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The inhibitor of the DNA- binding (Id) family of proteins, consisting of Id. Id. 2, Id. 3, and Id. HLH) family of transcription factors. The basic HLH (b. HLH) family of transcription factors regulates transcription by binding to DNA as either homodimers or heterodimers. Id proteins, which lack a DNA- binding domain, interact with b. HLH proteins to prevent dimer formation and/or DNA binding. In addition, Id. 1 can associate with members of the Ets protein family and Rb. Several observations support a crucial role for Id proteins in development, differentiation, and proliferation of cells, and in tumorigenesis. For example, it has been demonstrated that Id. Myo. D- mediated myogenic responses. Id. 1/Id. 3 double- knockout mice display abnormal angiogenesis characterized by enlarged, dilated blood vessels. Introduction of Id. ECs induces EC proliferation and migration. Because knockdown of Id. ECs treated with BMP perturbs EC activation, Id. BMP- induced EC activation. Loss of Id. 1 in tumor ECs leads to down- regulation of integrin . Although many b. HLH transcription factors have been implicated in EC angiogenic activities, which proteins Id. We have reported that Hey. Herp. 2/Hesr. 1, one of the b. HLH proteins induced by Notch signaling, antagonizes activated BMP receptor- induced EC migration. This antagonism is caused by the degradation of Id. Hey. 1/Herp. 2/Hesr. ECs. Thus, Id. 1- induced EC migration is blocked by Hey. Herp. 2/Hesr. 1. 2. However, the mechanism by which Id. EC angiogenic activation is still poorly understood. To gain more insight into the molecular mechanisms by which Id. EC activation, we searched for Id. E2- 2. E2- 2 (also known as ITF2, TCF4, SEF2, and SEF2- 1. B) is classified into the E- protein family (or the class A type of b. HLH transcription factors), whose expression is virtually ubiquitous. In addition to E2- 2, E2. A and HEB also belong to the E- protein family. This family of transcription factors recognizes a consensus DNA sequence known as the E- box (CANNTG) in dimer form, whereas monomeric forms have no discernible DNA- binding activity. The E- protein family of proteins is known to regulate lymphocyte development,2. Our previous study demonstrated that E2- 2 can inhibit the activity of VEGFR2 luciferase reporters in ECs. However, how E2- 2 counteracts the activity of the VEGFR2 promoter and whether E2- 2 influences the actions of ECs remain veiled. In this study, we explored the role of E2- 2 in angiogenesis both in vitro and in vivo. We found that E2- 2 represses VEGFR2 promoter activity to inhibit angiogenesis and that E2- 2–mediated EC inactivation can be alleviated through interaction with Id. Methods. Plasmids and adenovirusesc. DNAs for human and mouse E2- 2 as well as mouse LMO2 were cloned by reverse- transcription polymerase chain reaction (RT- PCR). Each c. DNA was sequenced before use. Mouse stem cell leukemia hematopoietic transcription factor (SCL) was a kind gift from Dr M. Ema (University of Tsukuba, Japan). DNAs were inserted into Flag- pc. DNA3 or Myc- pc. DNA3. DEF3 vector. 2. 9 DEF3- Flag- Id. DEF3- Myc- Id. 1, and DEF3- Id. MCKpfos- luc and p. GL2b- VEGFR2- luc (. Sigvardsson (Lund University, Sweden) and C. Hughes (University of California, Irvine), respectively. VEGFR2- luc mutant constructs were also generated by PCR. After verification of each sequence, reporter constructs were used for each experiment. Adenoviruses expressing Myc- E2- 2 were generated using the p. Ad. Track- CMV vector. After recombination of p. Ad. Track- CMV- Myc- E2- 2 with p. Ad. Easy- 1,3. 2 the resulting plasmid was transfected into 2. T cells, and adenoviruses were amplified. Adenoviruses expressing Flag- Id. Cell culture. COS7 cells and mouse embryonic endothelial cells (MEECs)1. Dulbecco modified Eagle medium (DMEM; Invitrogen) containing 1. FCS; Invitrogen), minimum essential medium nonessential amino acids (Invitrogen), and 1. U/m. L penicillin/streptomycin (Wako). Calf pulmonary aortic endothelial cells (CPAEs)3. DMEM with 1. 0% FCS, 2. M N- 2- hydroxyethylpiperazine- N. Primary human umbilical vein endothelial cells (HUVECs) were cultured in endothelial basal medium (Lonza Walkersville) supplemented with 2% FCS. MEECs and HUVECs were grown on 0. Adenoviral infections. Adenoviruses were incubated in DMEM containing polybrene (Sigma- Aldrich; 8. Two hours after infection, cells were washed and allowed to recover 2. If necessary, cells were starved by removal from the FCS overnight and then stimulated with 5. L recombinant human VEGF (Wako). Immunoprecipitation and Western blotting. To detect interactions among the proteins, plasmids were transfected into COS7 cells (5 . Forty hours after transfection, the cells were lysed in 5. Cell lysates were precleared with protein G- Sepharose beads (GE Healthcare) for 3. Protein complexes were immunoprecipitated by incubation with protein G- Sepharose beads for 3. Immunoprecipitated proteins and aliquots of total cell lysates were boiled for 5 minutes in sample buffer, separated by sodium dodecyl sulfate- polyacrylamide gel electrophoresis, and transferred to Hybond- C Extra membranes (GE Healthcare). The membranes were probed with anti- Myc 9. E1. 