Information

Can skin become denser?

Can skin become denser?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

I heard that after injury or repeated damage bone becomes denser, can skin become denser as well?


The structure of skin (epidermis) can change with damage, when the skin is broken the body repairs this partly by recruiting cells called fibroblasts. These fibroblasts lay down collagen fibres to repair the skin. These fibres a normal component of skin are not as neatly arranged as the original fibres and may also higher in number leading to 'denser' skin. This is essentially what a scar is. In some cases the above process can go awry forming what is known as keloid scars.

The other thing that can happen with repeated pressure exposure the skin can become callous, this is when there is thickening of the outer layer formed of cells called keratinocytes increase in number due to recurrent damage. These form typically on pressure points such as balls of feet.


BIO 140 - Human Biology I - Textbook

/>
Unless otherwise noted, this work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License..

To print this page:

Click on the printer icon at the bottom of the screen

Is your printout incomplete?

Make sure that your printout includes all content from the page. If it doesn't, try opening this guide in a different browser and printing from there (sometimes Internet Explorer works better, sometimes Chrome, sometimes Firefox, etc.).

Chapter 14

Layers of the Skin

  • Identify the components of the integumentary system
  • Describe the layers of the skin and the functions of each layer
  • Identify and describe the hypodermis and deep fascia
  • Describe the role of keratinocytes and their life cycle
  • Describe the role of melanocytes in skin pigmentation

Although you may not typically think of the skin as an organ, it is in fact made of tissues that work together as a single structure to perform unique and critical functions. The skin and its accessory structures make up the integumentary system , which provides the body with overall protection. The skin is made of multiple layers of cells and tissues, which are held to underlying structures by connective tissue (Figure 1). The deeper layer of skin is well vascularized (has numerous blood vessels). It also has numerous sensory, and autonomic and sympathetic nerve fibers ensuring communication to and from the brain.

Figure 1: The skin is composed of two main layers: the epidermis, made of closely packed epithelial cells, and the dermis, made of dense, irregular connective tissue that houses blood vessels, hair follicles, sweat glands, and other structures. Beneath the dermis lies the hypodermis, which is composed mainly of loose connective and fatty tissues.

Click on the link below to view an animation about the layers of the skin. The skin consists of two main layers and a closely associated layer. What are the basic functions of each of these layers?

The Epidermis

The epidermis is composed of keratinized, stratified squamous epithelium. It is made of four or five layers of epithelial cells, depending on its location in the body. It does not have any blood vessels within it (i.e., it is avascular). Skin that has four layers of cells is referred to as &ldquothin skin.&rdquo From deep to superficial, these layers are the stratum basale, stratum spinosum, stratum granulosum, and stratum corneum. Most of the skin can be classified as thin skin. &ldquoThick skin&rdquo is found only on the palms of the hands and the soles of the feet. It has a fifth layer, called the stratum lucidum, located between the stratum corneum and the stratum granulosum (Figure 2).

Figure 2: These slides show cross-sections of the epidermis and dermis of (a) thin and (b) thick skin. Note the significant difference in the thickness of the epithelial layer of the thick skin. From top, LM × 40, LM × 40. (Micrographs provided by the Regents of University of Michigan Medical School © 2012)

The cells in all of the layers except the stratum basale are called keratinocytes. A keratinocyte is a cell that manufactures and stores the protein keratin. Keratin is an intracellular fibrous protein that gives hair, nails, and skin their hardness and water-resistant properties. The keratinocytes in the stratum corneum are dead and regularly slough away, being replaced by cells from the deeper layers (Figure 3).

Figure 3: The epidermis is epithelium composed of multiple layers of cells. The basal layer consists of cuboidal cells, whereas the outer layers are squamous, keratinized cells, so the whole epithelium is often described as being keratinized stratified squamous epithelium. LM × 40. (Micrograph provided by the Regents of University of Michigan Medical School © 2012)

Click on the link below to view the University of Michigan WebScope to explore the tissue sample in greater detail. (Note: requires that you have Flash Player installed on your computer). If you zoom on the cells at the outermost layer of this section of skin, what do you notice about the cells?

Stratum Basale

The stratum basale (also called the stratum germinativum) is the deepest epidermal layer and attaches the epidermis to the basal lamina, below which lie the layers of the dermis. The cells in the stratum basale bond to the dermis via intertwining collagen fibers, referred to as the basement membrane. A finger-like projection, or fold, known as the dermal papilla (plural = dermal papillae) is found in the superficial portion of the dermis. Dermal papillae increase the strength of the connection between the epidermis and dermis the greater the folding, the stronger the connections made (Figure 4).

Figure 4: The epidermis of thick skin has five layers: stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, and stratum corneum.

The stratum basale is a single layer of cells primarily made of basal cells. A basal cell is a cuboidal-shaped stem cell that is a precursor of the keratinocytes of the epidermis. All of the keratinocytes are produced from this single layer of cells, which are constantly going through mitosis to produce new cells. As new cells are formed, the existing cells are pushed superficially away from the stratum basale. Two other cell types are found dispersed among the basal cells in the stratum basale. The first is a Merkel cell , which functions as a receptor and is responsible for stimulating sensory nerves that the brain perceives as touch. These cells are especially abundant on the surfaces of the hands and feet. The second is a melanocyte , a cell that produces the pigment melanin. Melanin gives hair and skin its color, and also helps protect the living cells of the epidermis from ultraviolet (UV) radiation damage.

