Saturday, July 5, 2008
Pregnancy often leaves women with stretch marks. Most women are keen to know about avoiding stretch marks during pregnancy.
When you gain weight rapidly, the skin stretches too fast and stretch marks appear. Known to dermatologists as striae, these stretch marks usually begin as red or purple blemishes that turn to silvery white lines on the skin. They mostly appear on the areas of the body that grow too quickly.
Looking for the Key to Avoiding Stretch Marks During Pregnancy?
During pregnancy the woman’s body undergoes major changes, and avoiding stretch marks during pregnancy is not always easy. It is not easy and cannot be done by everyone. Many women find that avoiding stretch marks during pregnancy is not possible even if they take great care. While there is a great chance that women acquire stretch marks during their pregnancy, very few women actually succeed in completely avoiding stretch marks during pregnancy.
The most important point to be kept in mind is to moisturize the area that is likely to be affected. Avoiding stretch marks during pregnancy is possible to some extent if areas such as the stomach, breasts, buttocks, arms and thighs are constantly moisturized. Products such as cocoa butter, shea butter and oils should be applied a minimum of twice a day to minimize the possibility of stretch marks.
Another tip that could help you avoid getting stretch marks during pregnancy is to make sure that the weight you gain is within the limits set by your obstetrician. If you are able to control (to a certain point) the amount of weight you gain during this time to these recommended levels, you have a great chance the stomach is going to be the only area that grows while the rest of your body will gain only smaller amounts of weight. This is a great tip to contain stretch marks, ensuring that they are limited to the stomach region.
However there are many women that are able to maintain their weight at levels recommended by their doctors but still cannot contain stretch marks to the stomach area, it is not possible for all women to do this. While it is inevitable that you will gain weight during you pregnancy, a slower increase kept within limits allows the skin the needed time to adjust to the growth of the belly, instead of a rapid increase in weight.
One of the most important factors to avoid getting stretch marks during pregnancy is to make sure your skin is moisturized at all time. Along with this approach another way is to keep weight gain at a lower but healthy level. After all these precautions if they still appear, a moisturizer is recommended, in the hope that the stretch marks will eventually disappear.
About the Author:
If you are searching for the best solution for removing your stretch marks, visit my website. I can show you how to get rid of stretch marks. You will find reviews of the best stretch marks cream on the market.
Friday, July 4, 2008
Looking beautiful can sometimes become quite a job. If you don’t have a clear cut plan of action and the right products for your skin. You can be using the best skin care products but still be missing something that can potentially stop you from looking your best.
Wrinkle Creams, skin moisturizes that nourishes dry skin and moisturizing creams that help keep your skin smooth and also silky! Scores of skin care companies at fine department stores entice you with the showy image and advertisements and naturally, seasonal rebates to make money out of us and still leave us in a pitch while always searching for solutions to the our problem - skin care with anti aging benefits.
Some Cosmetologists agree that proper skincare is the effortless program to deliver us from get too old too quick. Here are a few ways that could help us rejuvenate our skin’s vitality and maintain its health. Anti-aging skin care actually slows aging. We could easily slow down our aging process in the inexpensive and simplest ways. Here are six active suggestions for anti-aging skin care:
1. Eat a well-balanced diet: A balanced diet is key to preserving an effective body metabolism. Fruits and veggies are one of the greatest sources of fiber. They have a revitalizing force on our body. Do not eat oily and fatty foods since they lack in necessary nutrients and stimulate obesity and accelerate the aging process. 2. Do things that combat stress: Stress is one of the main things that accelerate our aging process. It has a damaging influence on our body. It lessens our appetite, interferes with our sleeping schedule and impacts our life as a whole.Respond to stress by seeing to our needs and taking care of ourselves, accelerates the aging process. Having a good balanced diet, getting adequate sleep, regular physical exercise and self-care are all sure ways of beating stress. 3. Drink enough H2O daily: This is one of the most inexpensive and easiest anti aging skin care answer. Water neutralizes and helps remove toxins from our body and keeps our skin clear and supple. 4. Adopt an exercise routine: An exercise routine is a great anti-aging skin care answer. All exercise programs improve blood circulation throughout our body, tones up our muscles and also helps keep the skin clean by purging out toxins in the form of perspiration. 5. Don’t use chemical-based products on your skin: Completely avoid usage of chemical containing skincare beauty products for your skin. Natural skin care products are a stronger alternative. Healthy skin nurturing products, whether home made or commercial ones are highly good as an antiaging skin care solution. 6. Safeguard your skin against damaging sun rays: UV radiation affect our skin and assists in speeding up the aging process. Use of good sun blocking lotion should be a frequent practice in our skin care regimen specially when we need to be exposed to the hot sun.