0 antibody (Santa Cruz Biotechnology). Primary antibodies were detected using horseradish peroxidase- conjugated goat anti–mouse antibody (GE Healthcare) and chemiluminescent substrate (Thermo Electron). Protein expression in total cell lysates was evaluated by Western blotting using anti- Flag M5 or anti- Myc 9. E1. 0 antibody. To detect the endogenous interaction between Id. E2- 2, either an anti–E2- 2 monoclonal antibody (anti- TCF4 M0. Abnova) or an anti- Id. Santa Cruz Biotechnology) was used. RNA isolation and RT- PCRTotal RNA was isolated using the RNeasy kit (QIAGEN). Reverse transcription was carried out using a First- Strand c. DNA Synthesis Kit (Takara). PCR was performed using Taq polymerase (Invitrogen) as directed by the manufacturer. Primer sets used are shown in supplemental Tables 1 and 2 (available on the Blood Web site; see the Supplemental Materials link at the top of the online article). Transcriptional reporter assay. MEECs were seeded at 5 . After 4. 0 hours of transfection, lysates were prepared and luciferase activity was measured using a luciferase assay system (Promega). Results were corrected by measuring . Each experiment was carried out in triplicate and repeated at least twice. Values represent the mean plus or minus SD (n = 3). Immunofluorescence. Immunofluorescence assay was performed as previously described. Briefly, MEECs grown on the cover glass were stimulated with 2. L BMP6 to induce Id. After treatment, the glasses were washed once with phosphate- buffered saline (PBS), fixed for 1. PFA; Wako), washed 3 times with PBS, subsequently permeabilized with 0. Triton X- 1. 00 in PBS for 5 minutes, and washed again 3 times with PBS. Glasses were blocked with 5% normal swine serum (Dako Denmark) in PBS at 3. The glasses were then washed 3 times with PBS, incubated with 5% normal swine serum (in PBS) including both fluorescein isothiocyanate- conjugated goat anti–mouse Ig. G antibody (diluted 1: 2. Invitrogen) and Texas red- conjugated goat anti–rabbit Ig. G antibody (diluted 1: 2. Invitrogen) at room temperature for 1 hour, and washed 3 times with PBS. To visualize the fluorescence, an immunofluorescence microscope (Axiovert 2. M; Carl Zeiss) was used. Migration assay. Cell migration assays were performed using a Boyden chamber. Costar nucleopore filters (8- . The chambers were washed 3 times with PBS. Adenovirus- infected HUVECs starved for 1. FCS were added to the top of each migration chamber at a density of 1. Angiogenesis - Wikipedia. Angiogenesis is the physiological process through which new blood vessels form from pre- existing vessels. The first vessels in the developing embryo form through vasculogenesis, after which angiogenesis is responsible for most, if not all, blood vessel growth during development and in disease. However, it is also a fundamental step in the transition of tumors from a benign state to a malignant one, leading to the use of angiogenesis inhibitors in the treatment of cancer. The essential role of angiogenesis in tumor growth was first proposed in 1. Judah Folkman, who described tumors as . It occurs in several well- characterized stages. First, biological signals known as angiogenic growth factors activate receptors on endothelial cells present in pre- existing blood vessels. Second, the activated endothelial cells begin to release enzymes called proteases that degrade the basement membrane to allow endothelial cells to escape from the original (parent) vessel walls. The endothelial cells then proliferate into the surrounding matrix and form solid sprouts connecting neighboring vessels. As sprouts extend toward the source of the angiogenic stimulus, endothelial cells migrate in tandem, using adhesion molecules called integrins. These sprouts then form loops to become a full- fledged vessel lumen as cells migrate to the site of angiogenesis. Sprouting occurs at a rate of several millimeters per day, and enables new vessels to grow across gaps in the vasculature. It is markedly different from splitting angiogenesis because it forms entirely new vessels as opposed to splitting existing vessels. Intussusceptive angiogenesis. In