text:
- Product Overview
Short description
- Nutritional formulation for older adults
- Provides powerful combination of antioxidants, vitamins and minerals to enhance vitality of senior adults
- Older individuals seeking to strengthen their body's natural defence system
- Those feeling worn down and seek a supplement to increase energy production
- Individuals who suffer from or prone to stress
- Those wanting to supplement with B12 to maintain blood health
- Those seeking a supplement to improve their general wellbeing
- Helps bolster the body's natural defence system
- Helps support energy production
- Can be beneficial during times of stress
- Is a source of Vitamin B12 which can assist in maintaining normal blood
- Helps improve general wellbeing
- Helps protect against free radical damage
Suggested dose
Adults- Take one tablet daily (with food), or as professionally prescribed
(per tablet)
Retinyl Palmitate688mcgequiv. Vitamin A1250IU
equiv. Retinol375mcg
Thiamine Hydrochloride (Vitamin B1)20mg
Riboflavin (Vitamin B2)20mg
Nicotinamide (Vitamin B3)30mg
Calcium Pantothenate27.8mg
equiv. Pantothenic Acid (Vitamin B5)25mg
Pyridoxine Hydrochloride30mg
equiv. Pyridoxine (Vitamin B6)24.7mg
Folic Acid90mcg
Cyanocobalamin (Vitamin B12)50mcg
Ascorbic Acid (Vitamin C)150mcg
equiv. Vitamin D3400IU
d-alpha-Tocopheryl Acid Succinate82.6mg
equiv. Natural Vitamin E100IU
Calcium (as Carbonate)50mg
Chromium (as Picolinate)50mcg
Iron (as Ferrous Fumarate)5mg
Magnesium (as Oxide-heavy)57mg
Manganese (as Amino Acid Chelate)700mcg
Potassium (as Gluconate)3.2mg
Selenium (as Selenomethionine)25mcg
Zinc (as Amino Acid Chelate)7.5mg
Glucosamine Sulfate-Potassium Chloride Complex266.7mg
equiv. Glucosamine Sulfate200mg
Choline Bitartrate30mg
Citrus Bioflavonoids extract5mg
Lecithin powder-Soy Phosphatidylserine -enriched Soy13.8mg
equiv. Soy Phosphatidylserine2.76mg
Herbal extract equiv. to dry:
Fucus vesiculosus (Kelp) whole plant100mg
equiv. Iodine20mcg
Free from: Gluten, nuts, egg, sesame seeds. No artificial colours or flavours
- WARNING: When taken in excess of 3000mcg retinol equivalents, Vitamin A can cause birth defects.
- If you are pregnant, or considering becoming pregnant, do not take Vitamin A supplements without consulting your doctor or pharmacist
- The recommended daily amount of Vitamin A from all sources is 700mcg retinol equivalents for women and 900mcg retinol equivalents for men
- Contains 37.6mg of Potassium
- If you have kidney disease or are taking heart or blood pressure medications, consult your doctor or pharmacist before use
- This product contains Selenium which is toxic in high doses. A daily dose of 150mcg for adults of Selenium from dietary supplements should not be exceeded
- Vitamin and mineral supplements should not replace a balanced diet
- If symptoms persist, consult your healthcare professional
- Derived from seafood
- Contains lactose
Other information
Storage: Store below 30°C in a dry place
- Specifications
0.25 kg
60 tablets
Maximum Quantity Allowed per customer:
- Customer Reviews


text:
Logan Stieber Athlete of the Week
Logan Stieber (Monroeville, Ohio/Ohio State University) has been named TheMat.com Wrestler of the Week.
Each week, TheMat.com will select an Athlete of the Week, based upon performance within wrestling for that week. The selection committee will consider any level of wrestling, from youth programs through the Senior level.
Stieber won a battle of returning NCAA champions by defeating Oklahoma's Kendric Maple 6-4 in overtime at 149 pounds in the NWCA All-Star Classic on Saturday night.
Stieber scored a reversal in the first tiebreaker period before riding Maple out in the second tiebreaker to earn the win in a dual held at George Mason University in Fairfax, Va.
The match was tied 4-4 in regulation after each wrestler scored a takedown and a pair of escapes.
Stieber moved up a weight class to wrestle Maple in the dual. Stieber, a junior, has won two NCAA titles at 133 and is moving up to 141 this season.
Maple is moving up to 149 after winning NCAAs at 141 last season.
Stieber is a past Junior World silver medalist for the U.S. in freestyle. He placed third at the 2013 U.S. Senior World Team Trials.
Note: To nominate a wrestler for TheMat.com Wrestler of the Week, send the athlete's name, accomplishments for the week and career accomplishments to Craig Sesker at email@example.com

subset: commoncrawl


text: As a one-time hip-hop head, I rarely find myself getting excited about it these days, but there are a handful of artists who continue to light my fire just when I'm about to give up on the genre. One of those is Big K.R.I.T. whose major label debut, Live From the Underground, is due on June 5th and will be getting purchased just on G.P. As an appetizer to that collection, he's just dropped a music video for the title track from his most recent mixtape, 4eva N a Day. The video for "4evaNaDay (Theme)" is part live action, part animation with K.R.I.T. spitting his verses in a cartoon world. The animation quite cleverly matches up with his lyrics and proved to be an enjoyable watch from beginning to end. Press play below and see for yourself.


text:
Can You See What I'm Saying?
Simpson Colloquium SC 101 – Can You See What I'm Saying?
Art has been a major force in shaping our thoughts and lives from the beginning of recorded time. As humans, our first communications were paintings on cave walls. These works of art are the beginning of our discovery of art. We will explore visual elements of art, properties of various media, major historical styles, and the purposes of art in society. We will critically analyze works of art through readings, videos, and discussions about how to interpret possible meanings the art is conveying. As part of the class, we will attend Simpson Forum events related to the arts and all the Farnham Gallery artists' presentations. We will also visit Des Moines Art Center and Pappajohn Sculpture Park to study public art installations.
Meet Your Professor
David Richmond, M.A., MFA
Professor of Art
David Richmond, Professor of Art at Simpson College, has enjoyed wide-ranging experiences in graphic design, photography and visual storytelling over his 30-year professional career.
His academic teaching background includes photography and design at the University of Iowa College of Art and Art History; graphic design at Dickinson University in North Dakota; and art and photography at Simpson College in Indianola, Iowa. At Dickinson University, Prof. Richmond developed the institution's first graphic design program.
Always curious and eager to inspire students, Prof. Richmond most recently led two different Simpson groups to China and to Ireland for photographic tours of those countries. He also led a committee that successfully acquired an NEA grant for Simpson College.
Prof. Richmond received his bachelor of fine arts, a master of arts and a master of fine arts from the University of Iowa.
Meet Your SC Leader
Kaitlyn Van Patten
My name is Kat Van Patten. I was raised in Indianola, along with an older brother and two cats. I will be a senior this fall. I plan to graduate in May 2015 with a double major in Graphic Design and Studio Art with a concentration in drawing. I will be your Simpson Colloquium Leader for Professor Richmond's Simpson Colloquium course.
I attended Indianola High School where I played golf and soccer. I was also very involved in French Club, Theater, Service Corps, 4H, choir, Art Club, orchestra, amongst many other things. At Simpson I am active in different organizations, including being president for Simpson's art club. When I have free time I love to work on artwork, go running, go for walks, watch movies, listen to music, spend time with my friends, and meditate.
I am a very open-minded person, creative, outgoing, and really enjoy meeting new people. My goal is to make all of you feel comfortable here on campus. Simpson has a lot to offer each of you in your time here and I hope I can do my part in helping you the best that I can. I am on Facebook, Twitter, and of course, email. Don't hesitate to add me, follow me, or shoot me an email (Students and parents alike!) I would love to get to know each of you. I look forward to meeting you in June!
Meet Your Writing Fellow
Maria Claussen
My name is Maria Claussen. I will be a sophomore during the 2014-2015 academic year, and will be the Writing Fellow for Professor Dave Richmond's Simpson Colloquium course. I am an Art major and would love to go into art after I graduate from Simpson. My goal in life is to make art that makes people think twice, art that affects people in ways they never imagined.
I was born and raised in Iowa, and I love it here. I tend to be quiet until I get to know you, and then sometimes I just never stop talking! In high school, I was super involved. I was in color guard, show choir, choir, art, cross country, track, speech, and musicals. I also had a job my junior and senior year, and I was involved with church and youth group, so I definitely had a lot to balance!
At Simpson, I am on the cross country team and I train with the track team for the next xc season. I also work at Sports Page a couple miles off campus, so time management is super important for me. Between classes, homework, practice, and work, I love to spend time with my friends and go to Salt. I'm a sucker for board and card games, so my friends and I end up playing cribbage and other games a lot.
I love to help people, and I am always there if you need me. I'll be in class to help with your writing, so don't hesitate to ask me questions or Facebook me!
Click below to continue viewing another option for Simpson Colloquium:


text:
Accused Abortionist Killer Barred from Using 'Necessity Defense'
The man accused of killing late-term abortionist George Tiller won't be allowed to use the "necessity defense" when he goes on trial next month, a district judge in Wichita, Kan., ruled this week.
While Judge Warren Wilbert said he would "leave the door open" for Scott Roeder to present evidence and arguments showing that his slaying of Tiller was done out of belief that he was saving the lives of fetuses, he will not allow Roeder to claim that he broke the law to prevent a greater harm.
The necessity defense is not recognized under Kansas law, the judge said Tuesday.
Roeder, a 51-year-old Kansas City native, is currently awaiting trial for the murder of Tiller, who had been strongly criticized by the pro-life community up until the May 31 shooting at Reformation Lutheran Church in Wichita, where Tiller worshipped.
As one of the few late-term abortion practitioners in the country, Tiller was regarded as among the most notorious figures in the pro-abortion movement and, at the time of his death, was under investigation by the Kansas State Board of Healing Arts for 11 petition allegations against him.
Despite their strong opposition to Tiller's late-term abortion practices, many Christian pro-life groups strongly denounced his murder.
Pro-lifers were also quick to adamantly reject any connections between the pro-life movement and Roeder, who has been described as being anti-abortion, anti-government, and "very religious" but in an Old Testament "eye-for-an-eye way."
Despite the criticism, Roeder has made clear in interviews following the shooting that he has no regrets and that he feels justified in shooting the prominent abortionist.
"Defending innocent life – that is what prompted me. It is pretty simple," Roeder told The Associated Press in 30-minute phone interview last month.
And having heard that at least four women who had sought abortions changed their minds and chose to have their babies, Roeder made it clear that he would do it again.
"[E]ven if one changed her mind it would be worth it," he told AP from jail. "No, I don't have any regrets."
In addition to Tiller's murder, Roeder has also been charged with two counts of aggravated assault for allegedly threatening two ushers who tried to stop him during the May 31 incident at Reformation Lutheran Church.
Beginning Jan. 11, some 300 potential jurors will be summoned to the courthouse. From that, 42 will move on to receive approval from lawyers. In the end, 14 jurors will be picked – 12 who will decide the case and two alternates.


