture, producing works to be appreciated primarily for their beauty or emotional power.  Science is thought of as the intellectual and practical activity encompassing the systematic study of the structure and behavior of the physical and natural world through observation and experiment.  But where do science and art blur the lines?

WHAT CAN WE TELL FROM THE SKULL:

The skull provides clues to personal appearance. The brow ridge, the distance between the eye orbits (sockets), the shape of the nasal chamber, the shape and projection of the nasal bones, the chin's form, and the overall profile of the facial bones all influence facial features in life. Using these bones, artists and forensic anthropologists work together to reconstruct facial appearance through the process of forensic facial reconstruction.  There are many ways of telling both the approximate age, and the approximate ethnic background of the victim.  To find age, you can pay attention to the cranial suture (or the place where the cranium fuses to other bones of the skull), the size of the skull can help, as well as the teeth and the formation of the bottom jaw.  When looking for the birth gender of the victim, scientists often pay attention to the brow ridge, eye sockets, mandible, and the slant of the jaw.  Sometimes, it is impossible to tell by looking at the skull what birth gender the victim was.  In cases like this, people look to the pelvis to tell if the human has given birth, and if not, males do not have a ventral arc.  It is often very difficult to find the race of a victim if they are mixed race, or if the skull is very worn out.  However, to find the ethnic background scientists will look at the shape of the skull, the nazel root, and the space between eye orbits.

WHAT ARE THE PROCESSES OF FACIAL RECONSTRUCTION AND ARE THEY ACCURATE:

Facial reconstruction is an exacting process. The finished product approximates the actual appearance, because the skull does not reflect the details of soft tissues-eye, hair, and skin color; facial hair; the shape of the lips; or how much fat tissue covers the bone. Yet, facial reconstruction can put a name on an unidentified body in a modern forensic case, or, in an archaeological investigation, a face on history.

Today, many forensic facial reconstruction techniques are in use, including two-dimensional (drawn), three-dimensional manual and three-dimensional computer-based.  In the manual techniques, including two dimensional a cast of the skull is required, so the facial markers do not become an anomaly when analyzing the skull.  Although all of these methods are used, it is most common that a trained sculptor, who is familiar with facial anatomy, works with a forensic anthropologist and uses clay to build the facial features. The forensic anthropologist interprets skeletal features such as the subject's age, sex, and ancestry, and anatomical characteristics such as facial asymmetry, evidence of injuries (a broken nose, for example), and loss of teeth before death.

Facial reconstruction is used when the victims dental records fail to identify them, and there is no dna to pull from the body.  The process of reconstruction starts with making a mold of the unknown skull with the jaw attached and false eyes in place.  Depth markers are placed on 21 different “landmark” areas of the mold of the skull to approximate the facial tissue thickness that lay on the skull.  These tissue thicknesses are approximated from averages of other people of the same age, sex, and race as the skull is assumed to be.  Facial muscles are placed on the mold next and then the face is built up with clay to within a millimeter of the depth markers as tissue.  The nose and eye setting are very difficult to estimate due to the enormous amount of variation possible, mathematical models are used to make the approximations, the mouth is assumed to be the same width as the distance between the pupils. In facial reconstruction the eyes, nose, and mouth are mostly guess work.  Characteristics such as birthmarks, wrinkles, scars, and such are guesses at best and cannot actually be determined from the skull.  Facial reconstruction is accurate because it has been using mathematics, and calculations as such, in order to determine spaces, amounts, as well as the shapes of the face themselves.

WHY IS FACIAL RECONSTRUCTION IMPORTANT:

Facial recognition, as well as facial reconstruction is very important in the forensic field.  Both have a very important role in catching murderers, and investigating crime.  Without having a facial reconstruction, often times, you cannot identify victims.  Assuming the body is historical and for museum purposes, then without an identity it becomes very difficult to fill in large gaps of information, and time that can be crucial to history.  Also, if you can’t identify a murder victim then scientists could only look into cause of death.  Learning the identity of a deceased victim is as important to crime investigations as learning the identity of the suspect. When human remains are found, then the top priority is often to find the identity of the victim.  Police often also will look for an identity out of respect, for both the victim and the victim’s loved ones if any.  Facial reconstruction has been used ever since 1890.  Before 1890, people mostly used few facial indicators such as the shape of the frontal bone, and the remains of flesh to help identify the victim.  Facial reconstructions, can also show what injuries were sustained previous to death.

WHAT CAN WE LEARN FROM FACIAL RECONSTRUCTIONS:

Our skeleton is an extensive record of our lives. The food we eat, the rate at which we grow as a child, the injuries we sustain, whether we have given birth; all can be determined from our bones. Experts can determine sex, age, and ethnicity, relatively easily from the skeleton, with the skull and pelvis playing pivotal roles in this analysis. Later this week, we’ll be taking a more detailed look at how to determine sex and ethnicity from a skull.Teeth can reveal information about diet and a comparison between dental records of the deceased and the recovered skull is often the primary method of identification.  By looking at the scull (or any bones in fact,) you can tell childhood injuries from injuries that might have been fatal.  You can also look at bone density and other factors to tell if the victim was suffering from any diseases.  People look for the sagittal suture – the squiggly line that runs the length of the skull – If it is fully fused, the remains are likely to be of someone older than 35. After that professionals look for a second line at the front of the skull -- the coronal suture – which fully fuses by age 40. Teeth are also looked at. If they're worn down it could be a sign of a poor diet. If they're well-maintained and/or have good dental work such as fillings, they were able to afford proper dental care—another clue as to the identity of your skeleton. Oftentimes professionals consult a scientist who specializes in teeth, known as an odontologist. They can determine how old a person was at death, what kind of health they were in and what kind of diet they had.