this type of vessel formation, the capillary wall extends into the lumen to split a single vessel in two. There are four phases of intussusceptive angiogenesis. First, the two opposing capillary walls establish a zone of contact. Second, the endothelialcell junctions are reorganized and the vessel bilayer is perforated to allow growth factors and cells to penetrate into the lumen. Third, a core is formed between the 2 new vessels at the zone of contact that is filled with pericytes and myofibroblasts. These cells begin laying collagen fibers into the core to provide an extracellular matrix for growth of the vessel lumen. Finally, the core is fleshed out with no alterations to the basic structure. Intussusception is important because it is a reorganization of existing cells. It allows a vast increase in the number of capillaries without a corresponding increase in the number of endothelial cells. This is especially important in embryonic development as there are not enough resources to create a rich microvasculature with new cells every time a new vessel develops. There is a significant amount of controversy with regard to shear stress acting on capillaries to cause angiogenesis, although current knowledge suggests that increased muscle contractions may increase angiogenesis. Nitric oxide results in vasodilation of blood vessels. Chemical stimulation. In general, FGFs stimulate a variety of cellular functions by binding to cell surface FGF- receptors in the presence of heparin proteoglycans. The FGF- receptor family is composed of seven members, and all the receptor proteins are single- chain receptor tyrosine kinases that become activated through autophosphorylation induced by a mechanism of FGF- mediated receptor dimerization. Receptor activation gives rise to a signal transduction cascade that leads to gene activation and diverse biological responses, including cell differentiation, proliferation, and matrix dissolution, thus initiating a process of mitogenic activity critical for the growth of endothelial cells, fibroblasts, and smooth muscle cells. FGF- 1, unique among all 2. FGF family, can bind to all seven FGF- receptor subtypes, making it the broadest- acting member of the FGF family, and a potent mitogen for the diverse cell types needed to mount an angiogenic response in damaged (hypoxic) tissues, where upregulation of FGF- receptors occurs. FGF- 2 is a more potent angiogenic factor than VEGF or PDGF (platelet- derived growth factor); however, it is less potent than FGF- 1. As well as stimulating blood vessel growth, a. FGF (FGF- 1) and b. FGF (FGF- 2) are important players in wound healing. They stimulate the proliferation of fibroblasts and endothelial cells that give rise to angiogenesis and developing granulation tissue; both increase blood supply and fill up a wound space/cavity early in the wound- healing process. Vascular endothelial growth factor (VEGF) has been demonstrated to be a major contributor to angiogenesis, increasing the number of capillaries in a given network. Initial in vitro studies demonstrated bovine capillary endothelial cells will proliferate and show signs of tube structures upon stimulation by VEGF and b. FGF, although the results were more pronounced with VEGF. Binding to VEGF receptor- 2 (VEGFR- 2) starts a tyrosine kinase signaling cascade that stimulates the production of factors that variously stimulate vessel permeability (e. NOS, producing NO), proliferation/survival (b. FGF), migration (ICAMs/VCAMs/MMPs) and finally differentiation into mature blood vessels. Mechanically, VEGF is upregulated with muscle contractions as a result of increased blood flow to affected areas. The increased flow also causes a large increase in the m. RNA production of VEGF receptors 1 and 2. The increase in receptor production means muscle contractions could cause upregulation of the signaling cascade relating to angiogenesis. As part of the angiogenic signaling cascade, NO is widely considered to be a major contributor to the angiogenic response because inhibition of NO significantly reduces the effects of angiogenic growth factors. However, inhibition of NO during exercise does not inhibit angiogenesis, indicating there are other factors involved in the angiogenic response. These receptors are tyrosine kinases. Thus, they can initiate cell signaling when ligand binding causes a dimerization that initiates phosphorylation on key tyrosines. Another major contributor to angiogenesis is matrix metalloproteinase (MMP). MMPs help degrade the proteins that keep the vessel walls solid. This proteolysis allows the endothelial cells to escape into the interstitial matrix as seen in sprouting angiogenesis. Inhibition