In a growing fetus, fingerprints form where the cells of the stratum basale meet the papillae of the underlying dermal layer (papillary layer), resulting in the formation of the ridges on your fingers that you recognize as fingerprints. Fingerprints are unique to each individual and are used for forensic analyses because the patterns do not change with the growth and aging processes.

Stratum Spinosum

As the name suggests, the stratum spinosum is spiny in appearance due to the protruding cell processes that join the cells via a structure called a desmosome . The desmosomes interlock with each other and strengthen the bond between the cells. It is interesting to note that the &ldquospiny&rdquo nature of this layer is an artifact of the staining process. Unstained epidermis samples do not exhibit this characteristic appearance. The stratum spinosum is composed of eight to 10 layers of keratinocytes, formed as a result of cell division in the stratum basale (Figure 5). Interspersed among the keratinocytes of this layer is a type of dendritic cell called the Langerhans cell , which functions as a macrophage by engulfing bacteria, foreign particles, and damaged cells that occur in this layer.

Figure 5: The cells in the different layers of the epidermis originate from basal cells located in the stratum basale, yet the cells of each layer are distinctively different. EM × 2700. (Micrograph provided by the Regents of University of Michigan Medical School © 2012)

Click on the link below to view the University of Michigan WebScope to explore the tissue sample in greater detail. (Note: requires that you have Flash Player installed on your computer). If you zoom on the cells at the outermost layer of this section of skin, what do you notice about the cells?

The keratinocytes in the stratum spinosum begin the synthesis of keratin and release a water-repelling glycolipid that helps prevent water loss from the body, making the skin relatively waterproof. As new keratinocytes are produced atop the stratum basale, the keratinocytes of the stratum spinosum are pushed into the stratum granulosum.

Stratum Granulosum

The stratum granulosum has a grainy appearance due to further changes to the keratinocytes as they are pushed from the stratum spinosum. The cells (three to five layers deep) become flatter, their cell membranes thicken, and they generate large amounts of the proteins keratin, which is fibrous, and keratohyalin , which accumulates as lamellar granules within the cells (see Figure 4). These two proteins make up the bulk of the keratinocyte mass in the stratum granulosum and give the layer its grainy appearance. The nuclei and other cell organelles disintegrate as the cells die, leaving behind the keratin, keratohyalin, and cell membranes that will form the stratum lucidum, the stratum corneum, and the accessory structures of hair and nails.

Stratum Lucidum

The stratum lucidum is a smooth, seemingly translucent layer of the epidermis located just above the stratum granulosum and below the stratum corneum. This thin layer of cells is found only in the thick skin of the palms, soles, and digits. The keratinocytes that compose the stratum lucidum are dead and flattened (see Figure 4). These cells are densely packed with eleiden , a clear protein rich in lipids, derived from keratohyalin, which gives these cells their transparent (i.e., lucid) appearance and provides a barrier to water.

Stratum Corneum

The stratum corneum is the most superficial layer of the epidermis and is the layer exposed to the outside environment (see Figure 4). The increased keratinization (also called cornification) of the cells in this layer gives it its name. There are usually 15 to 30 layers of cells in the stratum corneum. This dry, dead layer helps prevent the penetration of microbes and the dehydration of underlying tissues, and provides a mechanical protection against abrasion for the more delicate, underlying layers. Cells in this layer are shed periodically and are replaced by cells pushed up from the stratum granulosum (or stratum lucidum in the case of the palms and soles of feet). The entire layer is replaced during a period of about 4 weeks. Cosmetic procedures, such as microdermabrasion, help remove some of the dry, upper layer and aim to keep the skin looking &ldquofresh&rdquo and healthy.

Everyday Connection

Skin Color

The skin is the largest and most visible organ of the body. Variance in skin color is not only determined by the color of melanin which ranges from very light brown, red, to very dark brown, but also the position in which cells receiving melanin pigments from the melanosomes are situated in the skin strata. Cells situated closer to the outer surface of the skin will reveal more melanin pigmentation compared to cells located further away from the outer surface of the skin. Additionally, the amount of carotene and hemoglobin can contribute to skin color.

The figures above show melanin in the upper layers of the skin are more visible compared to those housed in the cells in the lower layers of the skin stratum. Thus a fair colored person may either have a darker melanin pigment housed in the lower cell layers of the skin stratum or alternatively, may have a lighter melanin pigment housed in the top layered cells of the skin stratum.

Watch the video in the link below to learn more about skin color.

Dermis

The dermis might be considered the &ldquocore&rdquo of the integumentary system (derma- = &ldquoskin&rdquo), as distinct from the epidermis (epi- = &ldquoupon&rdquo or &ldquoover&rdquo) and hypodermis (hypo- = &ldquobelow&rdquo). It contains blood and lymph vessels, nerves, and other structures, such as hair follicles and sweat glands. The dermis is made of two layers of connective tissue that compose an interconnected mesh of elastin and collagenous fibers, produced by fibroblasts (Figure 6).