Baby's bones begin to grow in the womb. At birth, the skeleton is partially formed. Many bones are still in "parts." The ends (epiphyses) and bony shafts (diaphyses) of long bones form separately in the womb. At birth, the ends of the long bones are mainly cartilage, with centers of bone beginning to form inside. As a child grows, the shafts get longer, and bone gradually replaces the cartilage epiphyses. Through the growing years, a layer of cartilage (the growth plate) separates each epiphyses from the bone shaft.  By paying attention to this, it is easier to tell age, and follow growth patterns to have a successful reconstruction.

Between 17 and 25 years, normal growth stops. The development and union of separate bone parts is complete. At this point, you and your skeleton are as tall as you are going to get - with many fewer bone parts than you started with.  The bones that enclose the brain grow together during childhood along lines called cranial sutures. During adulthood, bone "remodeling" may gradually erase these lines, at variable rates. Closure of cranial sutures gives general information about a person's age. It is best used with additional indicators to estimate age, or when other age indicators are unavailable.

WHAT ARE THE LIMITATIONS:

It is very hard to estimate a person’s weight and represent that with facial markers.  Since a chart of average thickness of soft tissue is used to estimate the way a person looked, if you were on the skinnier side, your head might appear a lot more overweight than usual and or skinnier.  To help determine weight, scientists look at the rest of the remains for a height.  Facial reconstruction relies on the relationships between the facial features, subcutaneous soft tissues and underlying bony structure of the skull. If there is no clue for potential identity because of impossibility to compare questioned remains with possible familiar material, in such cases one of the last chances is to recreate ante mortem appearance by face reconstruction. Many of the soft tissue thickness values are significantly different from those reported for comparable groups, suggesting that individuals from different geographical areas have unique facial features thus requiring population-specific values. This literature review attempts to throw some light on the important aspects that has to be taken into consideration while setting norms of soft tissue thickness among various populations.

Studying the unknown skeletal remains mostly becomes the only way to find out more information about individual characteristics, which could lead to identification of potential victim. If there is no clue for potential identity the most precise comparative techniques fail, because of impossibility to compare questioned remains with possible familiar material. In such cases one of the last options is to recreate ante mortem appearance by face reconstruction. Following the first introduction of reconstruction in the late 19th century, other techniques have been developed including radiography, 3D statistical model, ultrasound, MRI, CT and Cone Beam Computed Tomography (CBCT).  Facial contours were traditionally considered to be the result of positioning of underlying hard tissue followed by the soft tissue. However, current trend shows a paradigm shift from the conventional hard tissue analysis to also include both hard- and soft-tissue analysis.

IS FACIAL RECONSTRUCTION AN INTERDISCIPLINARY ART:

The skull is made up of 22 bones, 14 of those are facial and eight are cranial bones; it is a complex structure, and small variations during development and growth, together with soft tissue differences, create the enormous facial variation seen in the human population.  Artists have long been interested in the direct anatomical relationship between the skull and facial appearance.

Artist, Gaetano Guilio Zumbo (1656-1701), used facial reconstruction as an art because he believed that math and science are both forms of art.  His work can be found in the Wax Anatomical Collection at La Specola Museum, Florence, became famous for his macabre scenes depicting various stages of decomposition of the human body.  One of his most famous pieces is the head of a dead man, with facial muscles recreated in wax over a real skull.
This is the earliest surviving anatomical wax model created for didactic purposes and exhibits extraordinary anatomical precision alongside an artistic sense of horror and decay. Although we assume that Zumbo was less concerned with facial appearance than anatomical detail, he pioneered the development of scientific art and this work ranks as one of the finest examples of three-dimensional facial reconstruction.

By definition, an interdisciplinary art is relating to more than one branch of knowledge.  Facial reconstruction is often categorized as both a science and a mathematical equation.  Both science, math and art are human attempts to understand and describe the world around us. The subjects and methods have different traditions, and the intended audiences are different, think the motivations and goals, specifically for this purpose is fundamentally the same.


Does coloring affect the perception of depth? I have a question about the mechanics of human vision which may be as much of a physics question as it is a biology/physiology question. I noticed that if I try to imagine a clear blue daytime sky contrasted with a clear night sky and ask myself which of the two appears closer, my intuition says the daytime sky appears closer. My next thought was, given that a night sky is mostly black, visually the only difference between the two skies is their color. So why is that I want to "blue" is closer than "black"? And if the difference in color is truly what produces the difference in perceived depth, can similar effects be noticed with other color pairs at more familiar distance scales?

But then again, there are a couple of alternative explanations that seem more plausible to me on second thought. A black night sky could just as easily be called a dark sky, and the difference in perceived depth is really more a matter of shading. Then I remembered a night sky has stars of course, and it might be that my mind just wants to place the stars at normal "sky depth", forcing the black backdrop to appear even further away.

(Another related question I've been somewhat curious about: what precisely is the perceived "distance to the sky" as far as our intuitions are concerned?)

Yes, color and shading can certainly affect depth perception, as explained by wikipedia:

  Aerial perspective – Due to light scattering by the atmosphere, objects that are a great distance away have lower luminance contrast and lower color saturation. Due to this, images seem blurry the farther they are away from a person's point of view. In computer graphics, this is often called "distance fog." The foreground has high contrast; the background has low contrast. Objects differing only in their contrast with a background appear to be at different depths. The color of distant objects are also shifted toward the blue end of the spectrum (e.g., distant mountains). Some painters, notably Cézanne, employ "warm" pigments (red, yellow and orange) to bring features forward towards the viewer, and "cool" ones (blue, violet, and blue-green) to indicate the part of a form that curves away from the picture plane.