of MMPs prevents the formation of new capillaries. The presence of blood vessels where there should be none may affect the mechanical properties of a tissue, increasing the likelihood of failure. The absence of blood vessels in a repairing or otherwise metabolically active tissue may inhibit repair or other essential functions. Several diseases, such as ischemic chronic wounds, are the result of failure or insufficient blood vessel formation and may be treated by a local expansion of blood vessels, thus bringing new nutrients to the site, facilitating repair. Other diseases, such as age- related macular degeneration, may be created by a local expansion of blood vessels, interfering with normal physiological processes. The modern clinical application of the principle of angiogenesis can be divided into two main areas: anti- angiogenic therapies, which angiogenic research began with, and pro- angiogenic therapies. Whereas anti- angiogenic therapies are being employed to fight cancer and malignancies. One of the first applications of pro- angiogenic methods in humans was a German trial using fibroblast growth factor 1 (FGF- 1) for the treatment of coronary artery disease. Difficulties include effective integration of the therapeutic genes into the genome of target cells, reducing the risk of an undesired immune response, potential toxicity, immunogenicity, inflammatory responses, and oncogenesis related to the viral vectors used in implanting genes and the sheer complexity of the genetic basis of angiogenesis. The most commonly occurring disorders in humans, such as heart disease, high blood pressure, diabetes and Alzheimer's disease, are most likely caused by the combined effects of variations in many genes, and, thus, injecting a single gene may not be significantly beneficial in such diseases. In contrast, pro- angiogenic protein therapy uses well- defined, precisely structured proteins, with previously defined optimal doses of the individual protein for disease states, and with well- known biological effects. Oral, intravenous, intra- arterial, or intramuscular routes of protein administration are not always as effective, as the therapeutic protein may be metabolized or cleared before it can enter the target tissue. Cell- based pro- angiogenic therapies are still early stages of research, with many open questions regarding best cell types and dosages to use. Tumor angiogenesis. A malignant tumor consists of a population of rapidly dividing and growing cancer cells that progressively accrues mutations. However, tumors need a dedicated blood supply to provide the oxygen and other essential nutrients they require in order to grow beyond a certain size (generally 1. Growth factors such as b. FGF and VEGF can induce capillary growth into the tumor, which some researchers suspect supply required nutrients, allowing for tumor expansion. Unlike normal blood vessels, tumor blood vessels are dilated with an irregular shape. In normal cells (but not in cancerous ones), PKG apparently limits beta- catenin, which solicits angiogenesis. In either case, angiogenesis is a necessary and required step for transition from a small harmless cluster of cells, often said to be about the size of the metal ball at the end of a ball- point pen, to a large tumor. Angiogenesis is also required for the spread of a tumor, or metastasis. 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Recommendation. Take advantage of Advanced Dermatology’s Special Introductory Offer. Receive $2. 00 worth of products for $5. Visit their website to see if the offer is still available. ![]() Why Do I Have Jawline Acne? Two types of acne that are specific to adults tend to occur. Get the latest tips on diet. Suggest treatment for cystic hormonal acne on jaw line and. What diet should I Follow and how. Suggest treatment for cystic hormonal acne on jaw line and. 4 Signs Your Hormones Are To. Vegetables A Day To My Diet Cleared My Acne. Battling Your Jawline Acne. Factors such as stress, diet. ![]() ![]() ![]() Syndrome X – Liver Doctor. If you answer YES to 3 or more of these questions, you need the 1. Syndrome X Eating Plan – “Can’t Lose Weight? Unlock the Secrets that Keep you Fat” book which includes the diet and recipes to help with this syndrome. What is Syndrome X? ![]() ![]() Dr Cabot's new book provides the knowledge and thus the ability to overcome the metabolic problems that are causing Australians to become fatter. She asks: Do you suffer with Syndrome X? Try Dr Cabot's Syndrome X checklist. Can t Lose Weight You Could Have Syndrome X The Chemical Imbalance That Makes Men and Women Store Fatvisit http://dloadbooks.xyz/?book=0958613702. Advanced Search: Children & Young Adults. Activities & Games (41,305) All (41,305) Activities, Crafts & Hobbies (32,949) Puzzle / Maze Books & Quizzes (8,355). 