About the Author:
Slowing down aging is to a greater extent in our hands than in the departmental stores that sell cheap products. To get exceptional skin care products, find out about recipes of skin antiaging care creams, lotions, facials, serums and more, made at home You can get a unique content version of this article from the Uber Article Directory.
Thursday, July 3, 2008
Einstein's Monoclonal Antibody Shows Encouraging Results In Clinical Trial Of Novel Melanoma Treatment Pain Therapeutics, Inc. recently announced th
Pain Therapeutics, Inc. recently announced the successful completion of its first clinical study utilizing a novel melanoma treatment, which the company licensed from Albert Einstein College of Medicine of Yeshiva University. The treatment consisted of dosing patients with a monoclonal antibody labeled with a radioisotope.
A research team at Einstein, led by Arturo Casadevall, M.D., Ph.D., professor and chairman of microbiology & immunology, and Ekaterina Dadachova, Ph.D., associate professor of nuclear medicine and of microbiology & immunology, developed the novel approach to treat metastatic melanoma based on targeting melanin, a skin pigment that is released from dead melanotic tumor cells, with radiolabeled monoclonal antibodies. While the antibodies seek out the released melanin and destroy human melanoma cells with a lethal dose of ionizing radiation, melanin in normal, healthy tissue is not targeted because it is inside the cells and not accessible to the radio-labeled antibody. Small animal studies have demonstrated the feasibility of this approach.
In the recent clinical study, a team of researchers in Israel administered the radiolabeled monoclonal antibody to 12 patients diagnosed with advanced melanoma. Top-line results of this Phase I study indicate this antibody binds to melanoma tumor sites, as evidenced by powerful imaging data obtained by planar scintigraphy and SPECT/CT (single photon emission computed tomography combined with computed tomography). No serious drug-related, adverse events were observed in this study.
"Our initial findings demonstrated how basic research in one area of medicine can yield unexpected benefits for an entirely different field," said Dr. Casadevall. "We didn't set out to find a cure for melanoma. Instead, the advance emerged from my study of Cryptococcus, a fungus that can cause fatal infections in people with weakened immune systems and evolved from there. It is exciting when findings take such a promising turn and we are thrilled that this first clinical study using our monoclonal antibody has met with the success that it has thus far."
"Going from the laboratory to clinical application is what we researchers strive to do so that physicians and their patients can be offered more and better options for treatment," said Dr. Dadachova. "It is among the most rewarding aspects of conducting research and we are grateful to Pain Therapeutics and our colleagues at Hadassah Medical Center for their efforts to determine how useful this treatment can possibly be. We have great hopes for further success."
The objectives of the first Phase I study were to assess safety, pharmacokinetics and dosimetry to normal organs. As a result of encouraging data in all of these areas, Pain Therapeutics plans to initiate a second study in which patients will receive increasing amounts of radioactivity delivered by the radiolabeled antibody. The radioactive doses delivered to these patients will be significantly higher than those delivered to the patients of the first study.
At the Society for Nuclear Medicine Annual Meeting in New Orleans, last week, research teams from each of the collaborating laboratories - at Albert Einstein College of Medicine (New York) and Hadassah Medical Center (Jerusalem) presented data related to Pain Therapeutics' melanoma program. This meeting is considered to be the world's most significant technical meeting focused on breakthrough developments in clinical imaging and nuclear medicine.
At the meeting, Dr. Dadachova also was presented with an award by the Society's Young Professionals' Committee. The award is given in recognition of significant contributions to the fields of nuclear medicine and molecular imaging by young researchers.
About Albert Einstein College of Medicine of Yeshiva University
The Albert Einstein College of Medicine of Yeshiva University is one of the nation's premier centers for research, medical education and clinical investigation. It is the home to some 2,000 faculty members, 750 M.D. students, 350 Ph.D. students (including 125 in combined M.D./Ph.D. programs) and 380 postdoctoral investigators. Last year, Einstein received more than $150 million in grant funding from the National Institutes of Health (NIH). In addition, the NIH funds major research centers at Einstein in diabetes, cancer, liver disease, and AIDS. Other areas where the College of Medicine is concentrating its efforts include developmental brain research, neuroscience, cardiac disease, and initiatives to reduce and eliminate ethnic and racial health disparities. Through its extensive affiliation network involving five hospital centers in the Bronx, Manhattan and Long Island - which includes Montefiore Medical Center, Einstein's officially designated University Hospital - the College runs the largest post-graduate medical training program in the United States, offering approximately 150 residency programs to more than 2,500 physicians in training.