text:
Current evidence indicates that the ability of physical activity to sustain a normal phenotype of arterial endothelial cells (ECs) plays a central role in the beneficial effects of exercise (Ex) on atherosclerotic disease. Here we evaluate the strength of evidence that shear stress (SS) and/or circumferential wall stress (stretch) are the primary signals, produced by bouts of Ex, that signal altered gene expression in arterial ECs, thereby resulting in a less atherogenic EC phenotype. Current literature indicates that SS is a signal for expression of antiatherogenic genes in cultured ECs, in ECs of isolated arteries, and in ECs of arteries in intact animals. Furthermore, SS levels in the arteries of humans during Ex are in the range that produces beneficial changes. In contrast, complex flow profiles within recirculation zones and/or oscillatory flow patterns can cause proatherogenic gene expression in ECs. In vivo evidence indicates that Ex decreases oscillatory flow/SS in some portions of the arterial tree but may increase oscillatory flow in other areas of the arterial tree. Circumferential wall stress can increase expression of some beneficial EC genes as well, but circumferential wall stress also increases production of reactive oxygen species and increases the expression of adhesion factors and other proatherogenic genes. Interactions of arterial pressure and fluid SS play an important role in arterial vascular health and likely contribute to how Ex bouts signal changes in EC gene expression. It is also clear that other local and circulating factors interact with these hemodynamic signals during Ex to produce the healthy arterial EC phenotype. We conclude that available evidence suggests that exercise signals formation of beneficial endothelial cell phenotype at least in part through changes in SS and wall stretch in the arteries.
- nitric oxide
- prostacyclin
- endothelial nitric oxide synthase
- shear stress
- pressure
atherosclerotic cardiovascular disease is responsible for over 19 million deaths annually worldwide and coronary artery disease (CAD) remains the leading cause of death among cardiovascular diseases (93). Physical inactivity is recognized as a risk factor for the development of atherosclerotic CAD, and exercise training programs have been shown to be effective in prevention and treatment of CAD (7, 26, 29, 34, 88, 89, 94, 95, 102, 105, 129). Given these facts, there is growing interest in determining the mechanisms whereby physical activity and exercise produce beneficial effects in prevention and treatment of atherosclerosis. The primary mechanisms that underlie the effectiveness of physical activity in prevention and/or treatment of CAD are now being examined on several fronts but have not been fully established. Current evidence indicates that the ability of physical activity to sustain a normal phenotype of arterial endothelial cells plays a central role in the beneficial effects of physical activity (47). The purpose of this paper is to evaluate the strength of evidence that shear stress on the artery wall and/or circumferential wall stress (stretch on the artery wall) (Fig. 1) are the primary signals, produced by bouts of exercise, that signal altered gene expression in arterial endothelial cells, thereby resulting in a less atherogenic endothelial cell phenotype. There are several excellent, recent reviews outlining the general and specific effects of shear stress and stretch on endothelial cells (16, 51, 115, 136). Here we focus on the importance of these two hemodynamic signals in exercise training effects on endothelial cell phenotype. Available literature indicates that endothelial cell phenotype in vivo is determined via an intricate orchestration of many signals that interact with shear stress and cyclic strain in determining endothelial cell gene expression. The central hypothesis of our discussion is that shear stress and stretch, produced by exercise, modulate endothelial cell phenotype in a net antiatherogenic manner.
Before discussing the effects of these hemodynamic forces on endothelial cell phenotype, we first summarize evidence demonstrating the importance of normal endothelial phenotype in artery health and of changes in endothelial cell phenotype associated with development and progression of atherosclerosis. Next, we review evidence that the beneficial effects of physical activity on atherosclerosis and CAD are the result of exercise training-induced antiatherogenic endothelial cell phenotype. With this background we then discuss evidence in the literature that supports the hypothesis that shear stress and/or circumferential wall stress (stretch) are important signals responsible for exercise-induced expression of antiatherogenic genes in endothelial cells. First we discuss evidence that shear stress can signal antiatherogenic gene expression in cultured endothelial cells. We then summarize evidence indicating that in vivo shear stresses produced in the human arterial tree during exercise are in the range known to cause these beneficial effects on gene expression in endothelial cells. We also discuss how recirculating flow patterns and oscillatory flow can have deleterious effects on endothelial cell phenotype. After the discussion of shear stress we consider evidence that circumferential stress on the walls of arteries can signal antiatherogenic gene expression in arterial endothelial cells. Finally, we evaluate evidence that the interaction of these hemodynamic signals, as occurs in vivo, is critical in producing the antiatherogenic phenotype in endothelium of arteries of physically active subjects.
Importance of Endothelial Cell Phenotype in Artery Health
It is generally accepted that an early event in the pathogenesis of atherosclerosis is endothelial cell dysfunction. Endothelial cell dysfunction can be characterized by one or more of the following features: 1) reduced endothelium-mediated vasodilation, 2) enhanced endothelial cell turnover, 3) increased expression of adhesion molecules and other inflammatory genes of endothelial cells, 4) increased oxidant stress, and 5) increased permeability characteristics of the endothelial barrier. These changes in endothelial function represent the change in endothelial cell phenotype that, in this paper, we will refer to as proatherogenic phenotype.
Current evidence indicates that endothelial dysfunction is present prior to and throughout all stages of atherosclerosis, suggesting that the change of endothelial cell phenotype from normal to proatherogenic plays a key role in initiating atherosclerosis and in the development of atherosclerosis (20, 27, 32, 77, 130–132). Indeed, it has been proposed that decreased endothelium-dependent dilation and/or nitric oxide (NO) bioavailability are key components of the proatherogenic endothelial cell phenotype as one develops this disease. The progressive atherosclerotic process involving endothelial cell-leukocyte adhesion and transmigration, vessel wall inflammation, lipid accumulation/foam cell formation, and conversion to the synthetic smooth muscle cell phenotype has been reviewed in detail previously (26, 35, 74, 93, 117, 118). Accumulating evidence demonstrates, however, that the progression of atherosclerosis and CAD can be slowed, stopped, or even reversed by various interventions, including regular physical activity, and that these effects are accompanied by improved endothelium-dependent vasodilation and/or NO bioavailability (48, 117, 118).
Several studies have examined the effects of exercise training in patients with advanced atherosclerotic CAD (37, 38, 47, 49, 101). For example, Hambrecht and colleagues (49) reported that 4 wk of exercise training resulted in improved endothelium-dependent dilation in conduit arteries (Fig. 2A) and resistance arteries/arterioles (Fig. 2B) in CAD patients. In conduit arteries intracoronary infusion of acetylcholine (ACh) produced less constriction after 4 wk of exercise training and exercise training increased ACh-induced dilation in the coronary microcirculation as shown by measures of total coronary blood flow obtained with a Doppler wire in the coronary artery (Fig. 2B) (49). Lifestyle changes, including increased physical activity, have also been reported to decrease the rate of progression of CAD and/or reverse CAD in patients (38, 48, 101). In summary, research over the past few years provides substantial and increasing evidence that these beneficial effects of exercise are the result of effects of exercise on endothelial cells (75, 80, 90).
Exercise Training Produces Antiatherogenic Endothelial Cell Phenotype in Atherosclerotic Arteries
The balance of proatherogenic and antiatherogenic factors in artery tissue determine whether or not areas of lipid-laden foam cells in the intima of the artery develop into atherosclerotic lesions (35, 75, 117, 118). As outlined above, the proatherogenic phenotype in arterial endothelial cells is characterized by reduced endothelium-dependent dilation (i.e., endothelial dysfunction), decreased expression of enzymes involved in endothelial cell signaling pathways (i.e., pathways for producing NO, endothelium-derived hyperpolarizing factor (EDHF), and prostacyclin), increased expression of adhesion factors, inflammatory mediators, increased oxidative stress, and increased expression of other atherogenic genes (51, 75, 131, 132). Hypercholesterolemia has been reported to cause signs of proatherogenic endothelial cell phenotype (decreased endothelium-dependent relaxation) in conduit arteries of humans (8, 9), monkeys (52, 76), and pigs (6, 17, 63, 113, 114, 124, 139, 140). In addition, the established risk factors (i.e., hypertension, diabetes, smoking, obesity, etc.) also cause signs of proatherogenic endothelial cell phenotype and decreased endothelium dependent relaxation (51, 75, 131, 132). A growing body of evidence indicates that disruption of the NO synthase (NOS) pathway (26, 86, 95) and/or reduced bioavailability of NO are important components of the proatherogenic endothelial cell phenotype (75, 131, 132).
Sustained physical activity has been shown to improve or maintain normal endothelial function in peripheral arteries (57, 68, 80, 84, 90, 119, 140) and coronary arteries (91, 104, 134) and to have similar effects in the presence of vascular disease (47, 124, 139). This improved endothelial function produced by exercise appears to be partially the result of changes in regulation of the endothelial NOS (eNOS) pathway (68, 71, 73, 91, 139) that involve increased expression of eNOS protein (47, 72) and activation by phosphorylation of eNOS serine 1177 by Akt (47). It is important to emphasize that in the key studies of Hambrecht and colleagues (47, 49) as well as studies in experimental animals (68, 71, 73, 91, 139) outlined above, the increased expression and activity of eNOS was associated with improved endothelial function. Other signs of an antiatherogenic endothelial cell phenotype induced by increased physical activity include increased expression and activity of superoxide dismutases (SOD) (31, 110, 111) and of catalase (40) and decreased oxidative stress (75). These changes would serve to increase NO bioavailability by reducing reactive oxygen species (ROS) that catabolize NO to peroxynitrite leading to the formation of nitrotyrosine (51, 75, 110). Work examining the effects of exercise training on the development of atherosclerosis in rabbit aortas demonstrated that exercise training reduces atherosclerosis and improves endothelial function and phenotype as shown by decreased expression of adhesion molecules (e.g., P-selectin, VCAM-1) as well as inflammatory markers such as MCP-1 (16) and inducible NOS (iNOS) (143, 144). The opposing effects of exercise and hypercholesterolemia on eNOS expression, NO bioavailability, and endothelial function in arteries are consistent with the hypothesis that exercise has its beneficial effects through modulation of endothelial gene expression.
Thus there is substantial epidemiological and clinical evidence indicating that exercise training has beneficial effects in prevention and treatment of CAD (75) and, as discussed above, that these effects are associated with changes in endothelial cell phenotype. As shown in Fig. 3, we interpret currently available data as support for the hypothesis that the effects of exercise on expression of endothelial genes making the cells antiatherogenic (reflected as improvement of endothelial phenotype) represents a major mechanism whereby exercise limits or reverses atherosclerosis. The preponderance of evidence in this regard supports the widely held contention that the exercise related signal for antiatherogenic endothelial gene expression is increased shear stress produced by the increased cardiac output and regional blood flows required to provide oxygen to active cardiac and skeletal muscle during exercise (75). Locomotory exercise at intensities that produce maximal levels of oxygen consumption is associated with dramatic stress on the cardiovascular system. The demands for muscle blood flow cause dramatic increases in cardiac output (5–6 l/min to 25 l/min) and increases in shear stress, produced by movement of blood along the walls of the arteries. Also, high-intensity exercise increases stretch on the artery walls associated with increases in systolic arterial pressures and increases in heart rate that alter the magnitude and frequency of systolic stretch. Because of the magnitude of these hemodynamic effects of exercise on the conduit arteries, many have proposed that the beneficial effects of exercise on endothelial phenotype are the result of these hemodynamic, mechanical signals (36, 75).
Shear Stress as a Signal for Altered Endothelial Cell Phenotype
Regular exposure to increased "shear stress" on endothelial cells that results from increases in blood flow during bouts of exercise is considered by many investigators in this field to be the primary signal for exercise training-induced adaptations of endothelial function and phenotype (50, 87, 92, 112). Acute changes in shear stress on the wall of arteries are a well-known signal for flow-induced vasodilation (62, 65, 66, 109). Wall shear stress is increased by an increase in blood flow (Q̇) as described by the following equation: SS = 4ηQ̇/πRi3 (where SS is shear stress, η is viscosity, and Ri is internal radius of the artery).
Accordingly, at a given vessel radius, when flow increases, shear stress at the vessel wall also increases (Fig. 1). Acutely, flow-induced dilation of the artery increases radius and thereby returns shear stress toward normal levels. It appears that substances that signal remodeling and altered phenotype of endothelial and coronary smooth muscle cells are also released in response to increased shear stress (50, 75, 77).
There is a growing body of evidence that increased shear stress is a signal for increased eNOS, decreased endothelin-1 (ET-1) and decreased VCAM-1 gene expression in endothelial cells. Early studies involving cultured endothelial cells suggested that this may underlie training-induced increases in endothelium-dependent vasodilation. In 1992, Harrison and colleagues (96) reported that increases in eNOS mRNA and eNOS protein were observed when cultured endothelial cells were exposed to 24 h of a sustained increase in shear stress. These investigators subsequently demonstrated that as little as 3 h of increased shear stress promoted increased eNOS gene transcription (125, 127, 128) and that eNOS mRNA expression exhibited a dose-response relationship with shear. These findings were later confirmed by other investigators (97, 107). Several intracellular signaling mechanisms have been identified that mediate increased transcription of the eNOS gene in endothelial cells when exposed to shear stress (51). These mechanisms include G proteins (82), Ca2+ (82), and c-Src (21, 22, 51). c-Src is a proto-oncogene product that acts as an intracellular signaling molecule via its tyrosine kinase activity. In addition to an increase in transcription of the eNOS gene, exercise training may lead to elevated eNOS mRNA levels via posttranscriptional mechanisms. One such mechanism is increased mRNA stability as shown in Fig. 4. Recent work by Harrison and colleagues (51) has shown that cultured endothelial cells exhibit increased poly(A) tail length in response to shear stress, inferring a prolonged half-life on eNOS mRNA.
Recent evidence obtained with chip array analysis indicates that "…mean shear stress significantly affects the expression of about 3,000 endothelial cell genes" (53). Space does not allow us to discuss all the endothelial cell genes for which shear stress has been shown to influence expression. For the remainder of this discussion we focus on expression of eNOS and SODs as markers of an antiatherogenic endothelial phenotype and on expression of ET-1, adhesion molecules (VCAM-1, ICAM-1, selectins), and ROS as markers of a proatherogenic endothelial cell phenotype. Shear stress has been demonstrated to signal increased expression of antioxidant genes (96, 97, 107), increased production of prostacyclin (30, 39, 147), and increased expression of COX-1 and PGI2 synthase (98) in cultured endothelial cells, in addition to increased expression of eNOS. Also, increased shear stress in isolated perfused coronary arterioles produced increased eNOS and SOD-1 expression, demonstrating that it is not just cultured endothelial cells that exhibit these effects of increased shear stress (138). There is limited evidence from in vivo experiments evaluating the effects of shear stress on endothelial phenotype. There is evidence that chronic increases in blood flow produced by arteriovenous fistulas in dogs result in increased endothelium dependent relaxation, decreased production of endothelin and altered vasomotor responses to endothelin (87). Also, in rats arteriovenous fistulas have been reported to cause increased eNOS activity, mRNA levels, and protein content (92). Although the results of these experiments support the hypothesis that shear stress may signal antiatherogenic endothelial cell phenotype in vivo, they did not evaluate the effect of shear stress on other anti- or proatherogenic genes.
As summarized above, shear stress has been shown to produce increases in eNOS expression in cultured endothelial cells, in a dose-related manner, across the range of shear stress from 4 to 15 dyn/cm2 (128). Although it is clear that mean wall shear stress levels are not uniform in the arterial tree of mammals (11), recent results indicate that shear stress levels are generally in the range of 1 to 15 dyn/cm2 in human arteries. Areas prone to atherosclerosis in the arterial circulation generally exhibit low shear stress that can be caused by low velocity of laminar flow due to low blood flow levels and/or secondary recirculating flow patterns (separation, reattachment, and recirculation) around branch points and distal to stenoses (136). During exercise both causes of low shear in arteries appear to be decreased. For example, MR imaging allows measurement of shear stress in human arteries at rest and during exercise (12, 25, 122) and indicate that at rest, shear stress is in the range of 1 to 2 dyn/cm2 in the human abdominal aorta and increases to an average of 7 to 20 dyn/cm2 during moderate exercise (122). Also, Cheng et al. (11) report that review of the literature indicates that in nonatherosclerotic human arteries mean wall shear stress levels are in the range of 2 to 15 dyn/cm2 and that wall shear stress is inversely related to the diameter of the artery. Thus the magnitude of shear stress in humans during exercise spans the range of values that produce antiatherogenic endothelial gene expression in cultured cells, suggesting that shear stress could be an exercise-induced signal in humans and large mammals.
The effects of body size on cardiovascular hemodynamics should be considered as one evaluates available literature relative to the magnitude of shear stress produced in the arteries of the mammal. For example, in contrast to the values of shear stress in the aorta of humans outlined above, values of shear stress are much greater in the aortas of rats and mice. Greve et al. (45) report that shear stress values range between 60 and 120 dyn/cm2 in rodent aortas. Also, Cheng et al. (11) report that average mean wall shear stress levels in the common carotid artery of small rodents (rat and mouse) are in the range of 50 to 70 dyn/cm2 whereas larger mammals (human and dog) are in the range of 10 to 20 dyn/cm2. Given these observations, exercise-induced changes in shear stress may have a relatively different effect on endothelium in rodents than in arteries of large mammals.
Considering effects of exercise on shear stress, it is important to remember that increases in blood flow do not necessarily produce increased shear stress if radius of the artery also increases. This may explain some reports in the literature of no increase in eNOS expression in some arteries after exercise training (58, 83, 99, 100, 103).
Another important effect of exercise on shear stress may be that exercise can influence the frequency and magnitude of pulsations in flow (unidirectional) and/or oscillatory flow (antegrade and retrograde flow) and resulting shear stresses. It is well known that under some circumstances coronary blood flow can be retrograde and that retrograde flow also occurs in other areas of the cardiovascular system (12, 13, 43, 122). Oscillatory shear stress, as occurs with retrograde and antegrade flow, has been reported to produce the opposite effects on expression of many endothelial genes as does unidirectional shear stress (46). For example, unidirectional shear stress decreases expression of ET-1 (64, 81) and VCAM-1 (53) whereas oscillatory shear stress produces increased expression of ET-1 (147), increases expression of adhesion molecules (i.e., VCAM-1) (10, 53), decreases eNOS expression (even below zero shear stress levels) (55), increases expression of enzymes that produce ROS (i.e., NADPH oxidase) (23, 55), and increases the release of superoxide (85). As summarized in Table 1, current literature clearly demonstrates that oscillatory shear stress produces an increased expression of proatherogenic genes in cultured endothelial cells and a decrease in antiatherogenic genes (51).