Figure 6: This stained slide shows the two components of the dermis&mdashthe papillary layer and the reticular layer. Both are made of connective tissue with fibers of collagen extending from one to the other, making the border between the two somewhat indistinct. The dermal papillae extending into the epidermis belong to the papillary layer, whereas the dense collagen fiber bundles below belong to the reticular layer. LM × 10. (credit: modification of work by &ldquokilbad&rdquo/Wikimedia Commons)

Papillary Layer

The papillary layer is made of loose, areolar connective tissue, which means the collagen and elastin fibers of this layer form a loose mesh. This superficial layer of the dermis projects into the stratum basale of the epidermis to form finger-like dermal papillae (see Figure 6). Within the papillary layer are fibroblasts, a small number of fat cells (adipocytes), and an abundance of small blood vessels. In addition, the papillary layer contains phagocytes, defensive cells that help fight bacteria or other infections that have breached the skin. This layer also contains lymphatic capillaries, nerve fibers, and touch receptors called the Meissner corpuscles.

Reticular Layer

Underlying the papillary layer is the much thicker reticular layer , composed of dense, irregular connective tissue. This layer is well vascularized and has a rich sensory and sympathetic nerve supply. The reticular layer appears reticulated (net-like) due to a tight meshwork of fibers. Elastin fibers provide some elasticity to the skin, enabling movement. Collagen fibers provide structure and tensile strength, with strands of collagen extending into both the papillary layer and the hypodermis. In addition, collagen binds water to keep the skin hydrated. Collagen injections and Retin-A creams help restore skin turgor by either introducing collagen externally or stimulating blood flow and repair of the dermis, respectively.

Hypodermis

The hypodermis (also called the subcutaneous layer or superficial fascia) is a layer directly below the dermis and serves to connect the skin to the underlying fascia (fibrous tissue) of the bones and muscles. It is not strictly a part of the skin, although the border between the hypodermis and dermis can be difficult to distinguish. The hypodermis consists of well-vascularized, loose, areolar connective tissue and adipose tissue, which functions as a mode of fat storage and provides insulation and cushioning for the integument.

Everyday Connection

Lipid Storage

The hypodermis is home to most of the fat that concerns people when they are trying to keep their weight under control. Adipose tissue present in the hypodermis consists of fat-storing cells called adipocytes. This stored fat can serve as an energy reserve, insulate the body to prevent heat loss, and act as a cushion to protect underlying structures from trauma.

Where the fat is deposited and accumulates within the hypodermis depends on hormones (testosterone, estrogen, insulin, glucagon, leptin, and others), as well as genetic factors. Fat distribution changes as our bodies mature and age. Men tend to accumulate fat in different areas (neck, arms, lower back, and abdomen) than do women (breasts, hips, thighs, and buttocks). The body mass index (BMI) is often used as a measure of fat, although this measure is, in fact, derived from a mathematical formula that compares body weight (mass) to height. Therefore, its accuracy as a health indicator can be called into question in individuals who are extremely physically fit.

In many animals, there is a pattern of storing excess calories as fat to be used in times when food is not readily available. In much of the developed world, insufficient exercise coupled with the ready availability and consumption of high-calorie foods have resulted in unwanted accumulations of adipose tissue in many people. Although periodic accumulation of excess fat may have provided an evolutionary advantage to our ancestors, who experienced unpredictable bouts of famine, it is now becoming chronic and considered a major health threat. Recent studies indicate that a distressing percentage of our population is overweight and/or clinically obese. Not only is this a problem for the individuals affected, but it also has a severe impact on our healthcare system. Changes in lifestyle, specifically in diet and exercise, are the best ways to control body fat accumulation, especially when it reaches levels that increase the risk of heart disease and diabetes.

Pigmentation

The color of skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred into the keratinocytes via a cellular vesicle called a melanosome (Figure 7).

Figure 7: The relative coloration of the skin depends of the amount of melanin produced by melanocytes in the stratum basale and taken up by keratinocytes.

Melanin occurs in two primary forms. Eumelanin exists as black and brown, whereas pheomelanin provides a red color. Dark-skinned individuals produce more melanin than those with pale skin. Exposure to the UV rays of the sun or a tanning salon causes melanin to be manufactured and built up in keratinocytes, as sun exposure stimulates keratinocytes to secrete chemicals that stimulate melanocytes. The accumulation of melanin in keratinocytes results in the darkening of the skin, or a tan. This increased melanin accumulation protects the DNA of epidermal cells from UV ray damage and the breakdown of folic acid, a nutrient necessary for our health and well-being. In contrast, too much melanin can interfere with the production of vitamin D, an important nutrient involved in calcium absorption. Thus, the amount of melanin present in our skin is dependent on a balance between available sunlight and folic acid destruction, and protection from UV radiation and vitamin D production.

It requires about 10 days after initial sun exposure for melanin synthesis to peak, which is why pale-skinned individuals tend to suffer sunburns of the epidermis initially. Dark-skinned individuals can also get sunburns, but are more protected than are pale-skinned individuals. Melanosomes are temporary structures that are eventually destroyed by fusion with lysosomes this fact, along with melanin-filled keratinocytes in the stratum corneum sloughing off, makes tanning impermanent.

Too much sun exposure can eventually lead to wrinkling due to the destruction of the cellular structure of the skin, and in severe cases, can cause sufficient DNA damage to result in skin cancer. When there is an irregular accumulation of melanocytes in the skin, freckles appear. Moles are larger masses of melanocytes, and although most are benign, they should be monitored for changes that might indicate the presence of cancer ( Figure 8).