Wednesday, July 2, 2008
In the late 19th century Gregor Mendel used peas to show that one copy of a gene (allele) is inherited from the mother and one from the father. In the progeny, the inherited genes are expressed at the right time and in the right place, but until recently, it was thought that although gene products could be modified during the life of the organism, the genes themselves were unchanged, except for random mutation. Now it appears that one copy of some genes can alter the expression of the other copy, and those changes are passed down to the next generation.
These epigenetic alterations, called paramutations may be important in introducing changes when plants and other organisms are environmentally stressed. The exact mechanisms of how genes talk to other genes and change their behavior are being investigated, and recent results suggest that these processes could be important in engineering plants responsive to a variety of environmental conditions.
Dr. Vicki Chandler and her colleagues have studied paramutations in maize and other plants and have identified some of the genes and mechanisms that operate in this epigenetic process. Dr. Chandler, of the Department of Plant Sciences at the University of Arizona, Tucson, will be presenting this work at a symposium on Maize Biology at the annual meeting of the American Society of Plant Biologists in Mérida, Mexico (June 28, 9:10 AM).
The sequencing of genes, proteins, and, ultimately, whole genomes has revealed that genomes are not simply strings of genes, but rather complex, communicating, and interacting regions of information that could be compared to DNA computers controlling growth, development, and metabolism in each organism. The physical architecture of the genome is also highly complex. The nucleus, where the genome resides, is not full of strings of DNA like a pot of spaghetti. Rather, the strands of DNA are wrapped around proteins called histones and the whole is organized into an elegant and highly controlled structure called chromatin. When it is time for genes to be expressed, a section of chromatin is unwound and the DNA for that particular gene is made available to the machinery that transcribes DNA to RNA. Once the process is finished, the DNA is neatly folded back into the chromatin structure until needed again. Different parts of the genome can interact by direct contact or through intermediaries that can be proteins or RNA sequences. The exact mechanisms of how paramutagenic alleles communicate with their homologous partners are still unknown, but the work of Chandler and others suggests that both direct contact of homologous regions and changes induced by intermediary RNA molecules may be involved.
Peas also played an important role in the discovery of paramutations, as the first mutants of this type were observed in peas in 1915. Then, in the 1950s, Alexander Brink identified these types of mutations as interactions between alleles. He recognized that these interactions resulted in heritable changes to the expression of those genes. Since then, paramutations have been found in humans and other animals, as well as other plant species including tomato, tobacco, petunia, and maize. In animals, paramutations may be important in mediating the occurrence of diseases like diabetes. Chandler and her co-workers have been investigating paramutations in maize at the b1 gene, which regulates the distribution of the purple pigment anthocyanin in plant tissues.
At the b1 locus, the paramutagenic allele, which causes light or stippled pigmentation arises spontaneously from the wild-type allele, which causes dark purple pigmentation. If a plant with the paramutagenic allele is crossed with a wild-type allele, the progeny get both alleles. However, the paramutagenic allele silences the wild-type allele and produces a plant with stippled rather than purple pigmentation. The silent state is then passed on in subsequent crosses.
Several different components may be involved in paramutation, although they may differ among species. One important player is an array of repeated non-coding DNA sequences that lies upstream of the gene sequence of the paramutagenic allele. Seven of these tandem repeats are required for b1 paramutation. If only three tandem repeats are present, there is only partial paramutagenic activity. One possibility is that these tandem repeats are involved in direct interactions of chromatin regions, which results in paramutation changes. However, RNA also appears to be part of the process. The gene mediator of paramutation1 (mop1), an RNA dependent RNA polymerase is absolutely required for paramutation silencing at the b1 locus as well as for several other maize genes. In Arabidopsis, this RNA polymerase is associated with the production of small, interfering RNAs (siRNA) that function in gene silencing in other contexts. The siRNA could thus act as an intermediary molecule, being sent to silence the homologous allele. A third component is the placement of methyl groups on the control sequence (promoter) of the wild-type gene. Gene methylation has been known for some time as a cell defense mechanism for silencing foreign DNA but is also functional in other cellular processes. In several species, such methylation is also directed by RNA molecules. None of these processes is likely to be sufficient by themselves to effect paramutation, but rather all of them may interact, although to varying degrees in different species.