The effects of exercise on oscillatory flow and shear stress appear to be heterogeneous in different segments of the arterial tree. For example, in the human aorta, available information indicates that exercise decreases oscillatory flow and shear stress as total shear increases (122). Indeed, in human subjects, mild exercise was reported to abolish retrograde flow and shear in the supraceliac and infrarenal segments of the abdominal aorta (12). This is important because, whereas both oscillatory and steady shear stress stimulate increased NO production and eNOS expression in cultured cells, oscillatory shear stress produces substantial increases in the production of ROS whereas steady shear stress does not (51, 85). The effects of exercise on oscillatory flow in conduit arteries that perfuse active skeletal muscle are very complicated because exercise effects are dependent on interactions between the cardiac cycle and skeletal muscle contractions. For instance, Lutjemeier et al. (78) demonstrated that the amount of antegrade and retrograde blood flow during single-leg knee extension exercise was dependent on the point in the cardiac cycle where muscle contraction was initiated. Blood flow became oscillatory during contractions as the contraction would impede flow followed by augmented flow during skeletal muscle relaxation. As a result of these interactions of different combinations of timing of cardiac cycle and muscle contraction, blood flow patterns vary substantially during rhythmic exercise (78). Available evidence indicates that when going from rest to exercise antegrade flow increases to a greater extent than retrograde flow in arteries perfusing exercising skeletal muscle. The effects of exercise on oscillatory flow in conduit arteries that are not providing blood flow to exercising muscle tissue are also complex. For example, exercise has been reported to increase retrograde flow in the brachial arteries of humans performing leg exercise (42), in contrast to the decrease in oscillatory shear rate produced by exercise in the abdominal aorta.
Currently literature also suggests that oscillatory flow and shear stress may have different effects on endothelium in vivo than those observed in cell culture experiments (Table 1). For example, it has been reported that leg exercise produces increased blood flow and increased contribution of NOS generated NO release in brachial arteries of humans (42–44). Green et al. (44) demonstrated that leg cycling exercise produced oscillatory, antegrade/retrograde, blood flow patterns in the brachial artery and, importantly, that these conditions were associated with a larger contribution of NOS generated NO release from the brachial circulation. Green et al. concluded that these results may suggest an important role of oscillatory shear stress-mediated release of NO from the endothelium of the brachial circulation during leg exercise. On the basis of the literature summarized above, it is reasonable to propose that repetitive enhancement of NO production by brachial artery endothelial cells produced by leg exercise training would lead to an upregulation of eNOS expression, i.e., an antiatherogenic endothelial cell phenotype. However, at this time it is not possible to establish for sure that the increased NO production seen under these conditions in the arm vasculature is the result of the oscillatory shear, as proposed, or due to other stimuli in the arms during leg exercise, i.e., systemic effects of exercise on endothelial cell phenotype. Therefore, it is important that future work determine whether the increase in NO production in the arm, reported to occur during leg exercise, is evidence that oscillatory shear stress in the arm vasculature is a signaling mechanism underlying production of an antiatherogenic endothelial cell phenotype. More work is needed to understand these hemodynamic interactions and to pinpoint the impact of oscillatory flow and shear on endothelial cell phenotype in different arteries in vivo.
In summary, review of the current literature indicates that shear stress produces increased expression of antiatherogenic genes and decreased expression of proatherogenic genes in cultured endothelial cells and in endothelial cells of arteries in vivo. Also, the magnitudes of shear stress required for these alterations in gene expression are in the range of shear stress values reported in arteries during moderate levels of exercise in conscious humans. These observations indicate that shear stress during exercise is sufficient to induce antiatherogenic gene expression and are consistent with the hypothesis that shear stress is an important signal for exercise induced changes in endothelial cell gene expression. In cultured endothelial cells, oscillatory shear stress produces proatherogenic gene expression. Conversely, exercise appears to reduce retrograde flow in some arteries, thus decreasing oscillatory shear stress signals, whereas exercise increases retrograde flow in other arteries. More focused research in humans is needed to establish the importance of oscillatory flow in the effects of exercise on endothelial cell phenotype. Despite this current limitation in our knowledge, we conclude that available evidence strongly supports the hypothesis that shear stress is one signal for exercise-induced expression of antiatherogenic endothelial cell phenotype in arteries.
Pressure and Circumferential Stress (Stretch) as a Signal for Altered Endothelial Cell Phenotype
It is well known that arterial pressure fluctuates with systolic pressures of 120 mmHg and diastolic pressures of 80 mmHg at rest. During exercise peak systolic pressures can approach 200 mmHg and diastolic pressures remain normal or decrease (108). Arterial pressure waves pass through the arterial tree, and the magnitude of pulse pressure is determined by interactions between the compliance of the segments of the arterial tree and harmonics of the pressure waves. Thus arterial systolic and diastolic pressures in the femoral arteries can be significantly different from those measured in the aorta (108). Blood pressure can influence endothelial cells in at least two manners. First, cell culture experiments have demonstrated that exposure of endothelial cells to pressure affects growth rate of endothelial cells. Pressures in the range of 20 to 100 mmHg cause increased growth rates and higher pressures (>130 mmHg) cause inhibition of endothelial cell growth (115, 133). In addition to these effects on growth rates, pressure can signal altered endothelial cell gene expression. For example, exposure of endothelial cells in culture to pressures of 135 mmHg results in increased eNOS and iNOS protein content (133).
A second manner whereby changes in pressure can alter gene expression of endothelial cells results from stretch of the arteries. Because arteries are compliant, changes in pressure can stretch endothelial cells producing circumferential stress (strain) and the pulsatile nature of arterial blood pressure results in cyclic strain on the arteries. It appears that cyclic strain applied to endothelial cells produces even more dramatic effects on endothelial cell phenotype than does just compression (direct effects of pressure on the cells), as discussed in detail below.
Endothelial cells are exposed to cyclic circumferential stress (strain) from distention of arteries caused by increased blood pressure (which increases transmural pressure across the arterial wall) (25) and/or by relaxation of smooth muscle in the wall, which allows the blood vessel to increase in diameter, producing stretch of the endothelial cells lining the vessel. In vivo, arterial endothelial cells are exposed to cyclic distention during the cardiac cycle. Cyclic strain and wall movement have been measured in human thoracic aorta with MRI, and results demonstrate that peak strain usually occurs after peak flow in the aorta (25). The frequency and magnitude of this distention increases during exercise because of increased systolic pressure and heart rate (108). As summarized in Table 2, there is a growing body of evidence that cyclic strain alters endothelial cell gene expression patterns. Awolesi et al. demonstrated that cyclic strain increased transcription of eNOS in cultured endothelial cells (3) and increased eNOS enzyme activity of cultured endothelial cells (2). Since these observations, it has been proposed that distention (increased intraluminal pressure) of arteries is a signal for increased expression of the eNOS gene (148). There is also evidence that stretch increases expression of EDHF synthase (CYP450) (106), suggesting that cyclic strain may increase endothelium-dependent dilator pathways in general. Considering factors that may be proatherogenic, however, as summarized in Table 2, cyclic strain has also been reported to increase release of ROS (15) and to increase expression of adhesion molecules including ICAM (14, 145), selectin (145), and MCP-1 (141, 142, 145). These observations are consistent with many reports in the literature that indicate that chronic increases in blood pressure are associated with impaired endothelial function and increased progression of atherosclerosis (28). Also, Dancu et al. (19) reported that cyclic strain applied to cultured endothelial cells grown in silicon tubes caused a decrease in eNOS expression, in contrast to reports of studies using other methods of inducing stretch on cultured cells (3).
It is clear that the effects of cyclic strain on endothelial cells are complex and can be modified by a number of important variables. One important consideration in interpreting cyclic strain literature is evaluation of direct and indirect effects. For example, when endothelial cells in an intact artery are "stretched" because of increased pressure, there is an increase in superoxide and other forms of ROS in the artery (5) and an increase in adhesion molecules, such as VCAM-1 (126). The ROS produced by cyclic strain may indirectly cause increased expression of eNOS (4, 15). The major effect of rhythmic circumferential strain on endothelial cells appears to be proatherogenic, even though the changes in eNOS expression alone would be antiatherogenic because the increased ROS production and expression of adhesion molecules override the effects of increased eNOS expression (51). The increased eNOS expression, although insufficient to correct function, may be a compensation for the loss of bioactive NO through the actions of superoxide and other ROS species. Consistent with the proposal that increased eNOS expression may be secondary to ROS effects are the reports that increased blood pressure increases eNOS expression in rat aorta (4) in association with increased oxidant stress in the aorta as well (5). Exercise bouts are usually of 1- 2-h duration. Conversely, many studies of the effects of cyclic strain on endothelial cell phenotype have been designed so that the cells are exposed to cyclic strain 24 h/day. These different exposure times should be considered when interpreting results. For example, brief increases in blood pressure and ROS associated with bouts of exercise may signal increased eNOS expression and other beneficial effects of exercise, whereas chronic increases in blood pressure may elevate ROS chronically. Hence chronic elevations in blood pressure may trigger different changes in endothelial phenotype than do episodic increases in pressure and wall stretch. This hypothetically may explain the paradoxical enhancement in endothelial function associated with exercise, relative to the impaired endothelial function associated with primary hypertension.
In summary, cyclic strain on endothelial cells causes increased expression of eNOS. However, cyclic strain also signals upregulation of proatherogenic genes including adhesion molecules, MCP-1 expression, and markers of oxidant stress as summarized in Table 2. Also, chronic increases in blood pressure have been shown to result in proatherogenic endothelial cell phenotypes, and increased blood pressure is recognized as a risk factor for development of atherosclerosis (28). Therefore, we conclude that at this time it is unclear whether increased wall strain participates in signaling an antiatherogenic endothelial cell phenotype in physically active subjects. Given the duration of exposure to cyclic strain produced by exercise for 1 or 2 h/day, future research is required to determine whether increases in systolic blood pressures and heart rate produce important signals for the beneficial changes in endothelial cell phenotype associated with exercise training.
Interactions of Shear Stress and Circumferential Stress (Stretch) in Altered Endothelial Cell Phenotype
As outlined above, exercise produces complex hemodynamics that 1) increase the magnitude of blood flow and shear stress, 2) the frequency of pulsatile changes in pressures and flows, and 3) increased arterial systolic pressures. Available evidence indicates that the complexity of hemodynamics can contribute to expression of a proatherogenic endothelial cell phenotype especially when these hemodynamic parameters are asynchronous. Dancu et al. demonstrated that when pulsatile changes in diameter, flow and blood pressure occur synchronously these hemodynamic forces have different effects on endothelium lining silicon tubes than when the pulsatile changes are asynchronous (19). Figure 5 illustrates synchronous hemodynamics (on the left) and asynchronous hemodynamics on the right from data obtained in chronically instrumented, conscious pigs. Note on the left that aortic blood pressure, aortic blood flow, and aortic diameter have peak values during systole. This example is not truly synchronous because the time courses of the changes are similar though not identical. Truly synchronous hemodynamics would exist if these parameters in the aorta had the same time courses, i.e., minimal and maximal values at the same time points, so that peak pressure, flow, and diameter occurred at nearly the same time. In contrast to synchronous hemodynamics, an example of asynchronous hemodynamics is shown on the right of Fig. 5 in the coronary artery. Peak coronary flow occurs during early diastole, when pressure and coronary artery diameter are less than their peak values, i.e., asynchronous hemodynamics as defined by Dancu et al. (18). Dancu et al. examined the effects of synchronous and asynchronous changes in pressure, tube diameter, and gene expression on endothelial cells cultured in silicon tubes (18, 19). As shown in Fig. 6, Dancu et al.'s results demonstrate that asynchronous pulsations in shear stress and circumferential strain results in decreased eNOS expression but increased ET-1 expression in endothelial cells (18, 19). It is well known that asynchronous hemodynamics is the normal condition in the coronary circulation as illustrated in Fig. 5. That is, most coronary blood flow occurs during diastole, when blood pressure and coronary artery diameters are low (Fig. 5). Because of this, peak values of shear stress and circumferential strain are normally asynchronous in the coronary circulation. Perhaps of more interest, it is not uncommon to observe retrograde flow in the coronary arteries during early left ventricular systole at rest (59). These conditions may explain, in part, the propensity of the conduit coronary arteries to develop atherosclerosis. During exercise, coronary blood flow is normally no longer oscillatory but becomes pulsatile with positive flow in both systole and diastole. The pulsations in flow and pressure remain asynchronous during exercise, and it is not clear that the asynchrony of shear stress and circumferential strain would be decreased in the coronary arterial tree during exercise. It seems possible, however, that the relatively greater effect of exercise on shear stress (due to the four- to sixfold increases in coronary blood flow) and the fact that coronary blood flow is not oscillatory during exercise predominate during bouts of exercise resulting in a net antiatherogenic signal (69).
Enhanced external counterpulsation is a noninvasive treatment for CAD patients that has been shown to increase diastolic coronary blood flow and total coronary blood flow. Enhanced external counterpulsation increases diastolic pressures above the diaphragm by compressing the tissues below the diaphragm and driving blood toward the heart. In patients who received daily 1-h treatments of enhanced external counterpulsation for 6 wk, it was reported that plasma nitrate and nitrite levels were increased (indicative of increased release of NO in the blood) and ET-1 levels were decreased, suggesting improved endothelial function and phenotype in these patients (1). Similar results have been reported for enhanced external counterpulsation treatment in an animal model of CAD (146). Zhang et al. (146) proposed that enhanced external counterpulsation in a porcine model of CAD applied to the hindlimbs and hips of the pigs would increase shear stress and improve endothelial cell function/phenotype in the coronary and brachial arteries. They found that enhanced external counterpulsation resulted in a doubling of peak diastolic shear stress in the brachial artery. Application of enhanced external counterpulsation for 2 h a day for 7 wk also resulted in a more antiatherogenic endothelial cell phenotype in the left anterior descending coronary artery (146). On the basis of the analysis of the effects of hemodynamic stress presented above, it would be expected that the arteries in the hindlimb of these pigs and perhaps in the abdominal aorta, would have retrograde flow during counterpulsation, which drives blood back into the thoracic aorta. If this hypothesis is correct, we would further expect proatherogenic changes in endothelial cell gene expression in these caudal arteries. Zhang et al. did not report whether proatherogenic changes in endothelial gene expression were seen in the abdominal aorta and arteries of the hindlimb. Therefore, this hypothesis will have to be tested in future work.
Systemic Distribution of Exercise-Induced Arterial Vascular Adaptations
There are reports of exercise training-induced adaptations in vascular beds providing blood flow to tissues/muscle not heavily involved in training bouts (44, 56, 57, 61, 67, 69, 70) and within skeletal muscle that does not exhibit increased oxidative capacity with exercise training (62, 67, 137). For example, most (24, 79, 120) but not all (123) studies have reported that leg exercise training of healthy and diseased human populations produces improved endothelium-dependent dilation in conduit arteries of their relatively inactive arms. Such observations may suggest a systemic effect of exercise training on arterial endothelial cell phenotype. However, modest increases in blood flow (42), oscillatory shear rate (42), pulse rate (41, 42), and blood pressure have been reported in the arms of humans during lower extremity exercise (42, 60, 121). These results make it difficult to appreciate the importance of primary hemodynamic signals (shear stress and cyclic strain) that may signal phenotypic changes to endothelial cells in the brachial artery during leg exercise. In addition, it is unclear at this time whether hemodynamic forces or circulating factors are the underlying mechanisms involved in vasculature adaptations in conduit arteries that do not perfuse cardiac or skeletal muscle active during exercise. As a result, it has yet to be determined whether one or a combination of the four hemodynamic forces mentioned above are the underlying mechanism involved in the apparent systemic effects of exercise on endothelial cell function/phenotype.
In conclusion, the available literature reviewed herein shows that shear stress is a signal for expression of antiatherogenic genes in endothelial cells in culture, in isolated arteries, and in arteries of intact animals. Furthermore, shear stress levels in the arteries of humans during exercise are in the range that produces beneficial changes. In contrast, oscillatory flow patterns can cause proatherogenic gene expression in cultured endothelial cells. In vivo evidence indicates that exercise decreases oscillatory flow/shear in some portions of the arterial tree but may increase oscillatory flow in other areas of the arterial tree. We conclude that current evidence indicates that increased shear stress during exercise may be one signal produced by exercise that contributes to an antiatherogenic phenotype of arterial endothelial cells.
Our review of current literature indicates that circumferential wall stress can also increase expression of some beneficial antiatherogenic endothelial cell genes. However, this literature equally provides evidence that circumferential wall stress increases production of ROS and increases the expression of adhesion factors and other proatherogenic genes. These data suggest that circumferential wall stress produced during exercise may contribute to exercise-induced modulation of endothelial cell phenotype. It appears that interactions of arterial pressure and fluid shear stress may play an important role in arterial vascular health and likely contribute to how exercise bouts signal changes in endothelial cell gene expression. Given that the timing of these signals during the cardiac cycle (i.e., whether or not the changes are asynchronous or synchronous) can have major effects on the impact of these signals on endothelial phenotype, more detailed analysis of these hemodynamic variables during bouts of exercise training is required. We conclude that available evidence suggests that exercise signals formation of beneficial endothelial cell phenotype at least in part through these mechanical signals: shear stress and wall stretch. However, it is also clear that other local and circulating factors interact with these hemodynamic signals during exercise to produce the healthy arterial endothelial cell phenotype. Future research promises to reveal these factors and how they interact with hemodynamic forces.
This work was supported by National Institutes of Health Grants RR-18276, HL-36088, HL-52490, and AR-048523.
- Copyright © 2008 the American Physiological Society