Figure 8: Moles range from benign accumulations of melanocytes to melanomas. These structures populate the landscape of our skin. (credit: the National Cancer Institute)

Disorders of the&hellip

Integumentary System

The first thing a clinician sees is the skin, and so the examination of the skin should be part of any thorough physical examination. Most skin disorders are relatively benign, but a few, including melanomas, can be fatal if untreated. A couple of the more noticeable disorders, albinism and vitiligo, affect the appearance of the skin and its accessory organs. Although neither is fatal, it would be hard to claim that they are benign, at least to the individuals so afflicted.

Albinism is a genetic disorder that affects (completely or partially) the coloring of skin, hair, and eyes. The defect is primarily due to the inability of melanocytes to produce melanin. Individuals with albinism tend to appear white or very pale due to the lack of melanin in their skin and hair. Recall that melanin helps protect the skin from the harmful effects of UV radiation. Individuals with albinism tend to need more protection from UV radiation, as they are more prone to sunburns and skin cancer. They also tend to be more sensitive to light and have vision problems due to the lack of pigmentation on the retinal wall. Treatment of this disorder usually involves addressing the symptoms, such as limiting UV light exposure to the skin and eyes. In vitiligo , the melanocytes in certain areas lose their ability to produce melanin, possibly due to an autoimmune reaction. This leads to a loss of color in patches (Figure 9). Neither albinism nor vitiligo directly affects the lifespan of an individual.

Figure 9: Individuals with vitiligo experience depigmentation that results in lighter colored patches of skin. The condition is especially noticeable on darker skin. (credit: Klaus D. Peter)

Other changes in the appearance of skin coloration can be indicative of diseases associated with other body systems. Liver disease or liver cancer can cause the accumulation of bile and the yellow pigment bilirubin, leading to the skin appearing yellow or jaundiced (jaune is the French word for &ldquoyellow&rdquo). Tumors of the pituitary gland can result in the secretion of large amounts of melanocyte-stimulating hormone (MSH), which results in a darkening of the skin. Similarly, Addison&rsquos disease can stimulate the release of excess amounts of adrenocorticotropic hormone (ACTH), which can give the skin a deep bronze color. A sudden drop in oxygenation can affect skin color, causing the skin to initially turn ashen (white). With a prolonged reduction in oxygen levels, dark red deoxyhemoglobin becomes dominant in the blood, making the skin appear blue, a condition referred to as cyanosis (kyanos is the Greek word for &ldquoblue&rdquo). This happens when the oxygen supply is restricted, as when someone is experiencing difficulty in breathing because of asthma or a heart attack. However, in these cases the effect on skin color has nothing do with the skin&rsquos pigmentation.

The ABC video linked to below follows the story of a pair of fraternal African-American twins, one of whom is albino. Click on the link below to watch a video about the challenges these children and their family face. Which ethnicities do you think are exempt from the possibility of albinism?

Chapter Review

The skin is composed of two major layers: a superficial epidermis and a deeper dermis. The epidermis consists of several layers beginning with the innermost (deepest) stratum basale (germinatum), followed by the stratum spinosum, stratum granulosum, stratum lucidum (when present), and ending with the outermost layer, the stratum corneum. The topmost layer, the stratum corneum, consists of dead cells that shed periodically and is progressively replaced by cells formed from the basal layer. The stratum basale also contains melanocytes, cells that produce melanin, the pigment primarily responsible for giving skin its color. Melanin is transferred to keratinocytes in the stratum spinosum to protect cells from UV rays.

The dermis connects the epidermis to the hypodermis, and provides strength and elasticity due to the presence of collagen and elastin fibers. It has only two layers: the papillary layer with papillae that extend into the epidermis and the lower, reticular layer composed of loose connective tissue. The hypodermis, deep to the dermis of skin, is the connective tissue that connects the dermis to underlying structures it also harbors adipose tissue for fat storage and protection.


Stratum Basale

The stratum basale (also called the stratum germinativum) is the deepest epidermal layer and attaches the epidermis to the basal lamina, below which lie the layers of the dermis. The cells in the stratum basale bond to the dermis via intertwining collagen fibers, referred to as the basement membrane. A finger-like projection, or fold, known as the dermal papilla (plural = dermal papillae) is found in the superficial portion of the dermis. Dermal papillae increase the strength of the connection between the epidermis and dermis the greater the folding, the stronger the connections made (Figure 3).

Figure 3. The epidermis of thick skin has five layers: stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, and stratum corneum.

The stratum basale is a single layer of cells primarily made of basal cells. A basal cell is a cuboidal-shaped stem cell that is a precursor of the keratinocytes of the epidermis. All of the keratinocytes are produced from this single layer of cells, which are constantly going through mitosis to produce new cells. As new cells are formed, the existing cells are pushed superficially away from the stratum basale. Two other cell types are found dispersed among the basal cells in the stratum basale. The first is a Merkel cell, which functions as a receptor and is responsible for stimulating sensory nerves that the brain perceives as touch. These cells are especially abundant on the surfaces of the hands and feet. The second is a melanocyte, a cell that produces the pigment melanin. Melanin gives hair and skin its color, and also helps protect the living cells of the epidermis from ultraviolet (UV) radiation damage.

In a growing fetus, fingerprints form where the cells of the stratum basale meet the papillae of the underlying dermal layer (papillary layer), resulting in the formation of the ridges on your fingers that you recognize as fingerprints. Fingerprints are unique to each individual and are used for forensic analyses because the patterns do not change with the growth and aging processes.


Sun and Your Skin

Exposure to sunlight is the single biggest culprit in aging skin.