The molecular components of paramutation probably arose as cell defense mechanisms against viral or bacterial DNA. They have evolved to serve the needs of plants that grow in complex and changing environments from which they cannot escape, but to which they may be able to adapt through mechanisms like paramutation. Indeed, two instances of paramutation are known to be influenced by temperature. This work has implications for engineering crops that may be able to adapt to higher temperatures or drought conditions, as well as for applications in human and veterinary medicine.
Tuesday, July 1, 2008
The idea of a sun tan representing health or affluence is a recent trend. Before the 1950’s, people were very conscious of keeping their skin out of the sun. Indeed, someone that was heavily tanned may be thought of as some that worked outdoors in a poorly paid job and exposed to too much sun.
As prosperity became more tangible to people in the middle of the last century, having a lifestyle became more of a reality. The idea of leisure time was invented. People would dedicate time to going to the beach and spending time outdoors for relaxation. They had money to spend on vacations, often traveling to sunnier climates.
It was not long before having an all over tan was a sign of an affluent lifestyle. It represented the living of a healthy and vital life and was highly desirable. Pretty soon, getting a suntan became an activity in itself. People would spend many hours in the Sun ‘working on their tan’.
People wanted a permanent all over tan, regardless of the seasons. Other people wanted to get a tan before they went to a sunny climate for their annual vacation. Pretty soon the idea of the sunbed evolved.
Ever since the development of the sunbed they have proved to be very popular. Tanning salons pop up at every mall or shopping center. Many gyms have a tanning salon too which reinforces the link between a tan and a healthy lifestyle.
But the question that most people that use sunbeds have and then choose to forget is are sunbeds healthy ?
The answer is very simple. Current research suggests that any kind of tanning, be it in the Sun or being exposed to ultra violet radiation in some other way will eventually lead to skin cancer. The level or duration of exposure to UV rays before a skin cancer develops will vary from person to person depending on their skin type and other genetic factors.
Many tanning salon owners will make the distinction that the radiation that you are exposed to in the sun is different to that of a sunbed. UVB radiation causes the skin to burn and is the kind of radiation you will be exposed to in the Sun. Whereas, UVA radiation is the kind of radiation that you will be exposed to on a sunbed. It does not cause your skin to burn but it is believed to still be just as likely to cause skin cancer.
The salient point to all this is that any form of tanning of the skin will lead to skin cancer at some point. Maybe you will be fortunate and never reach that point during your life but the aim of skin cancer prevention is to limit a persons exposure to the cause of skin cancer, ultra violet radiation. That is why people should always wear sunscreen when outdoors. They should try to cover their skin with clothing and wear a hat and sunglasses when out in the Sun.
Lying on a sunbed once a week is like going in the sun with none of this protection. Under the circumstances, it seems like a potentially high price to pay to have a ‘healthy’ tan.
About the Author:
For more on the symptoms of skin cancer and details on the types of skin cancers that can develop, visit http://symptomsofskincancer.net
Monday, June 30, 2008
The 52-year-old patient's dramatic turnaround was the only success in a small study, leading doctors to be cautious in their enthusiasm. However, the treatment reported in yesterday's issue of the New England Journal of Medicine is being counted as the latest in a small series of successes involving immune-priming treatments against deadly skin cancers.
"Immunotherapy has become the most promising approach" to late-stage, death-sentence skin cancers, said Dr. Darrell Rigel, a clinical professor of dermatology at the New York University Medical Center in Manhattan who had no role in the research.
Still, the immune-priming experiments have yet to yield a consistent therapy. Even researchers who worked on the experiment involving nine patients and just one success are quick to couch the result. "This is only one patient," said study co-author Dr. Cassian Yee of the Fred Hutchinson Cancer Research Center in Seattle.
Researchers used a single infection-fighting cell from the man's immune system, CD4 T cell, copies of which were grown in a laboratory. The disease had spread to the man's lungs and a lymph node before he received the two-hour infusion of lab-grown immune system cells. Sixty days later, all signs of the disease were gone. He remained in remission for the following two years at which point he requested not to be contacted further by researchers or the media, a spokesman for the research center said.