Here are a few examples:

The above is Manet's "Luncheon on the Grass" - and if you look at it briefly it seems the bathing woman is sort of hovering amidst the trio instead of rinsing herself off in the background. This is because the warmer colors flanked by more saturated greens in the grass around her "pull" her forward into the same space as the rest of the painting. Here, scale is one of the major cues that she should be in the background.

Above is Cezanne's "The Bay" and is an excellent example of how warmer colors (reds, yellows, oranges) are used to add depth when contrasted with cool colors (blues, greens, violets). The image works very well, and that's partially because of the colors chosen. You can almost draw a diagonal line between the warm and cool portions of the painting.

  I noticed that if I try to imagine a clear blue daytime sky contrasted with a clear night sky and ask myself which of the two appears closer, my intuition says the daytime sky appears closer. My next thought was, given that a night sky is mostly black, visually the only difference between the two skies is their color. So why is that I want to "blue" is closer than "black"?

Well, there are many differences between the two! The daytime sky has numerous reference points - the horizon, mountains, clouds, airplanes, nearby buildings, etc. I would bet the reference points are the number one reason you perceive the daytime sky to be closer, as our brain is constantly taking them into account without us thinking about it. There are other cues, too: The daytime sky has a gradient to it - that is, the blue of the sky differs due to the curve of the atmosphere, and gradients increase depth perception with more saturated colors being perceived as closer (as opposed to the edges of the daytime sky, which are often less saturated).

The night sky, on the other hand, is pretty much solid black (if you live in suburban or urban areas). The lack of a gradient or other colors immediately robs the observer of some depth perception, and because of the inky blackness of night the other reference points - the horizon, nearby structures, airplanes, clouds, etc. - can practically disappear, robbing the observer of additional depth perception.

I had this same question.  I believe the answer is this is a known effect caused by aberrations between your eyes and the way they perceive color.  This effect is called Chromostereopsis.  I know this is an old topic but hopefully this information will be useful to people like me who were also trying to learn more.

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


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

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


Why do animal teeth get darker if exposed? I was wondering why the teeth of cats (And dogs, as far as I know, plus possibly some other animals or even humans) get darker if they are exposed to air / light?

Example:

(See the lower end of the tooth, which sticks out if the mouth is closed. No, the cat was not resisting, just slightly annoyed.)

So, my question is:

Why does this happen?
Would it happen to human teeth, if they would stick out of the mouth like the ones of cats do?

My guess is that it has something to do with the teeth reacting to air and corroding, but all my knowledge about biology comes from two years of biology in school, so I'm asking here.

The incisal and occlusal edges of teeth are more translucent since there is only enamel in this area and the dentin core is deeper inside. The dentin is more opaque and reflect the light back and it looks lighter whereas the enamel is translucent and allow more light to pass through and less light is reflected back so it looks darker. Many human teeth the incisal edge is translucent or darker for the same reason.

According to me animals use these teeth to chew meat particles etc. So because they don't brush these food particles get exposed to bacterial agents which in turn causes corrosion of teeth. As we see the structure of the animal teeth the food particles are trapped in between resulting into high bacterial corrosive activity. But in humans, regular maintenance and high use of water it decreases the acidity caused by the food in our mouth this prevents excessive corrosion and bacterial activity and growth. On the other hand canines have an initial use of tearing so the usually are not much affected by the food particles and also because of their protruding shape.
The exposure of air and light increase the bacterial activity.


Why does the apex of the human heart usually point to the left? In the majority of human beings, the apex of the heart (left ventricle) points towards the left side of the body.  Sometimes however (approx. 1/12000 births), a person is born with a condition known as "Dextrocardia", in which the apex of the heart points to the right side of the body instead.

Is there an evolutionary reason as to why the human heart usually points to the left side as opposed to the right side of the body?

(Note:  Please don't answer with, "because there is a notch in the left lung", because I will simply reply with, "is there an evolutionary reason for the apex of the heart AND the cardiac notch being on the left as opposed to the right side of the body").

From a quick look at the paper @ChinmayKanchi links to (Palmer, 2004) it seems that:

  All living vertebrates possess a heart that is conspicuously asymmetrical and normally displaced toward the left (Fishman & Chien, 1997).

So the heart orientation seems to be evolutionary conserved in vertebrates (as are many fundamental traits), and no specific explanation is needed for humans.

This is said with the reservation that human anatomy is not my subject field, and the refered paper also digs deeper into the molecular basis for the orientation/symmetry of organisms. For instance, it also says that:

  Second, the molecular pathway directing hearts leftward—the nodal cascade—varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system.

so the molecular mechanisms governing this seems to differ between species. This could indicate that there is a selective pressure molding species into the same heart orientation. This is pure speculation on my part though.

I also want to mention that evolutionary outcomes doesn't have to have a "reason" (i.e. a selective advantage). Much depends on chance events and evolution can only act on what is present at the moment (i.e. is restricted by earlier evolutionary history).

I think it is because of the reason that the left ventricle pumps blood throughout body, thus is bigger than the right ventricle. So, actually, the human heart is along the center septum, but seems just a bit to the right. 1.5 cm to be precise.


Blue light in a fridge. Is it really beneficial or just marketing? Recently while visiting a shop with electronics I saw a fridge with a huge advertisment sticker going more or less like this:

  There's blue light source in this fridge so there will be less bacteria inside and your fruits will have larger quantities of vitamins.

Can it be true? How can dead (picked, transported and refrigerated) fruit produce more vitamins? How does blue light affect this?

Furthermore I thought that only UV light kills bacteria.

Therefore my question is: how much truth was on that sticker?

Maybe a little bit?

There are two claims here, so let's talk about them individually. I'm not sure how this light is being produced (probably LED), but it'll have a wavelength somewhere between 400 and 500 nanometers.