Over time, the sun's ultraviolet (UV) light damages certain fibers in the skin called elastin. The breakdown of elastin fibers causes the skin to sag, stretch, and lose its ability to snap back after stretching. The skin also bruises and tears more easily and takes longer to heal. So while sun damage may not show when you're young, it will later in life.

Nothing can completely undo sun damage, although the skin can sometimes repair itself. Lasers can also help reverse some of the damage. So, it's never too late to begin protecting yourself from sun exposure and skin cancer. You can delay changes associated with aging by staying out of the sun, covering up, wearing a hat, and making a habit of using sunscreen.

Continued


What is the density of a human skin cell? - (Jul/19/2012 )

A colleague working in physics posed this question today and left myself and a number of fellow scientists, and his own dermatologist wondering.

"What is the density of a human skin cell?"

Understandably this will change depending on the layers of skin, which part of the body, with age etc but in general I could not locate any definitive answer.

Anyone know the answer? Or even how one would go about determining this?

My colleague looked quite exasperated when we said "google it".

Do you mean how many skin cells per unit volume or do you mean mass per unit volume?

When he was asking he mentioned if he had a kg of skin cells, what would the density be, so I presume mass per unit volume.

Well, you could take a series of samples of human skin (a few hundred thousand cells per sample) and put one sample into each of a series of aqueous solutions that have their densities increased over the series.

Humans are near enough neutrally buoyant so the density of each sample is going to be near 1gcm -3 but it&rsquos unlikely to be exactly that. Do this over a series of samples from different individuals to obtain a value for a mean human (or mean of the sub-set of humans you have selected by gender, age and race).

Of course I do have to ask where your &ldquofriend&rdquo is getting 1kg of human skin from. Should we be calling the authorities?

I see your point, the closest we got was that skin cells float on water so they must be less dense than water. I will pass on your suggestion, thank you.

I am still surprised that it is not an easily accessible piece of info.

Astilius on Thu Jul 19 15:54:16 2012 said:

He mentioned it was for testing the penetrating ability of a laser, but I fear that does little for our case. makes him sound like bond villain.

In my experience with cell culture, eukaryotic cells in general are more dense than a normal saline solution or PBS (they sink in these solutions), which means that they will be more dense than water, but how much more is hard to say. According to the wikipedia article(http://en.wikipedia. ical_properties) on adipose tissue, muscle cells have a density of 1.09, so I would expect skin cells to be slightly less dense.

FYI, the near enough neutral density of humans is due to fat deposits in the body (density about 0.9) and the presence of cavities such as the lungs that are full of air and thus more buoyant.

Thank you for the information, I passed it on this morning.

In your opinion would pig skin would be quite a close approximation to human skin with regard to density of epithelial layers. It would simplify matters quite a bit if he could use pig skin, but I would be nervous about the scientific merit of this.

Absolutely, pigs are a pretty good approximation for most things human. They do tend to have a bit more fat below the skin than humans though.


Why do my fingers absorb water and become wrinkled?

Human finger tips do not become wrinkled because they absorb water. Skin is a fairly good barrier that keeps out most of the external water. If our fingers did absorb a significant amount of water after staying in the pool or bath for several minutes, then our fingers would swell to round, plump shapes, which is the opposite of wrinkling. The wrinkling is actually caused by a reduction of fluid inside the finger tips.

How can our finger tips experience reduced fluid internally when exposed to increased fluid externally? From a physical perspective, this effect seems to be a paradox. The answer is that the wrinkling of wet finger tips is an active biological response, rather than a passive physical effect. Scientists have known for almost a hundred years that nerve damage in the hand can result in a person no longer being able to get wet-induced finger wrinkles. Finger wrinkling is therefore controlled by the nervous system. Nerve signals cause blood vessels in the finger tips to constrict, reducing the amount of fluid in the finger tips. Just as drying out a grape causes it to turn into a wrinkled raisin, the reduction of fluid in the finger tips causes them to shrivel and wrinkle.

Since finger wrinkling is an active neurological response, it is likely that evolution selected for it because this response confers some type of survival advantage. But how could wrinkles ever help one survive? This question has long been wondered and the answer is still far from settled. However, research done in 2011 seems to hint at an answer. As reported in the journal Brains, Behavior and Evolution, Mark Changizi and his associates at the 2AI Labs found evidence that finger tip wrinkles are shaped to improve the grip of wet fingers. They state, "We show that their morphology has the signature properties of drainage networks, enabling efficient removal of water from the gripped surface. Wet-induced wrinkles may, in fact, be substantially superior to 'rain treads' on shoes, which maintain a tread even when under compression and thus have a surface area of contact that is reduced. Wet-induced wrinkle treads, on the other hand, are pliable, and the act of pressing a finger tip down on a wet surface 'squeezes' the fluid out from under the finger through the channels, and upon completion of this single pulsatile flow the entire finger's skin contacts the surface." A human with an improved grip can better handle tools and weapons in the rain, as well as retrieve food from rivers and streams. In this way, the wrinkling of fingers in response to water could have provided a significant survival advantage to our ancestors.

Additional research carried out in 2013 by Kyriacos Kareklas and associates, as reported in Biology Letters, found that participants were able to transfer wet marbles and fishing weights between containers significantly faster if they had wet-induced finger wrinkles. They therefore showed that finger wrinkles indeed improve a human's ability to grip and manipulate wet objects. While more research is needed to confirm these results, these studies suggest that the improved-grip hypothesis is a plausible explanation to wet-induced finger wrinkling.