Doctors had long thought immune system cells, which so effectively attack foreign threats like viruses, were giving a pass to cancer cells. The theory was that because cancers cells are generated by the body, the immune system perceived them as part of the body.
But about 20 years ago, some scientists discovered that immune cells could latch onto and attack skin cancers. "There's a long history behind all of this," said Dr. Steven Rosenberg of the National Cancer Institute, a pioneer in that research.
In recent experiments, Rosenberg and other researchers have focused on souping up a certain kind of immune system cell, the "killer T cells" that envelop and kill foreign agents.
The new research took a different approach. The Hutchinson center scientists focused instead on specific helper T cells that are adept at locking onto a cancer cell and guiding the killer cells to their target. It's possible the treatment spurred his immune system to expand its cancer-fighting ability in new ways, Yee said. But the case raised many unanswered questions. The man had been treated earlier with other drugs. It's possible those treatments had already weakened or altered the cancer.
Also, none of the eight other patients in the study did as well. It's not clear why.
Professor Karol Sikora, a cancer expert at London's Imperial College, said of the research, "I think we will be able to harness the power of the immune system. Patients will live with their cancer, and die with their cancer, but not of their cancer; it will be like diabetes today."
Facts about melanoma
The most common and deadly form of skin cancer, it begins in the melanocytes, the cells found in the epidermis, the top layer of the skin. They make the brown pigment called melanin, which makes skin tan and protects deeper layers of the skin from the sun's harmful effects. Cancer begins when radiation overloads and damages the cells, causing mutations.
Because most of these cells still make melanin, melanoma tumors are often brown or black though they can also have no color. Melanoma most often appears on the trunk of fair-skinned men and on the lower legs of fair-skinned women, but it can appear other places, too. Having dark skin lowers the risk, but a person with dark skin can still develop melanoma.
Almost always curable in its early stages but likely to spread to other parts of the body if untreated.
More than 62,000 people in the United States will be diagnosed with melanoma in 2008. Almost 8,500 patients will die from it.
SOURCE: AMERICAN CANCER SOCIETY
Sunday, June 29, 2008
Quick! What's the biggest organ in your body?
You might be surprised to find out it's the skin, which you might not think of as an organ. No matter how you think of it, your skin is very important. It covers and protects everything inside your body. Without skin, people's muscles, bones, and organs would be hanging out all over the place. Skin holds everything together. It also:
• protects our bodies
• helps keep our bodies at just the right temperature
• allows us to have the sense of touch
Don't Miss Your Epidermis
The skin is made up of three layers, each with its own important parts. The layer on the outside is called the epidermis (say: eh-pih-dur-mis). The epidermis is the part of your skin you can see.
Look down at your hands for a minute. Even though you can't see anything happening, your epidermis is hard at work. At the bottom of the epidermis, new skin cells are forming.
When the cells are ready, they start moving toward the top of your epidermis. This trip takes about 2 weeks to a month. As newer cells continue to move up, older cells near the top die and rise to the surface of your skin. What you see on your hands (and everywhere else on your body) are really dead skin cells.
These old cells are tough and strong, just right for covering your body and protecting it. But they only stick around for a little while. Soon, they'll flake off. Though you can't see it happening, every minute of the day we lose about 30,000 to 40,000 dead skin cells off the surface of our skin.
So just in the time it took you to read this far, you've probably lost about 40,000 cells. That's almost 9 pounds (4 kilograms) of cells every year! But don't think your skin might wear out someday. Your epidermis is always making new skin cells that rise to the top to replace the old ones. Most of the cells in your epidermis (95%) work to make new skin cells.
And what about the other 5%? They make a substance called melanin (say: mel-uh-nun). Melanin gives skin its color. The darker your skin is, the more melanin you have. When you go out into the sun, these cells make extra melanin to protect you from getting burned by the sun's ultraviolet, or UV, rays.
That's why your skin gets tan if you spend a lot of time in the sun. But even though melanin is mighty, it can't shield you all by itself. You'll want to wear sunscreen and protective clothing, such as a hat, to prevent painful sunburns. Protecting your skin now also can help prevent skin cancer when you get older.
The Dermis Is Under the Epidermis
The next layer down is the dermis (say: dur-mis). You can't see your dermis because it's hidden under your epidermis. The dermis contains nerve endings, blood vessels, oil glands, and sweat glands. It also contains collagen and elastin, which are tough and stretchy.