10 Things Your Doctor Won. Do you have Syndrome X? Can't lose weight : you could have Syndrome X! Many adults have insulin resistance and don't know it. You can't lose weight because your body is in survival mode. Read Can't Lose Weight?: You Could Have Syndrome X PDF Online Like. Read or Download Now http:// Read Can't. ![]() ![]() ![]() Syndrome X is the most common cause of inability to lose weight. This is called a “liver roll”. You may also have excess fat in other parts of your body. Hyperinsulinemia (high insulin levels) Syndrome X is a metabolic disorder associated with high blood levels of the hormone insulin. Fatigue Obesity and insulin resistance can cause fatigue, so it is important to combat this symptom with diet and supplements to increase energy levels. What is insulin? Insulin is a hormone produced by the pancreas gland. What does it do? Its action is to put blood sugar (glucose) into the muscle and fat cells where it is used to make energy. What is insulin resistance and hyperinsulinemia? Insulin resistance leads to the high levels of insulin which cause Syndrome X. This means that the pancreas is forced to pump out higher and higher amounts of the hormone insulin to compensate for this resistance. Over time, high levels of insulin build up in the blood stream leading to the condition known as “hyperinsulinemia” or elevated insulin. What causes Insulin Resistance (IR)? ![]() Insulin resistance is often hereditary and is usually aggravated by a high carbohydrate diet and lack of exercise. Nutritional deficiencies of certain minerals (magnesium , zinc, manganese, chromium) can lead to insulin resistance. Liver dysfunction and/or fatty liver can lead to unstable blood sugar levels resulting in an aggravation of insulin resistance. Some cells in the body, for example the ovaries and adrenal glands, are more susceptible to insulin resistance. It is thought that around 1 in 4 people show signs of insulin resistance. What is the effect of IR on the female reproductive system? In many females insulin resistance and hyperinsulinemia (high levels of insulin) stimulate the ovaries to produce androgens (male hormone) and the androgens may exacerbate the collection of symptoms known as Polycystic Ovarian Syndrome. Absent periods can be a result. Many women with this condition have trouble with fertility. The excessive male hormones are also associated with symptoms such as excess facial and body hair, sometimes adult acne, hair loss from the temples and the crown (male pattern baldness). Other effects of high levels of insulin. High insulin levels are often associated with high blood sugar levels. Indeed a patient may be pre- diabetic or have type. Even though the insulin levels are higher than normal, the insulin does not work efficiently because the body cells are resistant to its effect. The insulin does not work effectively to bring down the high blood sugar levels. Those with Syndrome X have abnormalities in blood fat levels (cholesterol and triglycerides) and may have elevated blood levels of uric acid. Syndrome X significantly increases your risk of heart disease. Those who suffer with this condition often find they are consistently hungry and crave starchy carbohydrates. This makes sticking to conventional weight loss plans very difficult. Is it common? Professor Gerald Reaven, from Stanford University is the world’s leading expert on Syndrome X. Reaven tells us that there are approximately 3. USA with Syndrome X. Syndrome X is present in 7. Do men suffer with Syndrome X? Yes – Syndrome X is more common in men than women. Who suffers from Fatty Liver and Syndrome X? Fatty liver is very common in populations where fast food and refined food is easily available. The food keeps getting faster and faster and we keep getting slower and slower! It is more common in women over 4. It can affect people of all ages, and is not rare in adolescents and young children. Why can’t people with Syndrome X lose weight? If you are battling with a fatty liver and a ravenous hunger your chances of long- term success are slim indeed; unless you have the 2 missing parts to the jig- saw puzzle – 1. Normal insulin levels. Victims of Syndrome X cannot lose weight because of 2 reasons –Their liver is storing fat, when it should be burning fat. In other words they suffer with a dysfunctional liver. A healthy liver is able to burn fat and pump excess fat out of the body through the bile. In those with a fatty liver the reverse happens so they just keep on getting fatter, especially around the abdomen. The high levels of insulin make them very hungry. Indeed high insulin levels give you a ravenous appetite with cravings for carbohydrates such as sweets, savoury biscuits with cheese, chips, and sometimes sweet drinks and alcohol. This high intake of carbohydrates stimulates the insulin levels to become higher, which makes you even hungrier. Furthermore insulin preferentially converts sugar into fat storage deposits, instead of muscle and liver glycogen stores. This insulin encourages the deposition of fat in your body. Both of the above factors keep you locked into a viscious circle of ever increasing weight. After 2. 