6. Phlebotomist

Average salary: $33,670 / £22,500

We guarantee that, when you were six years old, you shouted to the heavens that you want to be a phlebotomist when you grew up. Well, 20 years later, and you are about to enter this field, which is in part because of your desire to find careers in biology.

For the uninitiated, a phlebotomist uses venepuncture – an incision in the vein to draw blood – to collect blood samples for a whole host of reasons, from transfusions to testing to research. If you’re nervous around needles and if blood makes you ill, then perhaps this is not the job for you. If they don’t, then phlebotomist is great for new graduates.


Density of Body Fat

A person's body density depends on how much fat and fat-free mass he carries. Fat is found under the skin, around the internal organs, as an essential part of the central nervous system, as part of the structure of some internal organs and inside the bone marrow. The density of fat is fairly consistent at 0.91 kilogram per liter and is less dense that most of your fat-free mass.

When you know your total body density, you still don't know what percentage of it is fat. But you can plug your body density into the following equation to get a general idea: percent body fat = (495 / Body Density) - 450.


Genes responsible for diversity of human skin colors identified

Human populations feature a broad palette of skin tones. But until now, few genes have been shown to contribute to normal variation in skin color, and these had primarily been discovered through studies of European populations.

Now, a study of diverse African groups led by University of Pennsylvania geneticists has identified new genetic variants associated with skin pigmentation. The findings help explain the vast range of skin color on the African continent, shed light on human evolution and inform an understanding of the genetic risk factors for conditions such as skin cancer.

"We have identified new genetic variants that contribute to the genetic basis of one of the most strikingly variable traits in modern humans," said Sarah Tishkoff, a Penn Integrates Knowledge Professor and the David and Lyn Silfen University Professor in Genetics and Biology with appointments in the Perelman School of Medicine and School of Arts and Sciences. "When people think of skin color in Africa most would think of darker skin, but we show that within Africa there is a huge amount of variation, ranging from skin as light as some Asians to the darkest skin on a global level and everything in between. We identify genetic variants affecting these traits and show that mutations influencing light and dark skin have been around for a long time, since before the origin of modern humans."

The findings are published in the journal Science. Tishkoff, senior author, collaborated with first author and lab member Nicholas Crawford, a postdoctoral fellow, and a multi-institutional, international team.

Tishkoff has long studied the genetics of African populations, looking at traits such as height, lactose tolerance, bitter-taste sensitivity and high-altitude adaptation. Skin color emerged as a trait of interest from her experience working on the continent and seeing the diversity present across groups.

"Skin color is a classic variable trait in humans, and it's thought to be adaptive," Tishkoff said. "Analysis of the genetic basis of variation in skin color sheds light on how adaptive traits evolve, including those that play a role in disease risk."

Both light and dark skin pigmentations confer benefits: Darker skin, for example, is believed to help prevent some of the negative impacts of ultraviolet light exposure, while lighter skin is better able to promote synthesis of vitamin D in regions with low ultraviolet light exposure.

To objectively capture the range of skin pigmentation in Africa, Tishkoff and colleagues used a color meter to measure the light reflectance of the skin of more than 2,000 Africans from ethnically and genetically diverse populations. They took the measurement from the inner arm, when sun exposure is minimal. The measurements can be used to infer levels of the skin pigment melanin. They obtained a range of measurements the darkest skin was observed in Nilo-Saharan pastoralist populations in eastern Africa, and the lightest skin was observed in San hunter-gatherer populations in southern Africa.

The researchers obtained genetic information from nearly 1,600 people, examining more than 4 million single nucleotide polymorphisms across the genome, places where the DNA code may differ by one "letter." From this dataset the researchers were able to do a genome-wide association study and found four key areas of the genome where variation closely correlated with skin color differences.

The region with the strongest associations was in and around the SLC24A5 gene, one variant of which is known to play a role in light skin color in European and some southern Asian populations and is believed to have arisen more than 30,000 years ago. This variant was common in populations in Ethiopia and Tanzania that were known to have ancestry from southeast Asia and the Middle East, suggesting it was carried into Africa from those regions and, based on its frequency, may have been positively selected.

Another region, which contains the MFSD12 gene, had the second strongest association to skin pigmentation. This gene is expressed at low levels in depigmented skin in individuals with vitiligo, a condition where the skin loses pigment in some areas.

"I still rememeber the 'ah ha!' moment when we saw this gene was associated with vitiligo," said Crawford. "That's when we knew we'd found something new and exciting."

The team found that mutations in and around this gene that were associated with dark pigmentation were present at high frequencies in populations of Nilo-Saharan ancestry, who tend to have very dark skin, as well as across sub-Saharan populations, except the San, who tend to have lighter skin. They also identified these variants, as well as others associated with dark skin pigmentation, in South Asian Indian and Australo-Melanesian populations, who tend to have the darkest skin coloration outside of Africa.

"The origin of traits such as hair texture, skin color and stature, which are shared between some indigenous populations in Melanesia and Australia and some sub-Saharan Africans, has long been a mystery." Tishkoff said. "Some have argued it's because of convergent evolution, that they independently evolved these mutations, but our study finds that, at genes associated with skin color, they have the identical variants associated with dark skin as Africans.