text:
- +1 573 427 7326
- email@example.com
Rep. Lyndall Fraker really likes Country Clubs. He likes to hold public hearings at them, and he also likes to give them tax breaks.
Rep. Lyndall Fraker, R-Marshfield, wants to offer a sales tax exemption on initiation fees or dues on private country clubs.
"It's just really hitting some of these clubs really hard," Fraker said.
Fraker acknowledges that tax credits do take a toll on the state budget.
"I'm not totally against tax credits, but I also feel there is a need to rein them in," Fraker said.
Yesterday, he filed the bill he said he would — HB 833: Authorizes a sales tax exemption on initiation fees or dues of private country clubs, golf courses, and golf clubs not open to the public.
There have been worse bills filed in the Missouri Legislature, but the timing was impeccable.
Yesterday was also the day legislative leaders sent ALEC's so-called "Right to Work" bill to the governor's desk, yielding to the demands of millionaires and billionaires and special interest groups.


text:
Peter Moody's King's Rose will attempt to continue her impressive spring carnival performance when she competes in the $3 million Cox Plate tomorrow October 22, 2011.
King's Rose has blossomed since being transferred from New Zealand to Moody's Caulfield stables and has proven herself over three tough runs.
The four-year-old mare won both the Group 2 Memsie Stakes and Stock Stakes this spring before finishing a close second to Secret Admirer in the Group 1 Toorak Handicap last start.
King's Rose, who has drawn well in barrier two for tomorrow's Cox Plate 2011, appears to be a forgotten danger in the race and below you can see why.
Horse Facts – King's Rose
- Jockey: Luke Nolen
- Trainer: Peter Moody
- Owners: Dr G W W Tsoi
- Age: 4YO
- Gender: Mare
- Breeding: by Redoute's Choice out of Nureyev's Girl
- Career: 15 8-2-0
- Prize Money: $615,661
- Current Cox Plate Odds: $13 at Luxbet
Why King's Rose Can Win the 2011 Cox Plate
- King's Rose has won both of her two prior attempts at the Cox Plate's distance
- She has won her only previous run at Moonee Valley Racecourse
- She is proven on both dead and slow-rated tracks
- King's Rose has been in fantastic form, winning two and placing second in the other of her three Australian race starts
- She has drawn barrier 2
- She will carry the second lightest weight of 55.5 kilograms
Why King's Rose Can't Win The 2011 Cox Plate
- King's Rose is yet to win an open class race
- This will be her first attempt at weight-for-age conditions
King's Rose is currently paying odds of $13 to win the 2011 Cox Plate at Luxbet so open an account today to secure these fantastic odds now!
Luxbet offer the "Best of the Best" odds on all the top races around the country.
Just enter the exclusive promo code BONUSBET when you join and you will receive a bonus bet valued at 100% of your initial deposit when you bank between $25 and $500 into your new account for a limited time only.
Furthermore, Luxbet members can enjoy the latest best tote exotic + 5% offer which is available on all race meets this spring racing carnival that feature a Group 1 race.
Also, did you know that Luxbet is owned by TABCORP? So you can bet with a company you know and trust, while still getting the great odds that a small bookmaker can offer.
So share in the Sydney Spring Carnival riches by opening a Luxbet account today!