5 years of clinical research Dr Cabot has discovered the key to break this destructive cycle and get the weight off permanently. Improve the liver function so that the liver starts to burn fat again. Reduce the high levels of insulin, so that excess hunger is prevented. Do some regular exercise such as walking, swimming, sports or aerobics. Recommended supplements: Take 2 capsules twice daily –. Berberine helps to improve insulin sensitivity, thereby helping to reduce elevated insulin levels. Take. The eating plan in “Can’t Lose Weight? Unlock the Secrets that Keep you Fat” book . This is an excellent starting guide for low carb, dairy free recipes, which are good for the liver. The book is also a wealth of information on Syndrome X and its associated symptoms and gives you a. You need to limit starchy and sugary carbohydrates and include protein at every meal. Good sources of protein are legumes, seeds, raw nuts, lean red fresh meats, all seafood, eggs. A fruit breakfast for example would not be recommended for an overweight person with Syndrome X – this is too much simple carbohydrate without protein. Healthy Low Carbohydrate Sweetener Guide. Sweeteners to avoid: Aspartame Neotame Sucralose (Splenda) Acesulfame- K (Sunette, Sweet & Safe, Sweet One) Cyclamates Saccharin. Sweeteners to Use: “Stevia”Xylitol. Benefits of Exercise. Studies on patients who exercise suggest that the exercise prompts the transport of the GLUT4 structures to the outer edge of the cell, which facilitates the entry of glucose into the cell, regardless of insulin resistance. Additionally, this factor appears to last for several days after exercise. How long does the Syndrome X Diet take to work? This varies depending upon the degree of fatty changes and the amount of fat in the liver. If you have only a mild degree of fatty liver the diet will work quickly. In other words you will start to lose weight within the first 2 weeks and the weight loss will be sustained. If you have a very fatty liver and moderate to severe insulin resistance, the weight loss will be slower and you may have weight loss plateaus when you find that weight loss stops for 2 to 3 weeks. After the plateau your weight loss will resume. Remember it takes time to remove the excess fat from the liver, and if you do not do this, long- term weight loss is impossible. Some patients with advanced degrees of fatty liver take up one year to completely remove all the excess fat from the liver. The liver formulas will speed up weight loss. The liver is the most important organ for longevity. By removing the excess fat from the liver you will not only lose weight, but improve the metabolic imbalances of Syndrome X such as high cholesterol & triglycerides, high uric acid and high insulin levels. This will result in healthier fat free blood vessels and a much lower risk of heart disease. Recommended books. This book is essential reading for anyone with sluggish liver function. It has sections on fatty liver, liver function tests and the implication of the results and high cholesterol. ![]() How to Set Up a Weight Loss Challenge . Setting up a weight- loss challenge among friends, family or colleagues inspires camaraderie and a little healthy competition. In the end, there may be one official winner, but everyone enjoys the reward of improved health. Set the dates for the challenge. Two to six months is an adequate amount of time for participants to lose noticeable amounts of weight. ![]() ![]() ![]() Weight loss resources to help you lose weight healthily. The 10,000 steps challenge. Sign up for email support. Mayo. Clinic. com recommends that a safe rate of weight loss is about 1 to 2 pounds per week. In a two- month challenge, participants can lose 8 to 1. Determine how to measure success. The most accurate way is by body fat percentage lost during the competition. Pounds lost is often an inaccurate assessment, since the weight could be water or muscle tissue instead of fat. Building muscle - - which weighs more than fat - - while losing body fat is the healthiest way to lose weight, so encourage