Reduced bacterial presence:

The intrinsic antimicrobial activity of blue light is well documented. Although the mechanism is not entirely understood and widely debated, the commonly accepted hypothesis is that the blue light triggers the production of reactive oxygen species like singlet oxygen that are highly toxic. However, this has only been observed under high-power light sources, and low levels of light may actually increase bacterial activity. What counts as a high-power source, you ask? The number from this article is $\frac{10mW}{cm^2}$. For a fridge with an internal surface area of >1 meter, such a power source should draw at least 100 W. Given that normal refrigerators use draw 100-200 watts, you'd essentially be doubling your electrical bill for the fridge.

It should also be noted that the above is a best-case scenario. As soon as you add anything to the fridge, you'll reduce the intensity and thus the effectiveness of the light source. Also, the light is unlikely to be on all the time- it probably turns on when you open the door and turns off when you close it. While this helps a lot with power use, it minimizes the effect of the blue light, which is constantly on in experiments.

Larger quantities of vitamins

There's no (reliable) evidence of light of any kind actually creating vitamins, so what the sticker suggests is that it doesn't degrade the vitamins already present as quickly as other kinds of light.

There's a good article here that discusses the stability of various vitamins. It's worth noting that most of these vitamins and essential amino acids are much more likely to be destroyed by cooking than light, which is probably why the fridge focuses its claim on fruits, which are less likely to be cooked.

There's very little research that I was able to find about the effect of different wavelengths of light on the stability of various vitamins, but as a whole I remain fairly skeptical that there's any notable difference. Most experiments that do study degradation of vitamins under light subject pure vitamins to high-intensity light for several days- unlikely to happen in your fridge.

TL;DR:

A claim like this shouldn't be a major factor in your buying decision. The effects of the blue light are probably negligible given the conditions in your fridge, but if you've got two very similar choices this feature could act as a nice tiebreaker. Besides, there's a lot to be said about how cool blue light looks and the confirmation bias present in your purchase.

Good question. Asian fridge moguls want to shine blue light on your chopped fruit, mostly, rather than save your life from a hazardous food.

Some research by National University of Singapore studied the effect of visible blue light diodes on some bacteria although not fungi which makes the fruit go moldy (mould propagation in apples is a common bio practical study).

The bacteria studied are not fruit surface bacteria. they are gut and skin bacteria.

The study did not test if fruit last longer in blue light. it just exposed gut and necrotizing bacteria to blue light.

You may get less E-Coli and salmonella, which is weird because you would have a very unwholesome fridge to have a E-Coli danger from it. fruit is not only consumed by bacteria. Salmonella dangers exist inside certain eggs, which is a dark environment. Fruit practically can't transmit major illnesses like S.Aureus, they live in different environments than fruit and are endemic to humans, but fruit do contain a lot of microorganisms necessary for their fermentation and to break them down.

Blue light perhaps increases your appetite too. https://www.sciencedaily.com/releases/2014/06/140602115916.htm

The raw scientific research for it from 2015 is not for funghi or yeasts, and it doesn't penetrate a steak properly, so it's fairly misleading marketing.


Exhalation while holding breath If you inhale to your maximum capacity and hold your breath for an extended period of time, it begins to feel uncomfortable; slowly releasing your breath at this point seems to provide relief from this discomfort.

Is there a biological reason why this is so, or is this something psychological?

The exact causes of the discomfort relief  after the breath-hold breakpoint  is unknown yet.

It has been stated that breath "pacemaker" continue to work independently of voluntary breath holding. Thus, while breath holding, the breath center is trying to activate the diaphragm and the afferent feedback from the diaphragm normally causes the feeling of discomfort. Thus, upon starting breathing again, i.e. actual diaphragm movements, the discomfort will diminish and the subject will feel relief.

Breath-holding and its breakpoint. Experimental Physiology Volume 91, Issue 1, January 2006.

full text of cited article

This occurs because the feelings of needing more air to breath result from changes in the concentration of carbon dioxide in the bloodstream. This happens because the carbon dioxide gets dissolved in blood, turning into carbonic acid (H2CO3). This, since it is an acid, dissociates into ions, and your body can detect that change in acidity. These changed PH levels are not desirable because they reduce the efficiency of proteins and can cause negative effects. Therefore, the body detects these changes and creates the discomfort from the desire to breath out. This also holds true for too little carbon dioxide, because it will result in the reverse effect on the acidity in the blood stream (it will raise the PH/make it more basic). Passing out occurs when the acid levels are too high and nothing is making them return to normal (breathing out) so the brain says "this idiot cannot breath correctly" and shuts off the control center to do it itself (unconsciousness).


Heritability of trait stronger from one sex over another? Given a trait that can be expressed (and measured) in both parents (e.g weight, height, strength, speed), are there ever traits in the child that correlate better with one sex parent than the other? If so, can you give some examples. This could be in any species.

It has been shown in Drosophila that cross-sex heritability is low for lifespan, where within-sex heritability was three times greater than cross-sex heritability. This means that, sons more closely resemble their fathers and daughters more closely resemble their mothers. This could be considered one such example, if you consider the trait to be a sex-specific thing, i.e. that fathers have a greater influence on lifespan in sons than mothers do.

In humans (and numerous other species, e.g. Indian Meal Moth), it has been shown that several traits have small cross-sex genetic correlations, suggesting that (in such traits) the parent of the same sex is a better predictor of a child's trait value.

It is common (in quantitative genetics circles) to consider homologous traits in two sexes as separate traits (e.g. male lifespan and female lifespan are separate traits), and analyse them in a multivariate framework such as a G-matrix. They often have some genetic covariance between the sexes because of pleiotropy and linkage disequilibrium (though covariance by LD is generally more transient: see books on quantitative genetics by Lynch & Walsh, Falconer & Mackay, or Roff, for more reading).