text:
Physicians highlighted ways to help prevent cancer, as well as how to cope with disease, during the 17th annual Tyler Breast Cancer Conference on Friday.
The community forum was open to the public, while Friday's presentations unite doctors as they receive a comprehensive review of advances in breast cancer research.
Friday night's topic focused primarily on how to adopt a healthy lifestyle.
Dr. Neil Spector, associate professor of medicine and associate professor of pharmacology and cancer biology at Duke Medical Oncology in Durham, N.C., detailed his experience as a heart transplant survivor.
In the 1990s, he went in circles with physicians about a mysterious medical condition, which ultimately left him with only 10 percent heart function. Doctors finally confirmed he had Lyme disease.
In 1997, he had a pacemaker installed. Instead of giving up, he began enjoying his life.
"Don't be defined by your disease," he told the audience.
Spector also reminded the crowd that while doctors have expertise in medicine and science, people still have to be their own advocate.
"If you don't feel like you're getting an answer and there's something inside of you that's telling you, 'This isn't right,' you better seek another opinion or figure it out until you feel comfortable," he said. "Otherwise, you could die.
"Trust your gut instincts. You're the only one who knows yourself. There is no one who knows your body like you do."
Spector said people should not discount meditation and other stress reducing techniques. It's all about the mind-body connection.
"Most Western medicine doesn't care about these things," he said. "All they care about is 'What can I prescribe for you?' It's reactive medicine."
He cited studies that showed 40 percent of premature deaths are caused by behavioral factors or things that people can control.
Ultimately, Spector said, individuals have to take back control of their health.
"I understood my doctors can only do so much for me and the rest of it is diet, exercise and stress reduction," he said. "Those are not just nice things to have. There's a real strong scientific rationale for why anyone with any cancer should lower their stress levels. Some of the things that stress does in the body fuel the growth of tumors."
"Anyone who goes to the oncologist, if they're doctor doesn't say, 'How are you coping with this? How is your stress?' It's almost as negligent as prescribing the wrong drug."
Spector said while medicine is ever changing and patients face limited face time with their doctors, there is a push for personalized medicine.
He said innovation in genomic research further limits time with physicians, as it may eventually allow patients to quickly present their profile to doctors.
But a change toward more time with their physician will only come from the patients demanding that time, Spector said.
Dr. Sasha Vukelja, a Tyler oncologist who has organized the conference each year, outlined ways to improve lifestyle.
This includes nutrition. Dr. Vukelja emphasized the need to eat slower, small frequent meals and to eat for the right reasons. She warns against dieting, which leads to binge eating and ultimately, weight gain.
"Don't make restrictions you can't keep up with," Dr. Vukelja said.
She also touted the benefits of exercise and taking supplements, particularly vitamin D3, which many people find are deficient in. Limiting alcohol consumption and eliminating tobacco products are other ways to improve health, she said.
As people are living longer after a cancer diagnosis, Dr. Vukelja said terminology and mindsets are changing. No longer are people diagnosed with cancer simply survivors. She prefers "thrivers." Her mission, she said, is to push the benefits of healthy living to her patients.
"We're curing cancer. We're making thrivers," she said. "But you now what? We want to prevent cancer."