"Our data are consistent with a proposed early migration event of modern humans out of Africa along the southern coast of Asia and into Australo-Melanesia and a secondary migration event into other regions. However, it is also possible that there was a single African source population that contained genetic variants associated with both light and dark skin and that the variants associated with dark pigmentation were maintained only in South Asians and Australo-Melanesians and lost in other Eurasians due to natural selection."

Also of interest was that genetic variants at MFSD12, OCA2, and HERC2 associated with light skin pigmentation were at highest frequency in the African San population, which has the oldest genetic lineages in the world, as well as in Europeans.

MFSD12 is highly expressed in melanocytes, the cells that produce melanin. To verify the gene's role in contributing to skin pigmentation, the researchers blocked expression of the gene in cells in culture and found an increase in production of eumelanin, the pigment type responsible for black and brown skin, hair and eye color. Knocking out the gene in zebrafish caused a loss of cells that produce yellow pigment. And in mice, knocking out the gene changed the color of their coat from agouti, caused by hairs with a red and yellow pigment, to a uniform gray by eliminating production of pheomelanin, a type of pigment also found in humans.

"Apart from one study showing that MFSD12 was associated with vitiligo lesions, we didn't know much else about it," said Crawford, "so these functional assays were really crucial."

"We went beyond most genome-wide association studies to do functional assays," Tishkoff said, "and found that knocking out MFSD12 dramatically impacted the pigmentation of fish and mice. It's pointing to this being a very conserved trait across species.

"We don't know exactly why, but blocking this gene causes a loss of pheomelanin production and an increase in eumelanin production," Tishkoff added. "We also showed that Africans have a lower level of MFSD12 expression, which makes sense, as low levels of the gene means more eumelanin production."

A collaborator on the work, Michael Marks, a professor in the departments of Pathology & Laboratory Medicine and of Physiology at Children's Hospital of Philadelphia and at Penn Medicine, demonstrated that the MFSD12 gene influences eumelanin pigmentation in a novel manner. Unlike other pigmentation genes, which are expressed mainly in melanosomes, the organelle where melanin is produced, MFSD12 is expressed in lysosomes, a distinct organelle from the melanosomes that produce eumelanin.

"Our results suggest there must be some kind of as-yet-uncharacterized form of cross-talk between lysosomes and the melanosomes that make eumelanins," Marks said. "Figuring out how this works might provide new ideas for ways to manipulate skin pigmentation for therapeutic means.

"In addition," Marks said, "the fact that loss of MFSD12 expression had opposite effects on the two types of melanins, increasing eumelanin production while suppressing pheomelanin, suggests that melanosomes that make pheomelanins might be more related to lysosomes than those that make eumelanin."

Additional associations with skin color were found in the OCA2 and HERC2 genes, which have been linked with skin, eye and hair color variation in Europeans, though the mutations identified are novel. Mutations in OCA2 also cause a form of albinism that is more common in Africans than in other populations. The researchers observed genetic variants in a neighboring gene, HERC2, which regulates the expression of OCA2. Within OCA2, they identified a variant common in Europeans and San that is associated with a shorter version of the protein, with an altered function. They observed a signal of balancing selection of OCA2, meaning that two different versions of the gene have been maintained, in this case for more than 600,000 years.

"What this tells us," Tishkoff said, "is there is likely some selective force maintaining these two alleles. It is likely that this gene is playing a role in other aspects of human physiology which are important."

A final genetic region the researchers found to be associated with skin pigmentation included genes that play a role in ultraviolet light response and melanoma risk. The top candidate gene in the region is DDB1, involved in repairing DNA after exposure to UV light.

"Africans don't get melanoma very often," Tishkoff said. "The variants near these genes are highest in populations who live in areas of the highest ultraviolet light intensity, so it makes sense that they may be playing a role in UV protection."

The mutations identified by the team play a role in regulating expression of DDB1 and other nearby genes.

"Though we don't yet know the mechanism by which DDB1 is impacting pigmentation, it is of interest to note that this gene, which is highly conserved across species, also plays a role in pigmentation in plants such as tomatoes," said Tishkoff.

The team saw evidence that this region of the genome has been a strong target of natural selection outside of Africa mutations associated with light skin color swept to nearly 100 percent frequency in non-Africans, one of few examples of a "selective sweep" in all Eurasians the age of the selective sweep was estimated to be around 60,000 to 80,000 years old, around the time of migration of modern humans out of Africa.

One additional takeaway from this work is a broader picture of the evolution of skin color in humans. Most of the genetic variants associated with light and dark pigmentation from the study appear to have originated more than 300,000 years ago, and some emerged roughly 1 million years ago, well before the emergence of modern humans. The older version of these variants in many cases was the one associated with lighter skin, suggesting that perhaps the ancestral state of humans was moderately pigmented rather than darkly pigmented skin.

"If you were to shave a chimp, it has light pigmentation," Tishkoff said, "so it makes sense that skin color in the ancestors of modern humans could have been relatively light. It is likely that when we lost the hair covering our bodies and moved from forests to the open savannah, we needed darker skin. Mutations influencing both light and dark skin have continued to evolve in humans, even within the past few thousand years."

Tishkoff noted that the work underscores the diversity of African populations and the lack of support for biological notions of race.

"Many of the genes and new genetic variants we identified to be associated with skin color may never have been found outside of Africa, because they are not as highly variable," Tishkoff said. "There is so much diversity in Africa that's not often appreciated. There's no such thing as an African race. We show that skin color is extremely variable on the African continent and that it is still evolving. Further, in most cases the genetic variants associated with light skin arose in Africa."