Merila & Sheldon 2000 (DOI=10.1086/303330) found:  "One striking, and unexpected, result from this study was that the heritability of lifetime reproductive success
in females was relatively high and significantly different
from 0. In contrast, the heritability of LRS for males was
lower and not different from 0 (although the estimate was
positive and broadly in line with that estimated by other
studies; see Burt 1995)."


Is there a good analogy that illustrates the difference between early DNA sequencing techniques and shotgun sequencing? My first university biology classes begin in September. In preparation, but increasingly out of curiosity, I've been studying some basic biology. Saying that to say, I know as much about DNA replication as the Khan Academy videos teach.

Presently, I'm reading about the two efforts to sequence the genome. From what I've read, Collins' project used "polymerase catalysis and nucleotide labeling"; whereas, Venter's project used "shotgun sequencing". I didn't know enough to understand the article I read on "shotgun sequencing" and couldn't find one that described the other technique.

I suspect that, in order to comprehend a concise description of the two techniques, I'd need to learn more than I could learn from an answer to this question. That said, it'd still be nice to have a very rough idea of what each process involves and how they differ from each other. A crude analogy to something concrete would be great.

The public effort, led by Collins, relied on a physical map of each chromosome.  Very large pieces of genomic DNA were sub cloned into cloning vectors and used to create genomic libraries in cosmids, BACs and YACs.  The sub clones are ordered using hybridization probes from either known genes, or RFLP genetic markers. In this way a physical map of each chromosome was built up, and then the project would march down the ordered clones, sequencing the sub clones.  If the physical map is good then you have a very good idea of where the sequence comes from.

Shotgun sequencing, in contrast, involves randomly fragmenting the entire genome into small fragments (using sonication, for example), sub cloning those pieces and sequencing everything.

In the first method each base is sequenced a minimal number of times, whereas in the second approach each base ends up being sequenced many times (on average).

For a whole genome, shotgun sequencing requires an excellent computer algorithm to "assemble" the resulting data into overlapping contigs.

PCR (polymeraze chain reaction) and shotgun sequencing are two somewhat complimentary approaches to sequencing. In the former case one uses chemical reaction to create multiple copies of the genome of interest, which allows to reduce the error in sequencing this genome. The latter is done by sequencing the data directly, i.e., without any genome multiplication.
PCR is more suitable when we are studying a particular genome or a few genomes, e.g., when sequencing the genome of a particular person or a particular type of organism. However, when some very different genomes are present, the amplification might be very uneven, and in fact introduce additional errors. This is why in some situations one prefers shotgun sequencing, e.g., when studying microbiome, containing many different types of bacteria, archaea, viruses, etc.
Both terms refer to the so-called High-Throughput Sequencing (HTS). You could learn a bit more about sequencing technologies from this popular science article.


How do marine mammals and penguins maintain bone density? After much searching on Google with no results, I decided to ask my question here.

If I'm not mistaken, swimmers' bone density is less than normal; at least for lifetime swimmers. Astronauts also lose bone mass from the lack of stress (from gravity) on their bones; it stands to reason that being in the water and thus being weightless, would lead to bone loss.

So my question is, how do marine mammals and penguins maintain their bone mass?

I wouldn't refer to it as "bone loss" but more as bone strength. Lifetime swimmers spend a lot of their time in the water. As in water yes they are almost "weightless" and their bone strength will decrease because it has gotten used to the "low" gravity. Now in the case of penguins and other Marine mammals, they have adapted to the force that the water applied to them.

Here is a link to a picture of penguin's flipper.


Non Coding DNA and its effect on evolution I had a discussion with a friend of mine; from his understanding, bacteria and other small organisms have higher amounts of "coding" DNA and, as such, are able to evolve much faster than organisms like us.  His argument was that if bacteria are able to evolve so much faster than us, then they should have become the Apex Predators on Earth instead of humans.

I argued that the 2% of the "coding" DNA is probably as long as the 90% of a bacterium (I'm guessing at this point) and that it is the bacterium's small life span that makes it evolve so fast.  Was hoping to get clarification from someone with more experience in the field.

Richard Dawkins discusses this in his book The Greatest Show on Earth: The Evidence for Evolution

Bacteria and other microorganisms, specifically Archaea, are able to exchange in a sort of 'copy and paste' genetic exchange that differs wildly from sexual reproduction.  They can even exchange genes with other distantly related species.  This, coupled with their short (compared to Humans) lifecycle, accounts for much of the difference in evolutionary rates.  Often, it makes sense to speak in terms of evolution in terms of specific genes themselves (in the case of bacteria), as opposed to evolution of the species as a whole, due to the 'copy and paste' exchange that can take place.  For Bacteria, there is something to be said for compiling a 'true' family tree for each gene separately, regardless of which kind of bacteria in which it resides.

Dawkins remarks, "The philosopher Dan Dennett has put it, 'Where the tree of life for animals is a majestically spreading oak, that for bacteria is more like a banyan.'"

Also, evolution by Natural Selection and random mutation does act on 'non-coding' DNA, just to be clear.

http://www.livescience.com/46986-human-genome-junk-dna.html

Microorganisms are often able to adapt to new environments quickly, but they lack the specialized functions of macro-organisms. Consider that the micro-organisms of macro-organisms have developed to form machinery that builds solutions to problems, rather than being retrofitted themselves to counteract new threats. Each time a bacteria needs to adapt itself to attack, whereas the specialized cells of our body can manufacture a solution on the fly rather than waiting around for a random beneficial strait to show up in the population. It would be like a small manufacturer quickly retrofitting it's production system to produce a new product. Sure, it can produce a new product, but it takes time for setup, and the company can only produce a limited number of varied products at a time, whereas a giant production company may have a huge amount of preset equipment for manufacturing a enormous variety of products with no need for retrofitting (evolution). The larger factory could have the advantage when it comes to efficient production, with quicker turnaround.