text:
Welcome to 3G Telecom
3G Telecom Infra (3GTI), a leading provider of network infrastructure solutions and strategic network design services, fully owns a robust fiber network throughout Andhra Pradesh state. We create solutions that work on large scale. Companies need robust, scalable and affordable networks. 3G Telecom Infra (3GTI) understands and adds measurable value to an organization's search for connectivity.
3G Telecom Infra (3GTI) was planned from the ground up to be a different kind of Network Company. Here's exactly what we mean: We own our own network-unlike most other network companies who simply lease their network from other companies. That means we're 100% responsible for the service you get. If there is a problem, we fix it.
We're ridiculously easy to do business with. If we say "This is the install date", it really is. If we give you a price quote, we stick by it-with no hidden charges. Isn't that the way things should be?
Our Customers
Latest News
- August 1st, 2010Beam telecom Multiplies Bandwidth by connecting to 3G Telecom Infra optical fiber network
- June 1st, 20103G Telecom Infra Further Expands Metropolitan Fiber Optic Network in Hyderabad and Secunderbad City Area


text:
WILMINGTON, NC (WWAY) — The inaugural "One Cup of Tea" fundraiser fills the cup of many in need in support of Saludhondu.
The organization was started by local physicians to provide medical facilities to the people of central Honduras.
More than 200 folks enjoyed tea and a silent auction while raising money for urgent-care-like clinics in the remote Honduran mountains.
Saludhondu began in 2010, the facilities were built in 2012.


text:
|Bloomsbury Auction: Early Hobbit (10th impression)
Subject: Bloomsbury Auction: Early Hobbit (10th impression)
by Urulöké on 2008/7/28 22:19:46
Bloomsbury Auctions sent me an announcement about their upcoming "Bibliophile Sale" on August 7th 2008 at 1:00 pm at their London location.
Viewing beforehand on
Tuesday 5th August from 9:30 am to 5:30 pm
Wednesday 6th August from 9:30 am to 8:00 pm
Thursday 7th August from 9:30 am to 1:00 pm
63. Tolkien (J.R.R.) .The Hobbit, first edition, tenth impression, colour frontispiece, plain illustrations and map endpapers by the author, school library stamp on verso of front free endpaper, original pictorial green buckram, shelf-lean, dust-jacket, 2 closed tears, frayed at corners and spine ends with some loss, 8vo, 1958.
Estimates £75 - £100


text:
Among American Beacon's overachievers was its large-cap value fund, AMR Class (AAGAX), which won the 2010 Lipper Fund Award for the Best Large Cap Value Funds category for the 10-year period ended Dec. 31, 2009. The fund beat out 185 funds for the award, returning 5.2% as of Dec. 31, 2009, while the S&P 500 returned 0.45%. "Consistency, low cost, attention to detail are the real value propositions we bring to clients and we're able to take a lot of their workload off of them and their investment committees because of what we do," says Needles. "We may not have had some of those high highs as some of those single managers but we didn't give up as much as they might have in certain markets."
Morningstar agrees. "They're really looking for highly reputable, skilled managers that have a repeatable process and don't have a lot of volatility in their funds," says Ryan Leggio, an analyst for the mutual fund tracker. Leggio points out that nearly all American Beacon's funds earned an above-average Morningstar rating of three or four stars. "It's a fine firm that's very conservatively managed and has done very well for shareholders."
Even with the market turbulence, Youngblood has no regrets about closing the deal. "We purchased the asset at the top of the market, so the timing could have been better," he says. "But we never looked at this as a quick flip." Just like the firm's investment approach, Youngblood is in it for the long haul.


text:
Sustainable Transportation Partnership
Council was provided an update on the activities of the Sustainable Transportation Partnership. In March 2013, the partnership was established through an Intermunicipal Service Agreement between the local governments of West Kelowna, Kelowna, Lake Country, Peachland, Westbank First Nation and the Regional District of Central Okanagan. The partnership coordinates the regional delivery of sustainable transportation programs and projects in support of common regional policy, plans and interests.
Zoning Bylaw Adjustment
Council gave first and second reading to a Zoning Amendment Bylaw to address two specific setback clauses within the new Zoning Bylaw, adopted February 11. Since adoption of the new bylaw, the District has received a number of inquiries and development variance applications regarding the setback clauses. Council agreed to a zoning text amendment as a general housekeeping matter. The Zoning Amendment Bylaw will be taken to public hearing on April 22, 2014.
Wildhorse Park Plan
Council directed staff to add the completion of a public consultation and preliminary park plan for Wildhorse Park, in the Smith Creek neighbourhood, to the 2014 operational plan and adjust the timing of other projects accordingly. Council also directed that $4,000 be put towards site cleanup and $8,000 for a preliminary park plan for the park in the 2014 Budget. The move is in response to a request from the Smith Creek Residents Association to pursue development of the park ahead of the recommended timelines in District's Parks and Recreation Master Plan.
Bartley Road Licence of Occupation
Council authorized the execution of a Licence of Occupation agreement between the District and the Province of BC for the westerly three acres of 2515 Bartley Road for a 20 year term commencing on March 25, 2014. The site will be used for municipal works activities and the District will continue to pursue a Sponsored Crown Grant for the entire parcel.
Westlake Road Upgrades – Tender Award
West Kelowna Council tendered the $5.1 million Westlake Road Upgrade construction project on April 8, 2014 with work expected to begin this month on this important transportation corridor. TT Contractors Ltd. was the lowest bidder on the construction project which will see Westlake Road, between Highway 97 and Starlight Crescent, transformed from a rural state to an urban arterial standard. The project is expected to take approximately five months to complete and will include the construction of:
- 3.6 metre wide travel lanes in each direction
- 1.5 metre cycling lanes in each direction
- Curb, gutter and underground storm drainage
- Replacement watermain
- 1.8 metre wide sidewalks at in each direction from Stevens Road to Highway 97
- 1.8 metre wide sidewalks on the east side from Stevens Road to Starlight Crescent
- 56 streetlights
- A roundabout traffic circle at the intersection of Stevens Road and Westlake Road.
During construction, motorists can expect traffic disruptions and road closures. Signage will be placed at key intersections indicating alternate routes during construction. Detour routes will be established to access homes and businesses throughout the construction period with a detailed detour map available on the District's website. Residents can watch the website for traffic notifications related to Westlake Road or to sign up to be emailed this information directly via the District's e-Notification system. The District's Facebook and Twitter followers will also be notified of construction activity. The total Westlake Road Upgrade project is expected to cost $6.2 million with the following funding sources:
- Development Cost Charges: $3.876 million
(from new construction projects over the past several years).
- Gas Tax Funds: $500,000
(provided by the Government of Canada and Province of British Columbia).
- District Capital Reserves: $479,300
- Reserves for Future Expenditures: $250,000
- Water Reserve: $1.038 million
- Donation: $95,000
MADD Signage
Council provided support for the installation of 16 signs as part of the Mothers Against Drunk Driving (MADD) "Campaign 911" within the community. The Canada-wide campaign is intended to provide awareness and encourage the public to report suspected drunk driving and boating. MADD will cover the costs associated with the signage and installation at seven locations (14 signs) on various District arterial roadways and two District boat launches.


text:
- Description
Product Highlights2 Cone step-down diffusers are constructed from 24 gauge steel with a durable white powder-coat finish. They feature a 2" 22 gauge collar, seismic support tab and 4-way air deflection.
- Specifications
Weight 7.70 Pounds Length 4.75 Inches Width 24.00 Inches Height 24.00 Inches Country of Origin VNM UPC or Barcode 803492203689 Hazardous Material No Brand TRUaire Curved Blade No Deflection 4-Way Adjustable No Application Air Ventilation Color White Composition Steel Finish Powder Coated Insulated No Shape Square Size 24" x 24" Type Sidewall and Ceiling Galvanized No Product Family 2003CD
- Documentation
To see the pricing of the equipment you need to be a licensed provider. Click here to become a licensed provider.