Skin changes are among the most visible signs of aging. Evidence of increasing age includes wrinkles and sagging skin. Whitening or graying of the hair is another obvious sign of aging.

Your skin does many things. It:

  • Contains nerve receptors that allow you to feel touch, pain, and pressure
  • Helps control fluid and electrolyte balance
  • Helps control your body temperature
  • Protects you from the environment

Although skin has many layers, it can generally be divided into three main parts:

  • The outer part (epidermis) contains skin cells, pigment, and proteins.
  • The middle part (dermis) contains skin cells, blood vessels, nerves, hair follicles, and oil glands. The dermis provides nutrients to the epidermis.
  • The inner layer under the dermis (the subcutaneous layer) contains sweat glands, some hair follicles, blood vessels, and fat.

Each layer also contains connective tissue with collagen fibers to give support and elastin fibers to provide flexibility and strength.

Skin changes are related to environmental factors, genetic makeup, nutrition, and other factors. The greatest single factor, though, is sun exposure. You can see this by comparing areas of your body that have regular sun exposure with areas that are protected from sunlight.

Natural pigments seem to provide some protection against sun-induced skin damage. Blue-eyed, fair-skinned people show more aging skin changes than people with darker, more heavily pigmented skin.

With aging, the outer skin layer (epidermis) thins, even though the number of cell layers remains unchanged.

The number of pigment-containing cells (melanocytes) decreases. The remaining melanocytes increase in size. Aging skin looks thinner, paler, and clear (translucent). Pigmented spots including age spots or "liver spots" may appear in sun-exposed areas. The medical term for these areas is lentigos.

Changes in the connective tissue reduce the skin's strength and elasticity. This is known as elastosis. It is more noticeable in sun-exposed areas (solar elastosis). Elastosis produces the leathery, weather-beaten appearance common to farmers, sailors, and others who spend a large amount of time outdoors.

The blood vessels of the dermis become more fragile. This leads to bruising, bleeding under the skin (often called senile purpura), cherry angiomas, and similar conditions.

Sebaceous glands produce less oil as you age. Men experience a minimal decrease, most often after the age of 80. Women gradually produce less oil beginning after menopause. This can make it harder to keep the skin moist, resulting in dryness and itchiness.

The subcutaneous fat layer thins so it has less insulation and padding. This increases your risk of skin injury and reduces your ability to maintain body temperature. Because you have less natural insulation, you can get hypothermia in cold weather.

Some medicines are absorbed by the fat layer. Shrinkage of this layer may change the way that these medicines work.

The sweat glands produce less sweat. This makes it harder to keep cool. Your risk for overheating or developing heat stroke increases.

Growths such as skin tags, warts, brown rough patches (seborrheic keratoses), and other blemishes are more common in older people. Also common are pinkish rough patches (actinic keratosis) which have a small chance of becoming a skin cancer.

As you age, you are at increased risk for skin injury. Your skin is thinner, more fragile, and you lose some of the protective fat layer. You also may be less able to sense touch, pressure, vibration, heat, and cold.

Rubbing or pulling on the skin can cause skin tears. Fragile blood vessels can break easily. Bruises, flat collections of blood (purpura), and raised collections of blood (hematomas) may form after even a minor injury.

Pressure ulcers can be caused by skin changes, loss of the fat layer, reduced activity, poor nutrition, and illnesses. Sores are most easily seen on the outside surface of the forearms, but they can occur anywhere on the body.

Aging skin repairs itself more slowly than younger skin. Wound healing may be up to 4 times slower. This contributes to pressure ulcers and infections. Diabetes, blood vessel changes, lowered immunity, and other factors also affect healing.

Skin disorders are so common among older people that it is often hard to tell normal changes from those related to a disorder. More than 90% of all older people have some type of skin disorder.

Skin disorders can be caused by many conditions, including:

  • Blood vessel diseases, such as arteriosclerosis
  • Diabetes
  • Nutritional deficiencies
  • Obesity
  • Reactions to medicines
  • Stress

Other causes of skin changes:

  • Allergies to plants and other substances
  • Climate
  • Clothing
  • Exposures to industrial and household chemicals
  • Indoor heating
  • Loss of elasticity (elastosis)
  • Noncancerous skin growths (keratoacanthomas)
  • Pigment changes such as liver spots
  • Thickening of the skin

Sun exposure has also been directly linked to skin cancers, including basal cell cancer, squamous cell carcinoma, and melanoma.

Because most skin changes are related to sun exposure, prevention is a lifelong process.

  • Prevent sunburn if at all possible.
  • Use a good quality sunscreen when outdoors, even in the winter.
  • Wear protective clothing and a hat when needed.

Good nutrition and adequate fluids are also helpful. Dehydration increases the risk of skin injury. Sometimes minor nutritional deficiencies can cause rashes, skin lesions, and other skin changes, even if you have no other symptoms.

Keep skin moist with lotions and other moisturizers. Do not use soaps that are heavily perfumed. Bath oils are not recommended because they can cause you to slip and fall. Moist skin is more comfortable and will heal more quickly.



Comments:

  1. Uilleam

    I'm sorry, but, in my opinion, they were wrong. I propose to discuss it. Write to me in PM, speak.

  2. Zuluktilar

    I apologize, but I think you are wrong. Enter we'll discuss it.

  3. Dorien

    I mean you are not right. I can prove it. Write to me in PM, we will discuss.



Write a message