participants to combine a balanced diet with exercise. However, body fat measurement by a human can be inaccurate, and other methods, such as hydrostatic underwater weighing, can be pricey. For accurate results, have the same professional, such as a personal trainer, take all measurements at the beginning and end of the challenge. This will reduce the margin of error. Decide whether participants will enter the challenge individually or as teams. ![]() Herbalife is a global nutrition and weight management company. An Herbalife Nutrition Independent Distributor. Weight Loss Challenge. You are here: Home / Weight Loss Challenge Sign up Sheet. Weight Loss Challenge Sign up Sheet. The Next Challenge Begins January 15 2013. Free Wellness Programs Vol. The first is a complete Employee Weight Loss Program and the second is a complete. For a smaller group, individual entries may work best; a larger group is ideal for a team challenge. Set the number of participants per team. Teams can choose their own members. Set the entry fee, if you're going to have one. Fees can be per person or per team. The money can cover expenses connected with the challenge - - T- shirts, advertising, a celebration at the end - - and can fund the prize. You can opt not to charge an entry fee if it might discourage people from participating. If you do collect an entry fee, put one person in charge of the funds throughout the challenge. Funds should be kept in a lock box or another secure place, and expenses should be documented. Choose the prize. Often, the reward is a cash prize generated from the entry fees collected, minus any expenses. However, prizes can also be material, such as a new laptop, or a gift certificate. If you are doing a company- wide challenge, ask your employer to furnish the prize; that way, participants pay only a minimal entry fee. Set up the infrastructure for weigh- ins and measurements for the beginning and end of the challenge and arrange a space for this purpose. Whether you simply use a bathroom scale or have a personal trainer take body fat measurements, have that process in place prior to advertising the contest. Some experts in the community, such as personal trainers and nutritionists, may be willing to take measurements or give talks in exchange for the opportunity to make contacts. Get permission from management if you are organizing the challenge at work. Have a member of management OK all plans and guidelines to be sure they conform to company policies. The company also may be willing to help cover expenses and the prize fund since the challenge will encourage employees to be healthier. Establish contest guidelines. Create a clear statement detailing the parameters, including dates; rules for entry; how measurements will be taken; any banned activities, such as taking weight loss supplements; prizes and any other information you think is important. If the challenge will be at work, ask management to sign off on the guidelines. Team accountability is key to weight loss success for Scott & White's Biggest Loser Challenge. You can implement a weight loss challenge in your workplace by.Plan mini- events along the way as well as a final celebration. Getting everyone together periodically during the challenge can help maintain interest and participation. It also gives people a chance to support each other, offer advice or share their weight- loss experiences. Events could include fun runs, yoga in the park or a healthy pot- luck. Get the word out. Whether you're setting up a challenge for friends, family, colleagues or the whole neighborhood, you must convince people to participate if your challenge is to succeed. Create fliers, send out emails or create a website where people can get more information and sign up. ![]() Tip. Up the stakes by having each team choose its favorite charity; if that team wins, a portion or all of the prize money goes to the chosen beneficiary. If your challenge is among work colleagues, ask your company to match the donation. Recruit health and wellness professionals to give talks throughout the challenge on subjects related to weight loss. Invite a local chef to demonstrate healthy cooking. Warning. Encourage participants to schedule a checkup with their doctors before beginning the challenge. About the Author. Jody Braverman is a professional writer and editor based in Atlanta. She studied creative writing at the American University of Paris and received a Bachelor of Arts in English from the University of Maryland. She also received personal trainer certification from NASM and her 2. Yoga. Works. Photo Credits. Creatas Images/Creatas/Getty Images. |
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