text:
Anchors Monty Torres and Anna Laurel of Fresno's KMPH unexpectedly landed a spot in the trailer for upcoming blockbuster "Battle: Los Angeles" (video above).
The movie's producers contacted the Fox-affiliate after seeing Torres and Laurel's original broadcast on YouTube and asked if they could purchase the clip, according to the Fresno Bee.
"Neither Anna nor I knew we were going to be in one of the movie's trailers until some of our colleagues, friends, told us they were seeing it on television," Torres said.
Here's a clip of the original newscast from last July, in which Torress and Laurel report on a "real" UFO sighting over Fresno:


text:
Maidenhead older, discerning and careful
- I've now bought two of these beds in the last two months. They were both on sale in different shops. They are comfortable, modern but traditional and a doddle to assemble. You don't buy two if they are pants! {:o)
Published on: 18 April 2016
Chloe Frame


text:
Newspapers for the Haredi Global Village
The most important thing that has been happening in the ultra-Orthodox media in recent years is apparently taking place in the United States. After the English edition of the Haredi newspaper Hamodia registered a surprising breakthrough in recent years, and has become a daily, the English edition of the Haredi magazine Mishpacha (Family) has registered a similar breakthrough. The publisher of Mishpacha, Eli Paley, says that he is already selling 19,000 copies of the English edition, most of them in the United States. Within a short time, he estimates, the paper will print more copies in English than in Hebrew. Every week he flies three tons of newspapers to North America. But soon, says Paley, the moment may come when it will pay for him to print the newspaper in Canada. The children's supplement of the paper has been highly successful, says Paley, and it helps Mishpacha sell hundreds of copies to Haredi schools.
Hamodia now issues three separate editions in English - in the United States, in Europe and in Israel. The paper in the U.S. is also geared to religious people who are borderline Haredi, and therefore its policy is more moderate than that of the Hebrew edition. For example, whereas the Hebrew paper does not print pages with pictures of rabbis, the English edition does. In Hamodia in Israel, they make sure not to place ads with Internet addresses, because of the prohibition by the leading Torah scholars on use of the Internet. Hamodia in the United States has accepted the fact that there is no business without the Internet, and does not demand that the www. be erased.
A recently reported study published by the head of the Floersheimer Institute for Policy Studies, Prof. Amiram Gonen, focused on Haredim in London going out to work. In the study Gonen discusses, among other things, the Haredim custom of traveling often to concentrations of Haredim the world over, for family visits, and in order to spend time with the rabbis. He says this creates "a global Haredi village." Now this village already shares the same media, just as global secular society watches the same television channels. (S.I.)
Want to enjoy 'Zen' reading - with no ads and just the article? Subscribe todaySubscribe now


text:
The Cold War describes the tense and hostile relationship between the Soviet Union and the U.S. between 1945 and 1992. The communist government of the Soviet Union wanted to convert other countries to communism. The U.S. pledged to support free countries so they could resist communism. Both countries had nuclear weapons and were capable of launching a nuclear war.
Other countries took sides in this international conflict. Many Western European countries sided with the U.S. to form NATO (National Atlantic Treaty Organization) in 1949. Eastern European countries signed the Warsaw Pact and formed an alliance with the Soviet Union.
1945: Yalta Agreement1947: Truman Doctrine1947: Marshal Plan1948: Berlin Airlift1949: NATO formed1950: Korean War begins.1952: U.S. tests first hydrogen bomb in Marshall Islands.1953: Soviet Union tests first hydrogen bomb.1953: Korean War ends.1955: Warsaw Pact organized1957: Launch of Sputnik1950s: McCarthy Hearings1961: Berlin Wall built1961: Bay of Pigs1962: Cuban Missile Crisis1963: Installation of a Hot Line1969: Strategic Arms Limitation Talks (SALT) begins.1979: Invasion of Afghanistan1987: Intermediate Range Nuclear Forces Treaty1989: Berlin Wall comes down.1990: Unification of East and West Germany1991: Collapse of the Soviet Union
CNN: The Cold War
The Cold War Museum
The Cold War
Cold War Policies
National Archives Learning Curve: Cold War
Yahoo: The Cold War
Back to Top
Definition:A system of government in which all means of production are owned by a single party; a social system in which property and goods are owned in common
Context:During the 20th century, the Soviet Union and China were two powerful communist countries.
NATO (North Atlantic Treaty Organization)
Definition:An international political alliance formed to settle disputes peacefully and defend member countries against outside aggressors
Context:NATO was formed in 1949 by the United States and Western European nations in response to the threats associated with the Cold War.
Warsaw Pact
Definition:A military alliance of communist eastern European nations formed in 1955 in response to the Cold War
Context:The nations of the Warsaw Pact included the Soviet Union, Czechoslovakia, East Germany, Bulgaria, Hungary, Poland, and Romania.


text:
A body piercing shop could be set up in Downham if planners give the go-ahead.
Brian Johnson has submitted a change of use planning application to convert a financial services site in Cannon Square, Downham, into a body piercing salon.
The application was lodged with West Norfolk Council on April 3.


text:
Van Plows Through Crowd Outside London Mosque
London police are confirming that one person is dead after an apparent attack on Muslim worshipers in north London. At least eight people were taken to area hospitals and another two people were treated for minor injuries at the scene.
A little after midnight, local time, a white van rammed into Muslim worshipers outside the Muslim Welfare Center in the Finsbury Park area. Police have not confirmed the nature of the incident, but eyewitnesses say it was a deliberate attack and counter-terrorism officials are reportedly on the scene.
Police have one man in custody. Witnesses captured video of the alleged driver being taken into police custody.
Reports that this video shows an arrest of a man who could be linked to an incident in #FinsburyPark in London pic.twitter.com/2y7gGx1EnM— Rhys Kelly (@Rhysaphine) June 19, 2017
The leader of the Finsbury Park mosque is condemning what he called a "cowardly attack." Mohammed Kozbar tweeted early Monday morning saying "Our thoughts and prayers with those who got injured and effected by this cowardly attack in Finsbury Park area." Kozbar adds that there are "many casualties in the floor."
The incident comes as Londoners are on edge following an attack earlier this month that left eight people dead. In that attack a van rammed pedestrians on London Bridge and then the three attackers began stabbing people at nearby Borough Market.


text:
Here's a liitle drawing of Dorothy Gale from the Wizard of Oz.It took me two hours to fill her in with my tablet.
DragoArt members upload artwork and drawing tutorials! They are also allowed to leave comments on tutorials, profiles, etc. Many more features, as well; it's way better than just being a boring guest! Register Now!


text:
When Courtney McCool landed a bar dismount in practice Tuesday, her face lit up and she hugged associate head coach Jay Clark.
Her recent accomplishment - sticking a dismount on the hard mat - gave the Georgia gymnast the greatest joy before entering the second-ranked Gym Dogs' competition at Arkansas today. She is expected be a part of the uneven bars lineup for the first time this season.
McCool, back from a foot injury, is the 11th Gym Dog to compete on the event this season.
Twelve gymnasts vying for six spots in the lineup has left the Georgia coaching staff with difficult decisions as to who will compete each week. The team, however, has benefited from the daily competition in practice.
"That kind of depth just breeds excellence," said Clark, who coaches the gymnasts on uneven bars. "It requires that the top kids stay on top of their game in order to stay in the lineup."
In the Gym Dogs' meet last week at Kentucky, they scored a 49.475 on bars, resulting in a climb up to first place in the nation on the event.
A season-best 49.525 against Alabama on Jan. 23, in which two-time NCAA all-around champion and former U.S. Olympian Courtney Kupets scored the second 10.0 of her career on the event, helped to boost Georgia's ranking in the past month.
Success on bars has not been limited to just this season. Clark and Georgia coach Suzanne Yoculan have guided gymnasts to success on the event in past years, too.
They have coached gymnasts to 25 Southeastern Conference uneven bars titles and 26 perfect 10s on the event. They have also coached four gymnasts to eight NCAA bars titles. Kupets was the last Georgia gymnast to win one in 2006.
Just last season, Clark and Yoculan coached Tiffany Tolnay, Katie Heenan, Nikki Childs and Grace Taylor to All-American honors on bars. Tolnay and Taylor shared the SEC bars title.
"Our handstands are generally better than anybody in the country," Clark said. "That's something that we work very hard on all year long. We drill that daily as part of their workout."
While there may be teams that are throwing more difficulty in their routines, the coaches said Georgia usually has two major release moves and finishes with an E level dismount. The part that the Gym Dogs have tried to hone is out-executing everyone else. They work on perfecting the little things - fluidness between skills, vertical handstands, height on release moves and sticking dismounts.
"We're just now getting to where we are starting to stick our landings," Clark said.
Yoculan believes her team has a vast collection of skills on the event that can please any fan.
Kupets, who won a bronze medal on the uneven bars in the 2004 Olympics, has three release moves in her routine. But she is not performing the toughest routine she is capable of after coming off a season-ending Achilles tendon tear last season.
"This routine is almost compulsory for her," Clark said. "It is one of the most difficult, if not the most difficult, routines in the nation, but it's just easy for her."
While Tolnay and McCool's strengths are textbook execution, Taylor's is her individuality. The junior is the only collegiate gymnast performing the Comaneci release move, according to Yoculan.
"One of the biggest awe factors is Grace's Comaneci," Kupets said. "It's where she gets up to the high bar and does a little flip around. Every time you see it, you hear everyone go 'Ooooh.' I love that skill."
The Gym Dogs are hoping to stay in the top spot in the nation on uneven bars with a solid performance tonight at Arkansas. They will start the competition on what has been their most consistent event this season.
"It's been an event that we've been able to build on," Kupets said. "It's an event that we're all confident on now."
No. 2 Georgia at No. 7 Arkansas 8 p.m.
© 2017. All Rights Reserved. | Contact Us


text:
Thank you for your interest in the CM2F support group. This list is intended to provide a way for CM2F users and for the author to meet and discuss bugs and provide solutions, and to offer ideas and pose questions about the mod. For more specific info try the authors website:
Digital Graal


text:
" Hardcover: 10 pages / Publisher: Egmont Books Ltd / Published: 19 Feb 2011 "
* Prices may differ from that shown
My youngest daughter is 2 and her favourite characters are Peppa Pig and Fireman Sam, she is also a little book worm so when I was having a mooch through the Amazon site before Christmas I decided I would buy her this book.
The book cost me just under £5 with free delivery from Amazon but I have never actually seen it on sale anywhere else. The book is only about 6 inches square which is smaller than books I usually like to share with my daughters.
The front cover of the book has the Fireman Sam logo in the top corner and then the title on the opposite side to the logo. Fireman Sam and Station Officer Steel are pictured on the front of the book on either side of the cover and the cover pulls open to reveal Jupiter the fire engine inside with Elvis driving. On the bottom of the book it says "Who is driving Jupiter?" which Emily always shouts back Elvis when I ask her and gets excited when I tell her she is correct.
On each page of the book there is a little bit of text and then a question to which the answer can be found by sliding the page of the book out, the book is made of really thick cardboard to make this easier although not quite a board book.
The pages are all from episodes of the show and we have seen every one of them so Emily recognises the situations and could actually tell me who was going to be under the flap on 2 of the pages the first time we read it which I was very impressed with.
The scenes in the book are,
Norman with his foot stuck between 2 rocks and the tide coming in,
A whale being stuck on the beach,
James being stuck behind some fallen rocks,
A tent on fire on Norman, Trevor and Dilys camping trip
Penny and Helen being lost in the fog on Pontypandy Mountain.
The book is easy to handle and Emily loves to pull the pages open to reveal what is underneath however she has actually torn the front cover of the book by pulling the page out but not managing to push it back in quite straight so we have had to glue the front cover back together.
Emily doesn't seem to get bored of this book, she will pick this up at least once a day if not more and if she asks me to read it to her then we have to read it a few times over. Emily will sit on the floor with her legs stretched out and rest the book on her knees pulling the pages open and shouting out the character name and it amuses her for ages.
I would say this is a great value book, the pictures are exactly like the TV programme which means that they aren't very bright but that doesn't matter. The book entertains Emily and is well worth the cost just a shame it damages easily, 4 stars from our house.