The nerve endings in your dermis tell you how things feel when you touch them. They work with your brain and nervous system, so that your brain gets the message about what you're touching. Is it the soft fur of a cat or the rough surface of your skateboard?
Sometimes what you feel is dangerous, so the nerve endings work with your muscles to keep you from getting hurt. If you touch something hot, the nerve endings in your dermis respond right away: "Ouch! That's hot!" The nerves quickly send this message to the brain or spinal cord, which then immediately commands the muscles to take your hand away. This all happens in a split second, without you ever thinking about it.
Your dermis is also full of tiny blood vessels. These keep your skin cells healthy by bringing them the oxygen and nutrients they need and by taking away waste. These blood vessels are hard to see in kids, but you might get a better look if you check out your grandparents' skin. As the dermis gets older, it gets thinner and easier to see through.
The dermis is home to the oil glands, too. These are also called sebaceous (say: sih-bay-shus) glands, and they are always producing sebum (say: see-bum). Sebum is your skin's own natural oil. It rises to the surface of your epidermis to keep your skin lubricated and protected. It also makes your skin waterproof — as long as sebum's on the scene, your skin won't absorb water and get soggy.
You also have sweat glands on your epidermis. Even though you can't feel it, you actually sweat a tiny bit all the time. The sweat comes up through pores (say: pors), tiny holes in the skin that allow it to escape. When the sebum meets the sweat, they form a protective film that's a bit sticky.
An easy way to see this film in action is to pick up a pin with your fingers. Then wash your hands well with soap and water and dry them off completely. Now try to pick up that pin again. It won't be so easy because your sticky layer is gone! Don't worry — it will be back soon, as your sebaceous and sweat glands create more sticky stuff.
The Third Layer Is Subcutaneous Fat
The third and bottom layer of the skin is called the subcutaneous (say: sub-kyoo-tay-nee-us) layer. It is made mostly of fat and helps your body stay warm and absorb shocks, like if you bang into something or fall down. The subcutaneous layer also helps hold your skin to all the tissues underneath it.
This layer is where you'll find the start of hair, too. Each hair on your body grows out of a tiny tube in the skin called a follicle (say: fah-lih-kul). Every follicle has its roots way down in the subcutaneous layer and continues up through the dermis.
You have hair follicles all over your body, except on your lips, the palms of your hands, and the soles of your feet. And you have more hair follicles in some places than in others — there are more than 100,000 follicles on your head alone!
Your hair follicles rely on your sebaceous glands to bring on the shine. Connected to each follicle in the dermis layer is a tiny sebaceous gland that releases sebum onto the hair. This lightly coats the hair with oil, giving it some shine and a little waterproofing.
Skin Can Warm and Cool You
Your skin can help if you're feeling too hot or too cold. Your blood vessels, hair, and sweat glands cooperate to keep your body at just the right temperature. If you were to run around in the heat, you could get overheated. If you play outside when it's cold, your inner temperature could drop. Either way, your skin can help.
Your body is pretty smart. It knows how to keep your temperature right around 98.6° Fahrenheit (37° Celsius) to keep you and your cells healthy. Your skin can respond to messages sent out by your hypothalamus (say: hy-po-thal-uh-mus), the brain's inner thermometer. If you've been running around on a hot day, your blood vessels get the signal from the hypothalamus to release some of your body's heat. They do this by bringing warm blood closer to the surface of your skin. That's why you sometimes get a red face when you run around.
To cool you down, sweat glands also swing into action by making lots of sweat to release body heat into the air. The hotter you are, the more sweat your glands make! Once the sweat hits the air, it evaporates (this means that it changes from a liquid to a vapor) off your skin, and you cool down.
What about when you're ice-skating or sledding? When you're cold, your blood vessels keep your body from losing heat by narrowing as much as possible and keeping the warm blood away from the skin's surface. You might notice tiny bumps on your skin. Most kids call these goosebumps, but the fancy name for them is the pilomotor (say: py-lo-mo-ter) reflex. The reflex makes special tiny muscles called the erector pili (say: ee-rek-tur pie-lie) muscles pull on your hairs so they stand up very straight.
Keep It Clean!
Unlike other organs (like your lungs, heart, and brain), your skin likes a good washing. When you wash your skin, use water and a mild soap. And don't forget to cover scrapes and cuts with gauze or a bandage. This keeps the dirt out and helps prevent infections. It's just one way to be kind to the skin you're in!