Therefore, the specialization of micro-organisms leads to nature allowing the evolution of macro-organisms as the major factories of nature.

Excess, unused (or at least non-critical) DNA is useful because it allows evolution some wiggle room. If a bacteria suffers a deleterious mutation in a vital gene, then it's obviously not fit. But, that same bacterium with can accumulate potentially useful codes in the previously unused portion of it's genome, without needing to deal with risky mutations in vital genes. And again, as microorganisms specialize, they can fabricate new proteins and such, with lower risk, and less time, compared to micro-organisms which use evolution of their genome as the sole/primary means of short term adaption.


Are there certain symmetric-pair muscles that are slightly bigger and NOT due to handedness? Ok, hear me out, I was just thinking about an article in Nature I read in the past titled "Scrotal asymmetry in man and in ancient sculpture"$^{\dagger}$ and more recently an entire medical textbook detailing everything about hands wherein the author accounts the different types of blood vein topology categories there are in humans, and he touches on handedness too. The part about handedness stuck with me, and I began to notice (looking in the mirror, etc.) that my right neck muscles are slightly larger than the left ones, but so is my friend's who is left handed. I thought this might be due to handedness not translating to chewing behavior (chewing on the right or left predominantly). Anyway, all this is building up to my main question which is this:

  Is there something about our anatomy (organ placement, vein topology, etc.) that makes certain symmetric-pair muscle groups unavoidably asymmetrical or is it just handedness or the environment?

$\dagger$ Heard about it here: https://www.youtube.com/watch?v=Xyquv6SsLWg&t=0m56s

There are many variables that could affect the answer to this question. Such as what activities you partake in.

For example, I am a hockey player at the he varsity level in high school. I have noticed that my entire right side is more toned, muscular, and flexible (especially my right latisimus dorsi and deltoid). It just so happens that I rely on my right side for energy and strength more than my left when it comes to shooting pucks and just playing the game.

Typically what we see in humans is the dominant side of their body will tend to show more hypertrophy than the non-dominant side. When you look at a human anatomically, their dominant side shoulder will be bigger and will rest lower when relaxed. Even small things like sleeping habits can effect the visual difference of you symmetry. I will agree though that it is odd that your friend noticeably has more hypertrophy in his neck muscles on one side but is dominant on the other side. This could be due (but not limited) to small habits not taken into account. Like I mentioned before, sleep habits, any motion with the neck in a specific way, chewing could maybe be a factor, or (maybe not likely) a genetic mutation.

This is an interesting topic and I urge you to maybe look at some more people for evidence that dominance has a role in it. 2 people is maybe not enough evidence to really back up a claim you're going to make.

Hope this helped!

-Sartoaster


Why are not all species hermaphrodites? If a hermaphrodite animal (like slug, snail, etc) finds a partner they can mate immediately.

If another animal with "normal" reproduction (lets say a mouse) finds a partner they can only mate if they are opposite genders.

So it seems logical that the hermaphrodite way of reproduction is more successful than the "normal" way.

But it is not, as far as I know all higher developed species are using, the standard way of reproduction (male and female).

Why? What are the disadvantages of hermaphroditism?

Firstly I'll clarify that you are talking about simultaneous hermaphrodites rather than sequential hermaphrodites (1st one sex, then the other e.g. the limpet Patella vulgata).

It is perhaps easiest to address the question by countering it and asking why dioecy (2 sex systems/2 gonochoric types e.g. male and female) is better? As you have pointed out there are obvious advantages to being a hermaphroditic species such as more chance of mating - more likely to provide an advantage at very low population densities where interactions are infrequent.

There are two key disadvantages of hermaphroditism which I will briefly cover but have been discussed in this paper and probably other costs.

The first is energy costs. Maintaining the capacity to produce male and female gametes will be more costly than maintaining one. This gives the hermaphrodite a fitness disadvantage because energy is rarely an infinite resource. Therefore at higher population densities, when mating opportunities are not rare, the gonochoric individuals will have a higher fitness because they have more energy. Monogamy is also analogous to rare encounters but true monogamy is rare (1 partner for life).

The second disadvantage of hermaphroditism is self fertilisation. This will cause an increase in homozygosity and lead to inbreeding depression (reduced fitness).

So you are right to some extent...

  the hermaphrodite way of reproduction is more successful than the
  "normal" way.

...but the conditions which give rise to an hermaphroditic advantage are restricting. Overall, the above costs, combined with the obvious complexity of evolving the ability to produce male and female gametes, the ability to both fertilise and be fertilised, pregnancy and birth, and mating systems, mean that it is often more beneficial to be a dioecious species. Thus dioecy evolves.

EDIT: Question Raised by @Single_Digit

  I have been pondering this question for a while and I get what RG255
  is saying. I'm just not sure I entirely buy it. Take earthworms, for
  example. They are simultaneous true hermaphrodites (as far as I
  understand). The anatomy doesn't have to be that complex*. They simply
  have two genital openings (one for eggs and one for sperm) and they
  line up in a "69" (excuse the vulgarity) position. This should, in
  theory, minimize the inbreeding depression. However, it doesn't
  eliminate the maintenance of two sets of reproductive systems. But
  most organisms are not internally fertilized mammals with wildly
  complicated systems of internalized embryonic care. Most species lay a
  pile of eggs that a male squirts sperm on or squirt eggs while the
  male squirt sperm and then they hope for the best.