text: The Modern Mod–H&M are looking to the past to inform its new fall/winter 2014 collection currently being prepped for its launch. The brand are attempting to build a wardrobe for the 'modern mod' with the line, pairing some of the styles of 1960s British counter-culture with inspiration from Paris and New York. Model Paolo Anchisi has been photographed wearing pieces from the collection, adding considerable attitude to an already rebellious range.


text:
My cousin sent me these 4 tins of tea from the Great Wall Tea Co and it took me a long time to try this one because I'm not usually a fan of green teas. Anyway, this is leagues better than the Yogi Tea one that I tried. Rarely drink it, but it was nice today.
3 min, 0 sec


text:
Mundo Unico Conscience Brief 1220053
Sorry, no other customer-recommended styles found.
This product was discontinued June, 2013 and is no longer available. Please consider one of the Customer-Recommended Replacements above, or try a new search.
This sleek brief features a contour pouch and higher-cut front leg openings for comfort. Understated exposed elastic waistband has Unico logo.
Try these keyword searches with similar features:


text:
North Carolina headed down to Atlanta for a business trip to Georgia Tech Tuesday night and did what it had to do, claiming a 70-58 victory that was vital in UNC's ever-increasing hopes of reaching the NCAA Tournament.
UNC, which improved to 18-8 overall and 8-5 in ACC play with the win, didn't shoot particularly well on the whole, making just 30 percent of its three-pointers (six-of-20) and less than 40 percent on all shots, but the Tar Heel defense perplexed the Yellow Jackets and kept them off-rhythm and on the run much of the evening.
Playing for the third straight game with P.J. Hairston in a smaller starting rotation, UNC's perimeter-oriented approach forced Georgia Tech to pay a lot of attention to the outside, opening things up in the middle for James Michael McAdoo.
Article Continues Below
McAdoo, who has had a couple of recent rough outings, brought it all together against the Jackets, scoring 15 points in the first half alone and breaking the 20-point mark before the midway point of the second half.
By the time UNC had broken out to a 59-41 mark at the 8:47 mark of the final period, McAdoo was in double-double territory with 22 points and 10 rebounds. He finished with 22 points and 11 boards.
Before too long the Tar Heels were leading by 20 points---the kind of score that has been non-existent pretty much everywhere else on the road UNC has played this season---and the Yellow Jackets faithful were streaming towards the exits early.
And while Tech made it closer at the end, the final score didn't reflect the way in which UNC coolly and calmly controlled the game.
"You're always happy about a win in the ACC on the road, when especially it's an ugly game at times for both teams," said head coach Roy Williams after the game. "I thought we had 100 turnovers and we only had nine, but I think in the first half James Michael McAdoo having 15 points was really big for us. In the second half, I thought Reggie Bullock got out on the break and we found him on the break. He got nine points and all of those were in the second half. Marcus Paige had eight; all of them in the second half. Dexter Strickland had four, all in the second half because our starting guy is on the perimeter."
"Give North Carolina credit, they took control of the game at about the 12 minute mark in the second half," added Georgia Tech head coach Brian Gregory.
"They (UNC) took advantage of some turnovers and some missed shots to get some transition baskets.
"They're good," Gregory added about the Tar Heels. "They're going with the smaller lineup, ,and I thought we did a pretty good job against that, in particular guarding P.J. Hairston at the four, which was good to see because that was a new challenge for us."
"At the same time, their quickness, in particular McAdoo at the five gave us some problems. We didn't take care of the ball. In the second half our turnovers were a big key."
It was a reprieve for the Tar Heels on Georgia Tech's home court, as the old arena, known as Alexander Memorial, was a house of horrors for UNC over the years.
But so far so good in newly-refurbished McCamish Pavilion, as the Tar Heels picked up its first victory over the Yellow Jackets in Atlanta since 2008.
The teams stayed close throughout the first half, and while UNC shot below 40 percent over the first 20 minutes and three players scored all but four of Carolina's points, they held a 36-30 halftime margin behind their solid defense, which held the Yellow Jackets under 50 percent shooting and forced over twice as many turnovers as the Tar Heels had themselves.
For the game, the Yellow Jackets had 19 turnovers, compared to just nine for UNC.
"It's hard to win games shooting 38 percent. It's still a W and that's the way we'll look at it and that's the way we'll take it," said Williams.
McAdoo led three Tar Heels in double-figures---a group that included Leslie McDonald (15 points) and Hairston (10 points).
The Tar Heels held Georgia Tech without a single field goal for a stretch of over seven minutes in the second half as they gained a confidence-inspiring victory heading into Saturday's rivalry clash with N.C. State in the Smith Center.
"I don't like to look down and see that they outrebounded us 43-38 and in second chance points, 12-9. We don't like that. I do like the fact that we got out on the fast break a little bit more," said Williams.


text:
Pick Your Target
It's easy to get carried away with your goals—I call it Athletic Amnesia. Mere minutes after saying you want to run the fastest marathon of your life, you are proclaiming this will also be the year you swim the English Channel, and finally master speaking Japanese.
Don't get me wrong; lots of goals are great. But know which one is your most important one, and use that as your guide to help set up a year that will enable you to be your best.
More: Train Your Mind to Get Better Results
Work Backwards
Once you know what your big goal is for the season, work backwards towards race day. The bigger the goal race, the longer you need to plan. As an example, a marathon might take a six-month window of planning, from initial training to building actual race fitness. A 5K, on the other hand, might only take eight weeks of planning.
More: Your 3-Part Training Plan
Back planning also allows you to incrementally build your training and race selection to fit your goal race. Your half-marathon training might benefit from a 10K race a few weeks before the big day. Perhaps there are local tune-up races that would allow you to replace some of the longer, solo training days with friends and some fun.
More: 8 Reasons to Run With a Partner
Here are some additional tips to help you build out your best year.
How to Pick Your "A" Race for the Season
- Location: Keep it close to make it easy, or choose a fun destination race.
- Social: Pick a race that your friends might also do, and train together. Starting to train too early or waiting too long to race could mean you are on your own.
- Weather: Make sure the last eight to 12 weeks before your big race are conducive to training. Your stretch goal should be hard enough without having to deal with blistering heat, tornado season, daylight savings, etc.
- Time it right: Do everyone a favor and make sure the race doesn't conflict with key personal and professional milestones. If you're an accountant, you probably shouldn't pick a late April or early May key race.
More: How to Pick the Right Marathon For You
Keep It Fun and Fast Until 12 Weeks Out
- Train to be fit, not to race: If you are healthy and fit, you shouldn't need more than twelve weeks to peak for your big race.
- Local race calendar: Sign up for 5K and 10K events to stay focused and build critical speed without pressure.
- Get creative: Find new places to run, even if it means going out of your way. Those last few weeks will force you to do plenty of work when the time comes.
More: 3 Ways Out of a Running Rut
Get Focused and Do the Work
- Draw the line: Have the official start of your race preparation clearly marked so you know when it's time to bring your "A" game.
- Shop ahead: Have the gear and supplies your training requires so you can avoid missed workouts or last-minute shoe shopping issues.
- Remember to rest: Take at least one day off a week, if not for a physical break, then at least for your sanity.
- Set incremental targets: Pick some intermediary milestones to your stretch goal that you can test in a few key training sessions or tune-up races. This could be a specific pace, distance or time.
More: Should You Race a Half Marathon Before a Marathon?
There is no single right way to plan a season. Make sure you know the big goal on the horizon, and set the small steps in motion early on. This will keep you involved and consistent, and you'll be ready to start the real training when it matters. By the time you arrive at the starting line, you'll be confident knowing that you have given it your best shot ? all you'll have to do is run.
More: 5 Race-Day Mistakes to AvoidSign up for your next race.
- 2
- of
- 2


text:
I am level 16 atm. Do you get these at like 20 or 30? I know nothing about this game besides spvp. Can you craft or something?
How do you guys get such cool spvp armor and weapons?
Started by Flooth, Dec 27 2012 01:58 AM
1 reply to this topic
Posted 27 December 2012 - 01:58 AM
- 0
Posted 02 January 2013 - 05:04 PM
You can make new armor and weapons in the Mystic forge that is in the mists. You need a PvP Salvage kit and some of that armor you buy from the vendors. Once you have different components you just toss them in to the forge and see what you get!
- 0
0 user(s) are reading this topic
0 members, 0 guests, 0 anonymous users


text:
March. 20, 2014
Smith named national SOMA Board's political affairs director
The Student Osteopathic Medical Association appointed Matthew Smith, MS-II, political affairs director on the national organization's board of directors earlier this month. SOMA is the nation's largest network of osteopathic medical students.
In his new position, Smith will follow relevant political developments and work with the American Osteopathic Association to keep SOMA members across the U.S. informed about proposed legislation. He is responsible for federal SOMA legislative advocacy efforts and working with the AOA, the American Association of Colleges of Osteopathic Medicine and the Council of Osteopathic Student Government Presidents.
Smith is president of the OSU-COM SOMA chapter, a member of the Political Action Committee and secretary of the Wilderness Medicine Club. He was recently inducted into Omega Beta Iota, the national osteopathic political action honor society.