  I would think the advantages of simultaneous parenting (after all,
  many MANY species' males don't provide much in the way of child care)
  and its fitness advantage would vastly outweigh the burden of a second
  set of reproductive organs.

  With that said, I don't have a better explanation, but I find the
  question a very interesting one. The linked article is pay-walled,
  aside from the abstract, but I still disagree with some of its tenets.
  To me true hermaphroditism should be very common (I realize it isn't)
  in species that don't need two parents to raise offspring, but do
  benefit from some (as in one parent's) parental care. I recognize that
  it would do little to help species that merely dump gametes and leave
  because specialization of one reproductive system would likely do the
  job better and both genders equally contribute under that type of
  system.

  So, RG255 convince me! Clearly there are good reasons, since gender
  (or asexual repr) is the norm, but I need more/better evidence.

  Yes I realize they would need separate internal anatomies for each type of gamete, but still...

My response:

  You have presented one example of hermaphroditism and used that as
  evidence that all species should be hermaphrodites. Earthworms are
  small slow creatures living in soil, I don't imagine they have high
  rates of encounter, and therefore low rates of encountering the
  opposite sex, therefore hermaphroditism would be favoured as discussed
  above.

  Further, you say most species are external fertilisers (do you
  have a reference for this?) and therefore it is not costly be a
  hermaphrodite. I don't see your logic there, the cost is not
  necessarily to do with the cost of bearing child, producing &
  maintaining the gonads and gametes is also a costly process. I would
  argue that this is extremely complex. This is not just on a
  morphological level but also physiological: in non-hermaphroditic
  species the sexes have very different, and often, conflicting gene
  expression and hormone production patterns. Hermaphrodites would not
  be able to optimize to the fulfilling both the male and female roles.

  Finally, you pointed out that the worms do not inbreed. Inbreeding
  avoidance does not have to be the cause of the hermaphroditism
  persisting, if the environment/other factors favour hermaphroditism. I
  never said that both were simultaneously necessary.

  I hope this
  clarifies it for you, if not please expand as to why, I am on here
  because I want to help people understand biology properly!

Further response from @single_digit:

  Well fair enough about my external fertilizers comment. I don't have a
  reference, but I was thinking all multicellular life and I'd have to
  imagine that when you factor in plants, that external fertilization is
  relatively the norm (as is hermaphrodism (dioecy) for the plants). As
  to earthworms, I disagree about your description of them. Their
  densities are actually pretty high, so I'd wager they encounter each
  other frequently, so I'm not sure where that leaves them in terms of
  pressures for hermaphroditism. Your point on the physiologic/hormonal
  issues of maintaining the systems is one I haven't previously
  considered. I honestly don't have any clue as to how daunting (or
  simple) that is, but I'd imagine that the sophistication of the
  systems would play a pretty key role. Makes me wonder how much this
  has been researched in true hermaprhodites. I suppose the main thing I
  keep coming back to is the overwhelming disadvantage gender has in
  terms of potential to create offspring. Males in many (most?) species
  essentially act as little more than sperm donors, thus half the
  individuals have effectively zero fitness. That just seems like an
  overwhelming advantage for hermaphrodites.

My Response

  Why do you consider half of the individuals to have zero fitness?
  Fitness is widely accepted as the number of offspring a parent
  produces because this is directly related to number of copies of their
  genes passed to the next generation. Sperm donor type males achieve
  increased fitness by mating as do females - with out the male they
  would never be fertilized. The key disadvantage of dioecy is the
  halved (assuming equal sex ratio) frequency of potential encounters
  that could lead to mating. The general disadvantages of
  hermaphroditism are inbreeding depression and high cost & complexity.

Single_digit:

  Zero fitness isn't exactly correct, but if we look at parental care as
  conveying a survival advantage for K selected species, and huge
  numbers of offspring conveying an advantage for r-selected species
  (obviously the type of env affects this) does a deadbeat dad really
  optimize for either of these? Passing on genes is fine, but if
  offspring survival is low, does it matter? Does it simply boil down to
  the maintenance of two repr systems plus decreased fitness from
  inbreeding vs the increased reproductive success from extra child
  care? Or is there more?

My response:

  r/K selection theory has generally been disregarded in the
  evolutionary biology community due to the substantial evidence against
  it so it is unhelpful to think of selection in this way. As long as
  the 2 sexes strategy is more successful at passing on genes than a
  hermaphroditic strategy it will (should) prevail. Dioecy will be more
  successful if the hermaphroditism introduces to much cost through
  production and maintenance of sexual organs/gamete and inbreeding
  whilst not attaining substantial gains from higher potential mating
  frequency.

@Single_Digit

  Interesting about r/K selection. I hadn't heard that. Do you have any
  links? I'd be curious to learn more there. I incorrectly earlier made
  a comment about dioecy where I meant monecy. But this seems to beg the
  question, why is monecy/hermaphroditism so much more prevalent in
  plants? Obviously there are different survival pressures, but I'd
  think the same basic principles would apply as in animals, but the
  condition seems to be far more common than in animals.

My Response

  I seem to remeber there being a reason in plants, don't
  have time to look it up right now. The work about r/K selection was
  Reznick/Stearns/Charlesworth. Reznicks is the most recent and more
  overview type paper - best place to start:
  http://www2.hawaii.edu/~taylor/z652/Reznicketal.pdf

The female & male organs compete against each other.  A stud hermaphrodite has little incentive to have female organs.  A human stud who can have 1000s of kids would be slowed down considerably if he\it had to spend 9 months\year being pregnant & raising infants & it's costly to maintain female organs.


Is there a link between digestion and nightmares? A common belief is that eating too much before going to sleep can cause to have nightmares. In fact, I often experience it: I systematically have nightmares after eating too much in the evening.

Then I was wondering: is there really a link between digestive system's activity and unconscious brain's activity?

If it actually exists,
- is the influence linked to the neurons we have in out gut?
- or is it linked to the augmentation of the concentration of a nutrient in our bloodstream (which can then reach our brain and)?
- or is the neuronal activity which control digestion that interferes with the process of dreaming?

If the influence is linked to the augmentation of the concentration of a nutrient in our bloodstream, does this mean what we eat actually controls our mood or level of anxiety, or any subconscious process? (regardless of compounds known for having a particular effect, like theobromine, etc...)

A nightmare is basically an alarm; typically your subconcious mind trying to wake you. Nightmares often occur when you are experiencing pain or discomfort (like needing to use the bathroom).

Dreams are a way of sorting through questions in a "what if" sort of way. When it comes to a nightmare, you are in a panic-situation, often without a solution, or where a "logical" solution is unsuccessful.


How will changing the concentration of a Tris buffer affect amylase enzyme activity? For instance if you increase the amount of Tris but pH still does not change then will the enzyme activity still proceed normally?  If it does change the pH will it change enzyme structure and why?

I realize I'm 4 years late, but wanted to give an answer to this. It appears that tris often has inhibitory effects on amylase activity. Adding more Tris will lead to competitive inhibition with the substrate and will skew the results.

Binding of Tris to Bacillus licheniformis alpha-amylase can affect its starch hydrolysis activity
https://www.ncbi.nlm.nih.gov/pubmed/18289113

After 4 years of working in enzymology I've got say tris is really tricky first of all when you use more tris to keep pH at the same as before you will need to re adjust the pH as tris is about 9 but most enzymes work around 6to7.5 (for alpha amylase it's 5.8) if you don't then your enzyme wont work properly ,it needs very low or high pH grade to destroy 3D structure of enzyme ,so we can simply say it will lost it's functionality , if you adjust the pH high concentration can cause some problem such as surrounding substract here amylase and not letting it to connect to enzyme in some cases acid you use to adjust pH has toxic effects on enzyme chlorine in this case but pretty sure the best way is optimization to understand the reaction.
Best regards .


Limit on the Number of Facial Phenotype Individuals of each species all have unique facial structure variations (shape of nose, position of chin etc) from humans to birds and fish etc. We humans don't seem to be reaching mathematical limit of uniqueness easily (maybe till the end of the world) considering huge variation and all possible combinations that define our facial structure/traits. However some animal populations are way more larger than humans and each year they reproduce in large amounts.  Considering their huge populations, is it possible for some species to reach their mathematical limit of having unique facial structure variations therefore start repeating the same facial structures?  For example can individuals of some fish species (sardines, sea breams etc) be already sharing exact same facial structure/geometry as a result of reaching all posible facial structure  variation limit?

Okay, theoretically possible, but only in theory.  Practically, it's totally impossible.  Let's start by defining why it would theoretically be possible.
Theoretically, there are only so many possible arrangements of proteins in the face, which would represent a limited number of possible facial appearances.  However, as you probably guessed, there are zillions of proteins being expressed in each body organ, such as an eye.  So just from the perspective of the number of different possibilities, it would be impossible.
One might think that since the facial features are controlled by genetic variation, eventually these features will begin to repeat themselves, but such is not the case, for two reasons:

There are way to many genes - and alleles - that control facial features.  We're talking thousands if not millions.  When you raise that number of alleles to each others' powers, you start to see the impossibility of repeating the exact same combination, especially since every new generation is introducing new alleles from a new blood line.

Genetic code is not the only thing that changes how you look.  A whole branch of genetics, epigenetics, is devoted to the changes of gene expression unrelated to DNA sequence.  The expression can be changed by environmental factors, even as early as when the embryo is forming the placenta.  This is why identical twins (who have identical DNA) do not actually look exactly the same, or even have identical fingerprints.

Bottom line, totally impossible.

Sources:

Face shape is in the genes, PLOS, 2016
Epigenetics, Wikapedia, 2017
Why do identical twins have physical differences?, Anonymous, 2005
Introduction to epigenetics, University of Leicester, 2013
How many Proteins exist in human body?, Innovateus, 2013


Difference between going against and going down a concentration gradient The difference between facilitated diffusion and active transport is that facilitated distribution occurs down a concentration gradient and active transport occurs against a concentration gradient. I understand that, as a result of these differences, active transport uses ATP so that it can bind to the carrier protein, however I don't know what is meant by going against a concentration gradient or down a concentration gradient.

In short, I would like to know the difference between going against and down a concentration gradient. A definition of what a concentration gradient is might clarify things a little further as well, since the definition I have doesn't help much.

"Concentration" is "how much stuff is there someplace?" "Concentration gradient" is "how much is concentration changing from point A to point B?"

Imagine a terrain where concentration is represented by height.

"Down" a concentration gradient means from high concentration to low concentration - this is the direction things would move via simple diffusion.

"Up" or "against" a concentration gradient means from low concentration to high concentration. Moving in this direction requires some sort of energy input, such as active transport using ATP, or an electrical gradient, or something else.

Moving against a concentration gradient means that the substance is moving from a low concentration to a high concentration.
Moving down (descending) a concentration gradient means that the substance is moving from high concentration area to a low concentration area.


Is this plant lantana camara? If not what is it? I was in a botanical garden recently and wasn't able to find the tag on this plant. The diameter of the entire flower tended to be around 5cm.

Google seems to suggest its lantana camara but I'm not 100% convinced yet.

When rubbed, its leaves produced a minty aroma

It is Lantana camara, you can check here: https://en.wikipedia.org/wiki/Lantana_camara