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Students gain an understanding of the community services typically available in the United States and the role of the interpreter in each setting. Students study and practice basic techniques and modes of interpretation with relevant texts and oral passages by using monolingual and bilingual dictionaries, developing personalized glossaries, and familiarizing themselves with equipment to help improve their interpretation skills.
Course is offered On-line


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Francis the Phrenology Doll Lauretta Lowell(see more by this artist)
30" assemblage doll. Phrenology is the study of the structure of the skull to determine a person's character and mental capacity. Francis has her head/brain divided into sections that represent different parts of her personality that are noted on different parts of her body. One of a kind...that's for sure!!! Visit my Whimsical Curiosities website more more of my art at www.whimsicalcuriosities.com

subset: commoncrawl


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Back home from Austria!
The card I want to show you uses the German phrase "auf die Pauke hauen" which translates to "to hit the kettledrum" and means as much as partying wild and having a blast.
I made the following card for a musician's 60th birthday:
The little guy has a crazy stare, don't you think?


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This place is open even during hurricanes. Seriously. This Irish pub features a huge bar, booth and tabletop seating, a full menu, pool tables, and two large rooms. Fine whiskeys are available, and Bushmill's 16-year can be had for $12.50 a shot. Guests range from European tourists to South Beach locals and mainland Miamians. There's no dress code and no cover. But if you go there to eat, keep in mind that an 18 percent gratuity is added to all restaurant checks.
Though St. Patrick's Day is not a legal holiday in the United States, it might as well be. After all, everyone is Irish on St. Paddy's Day, and there are few professions that allow for drinking a beer... More »
Thank the good lord for the beautiful game. And thank the good folks at the many soccer bars in Miami for broadcasting what promises to be an epic clash of perennial futbol powerhouses, Euro 2012.For ... More »
Your last name may not be O'Neil or McCarthy, but here in Miami, we all share a lot in common with the Irish -- 95 percent of our population is comprised of immigrants that fled their homeland due to ... More »
Steve Cuozzo, restaurant critic for the New York Post, recently published his view on how to get back to the business of fine dining during these times of terror: "The mayor and the president urge us to get on with life. I'm ready to take the... More »
When Dubliners enter their local pub, the feeling is one of immediate comfort, like slipping into a pair of well-worn shoes. The spacious interior of the Playwright Irish Pub & Restaurant handsomely mimics the antique look that comes naturally to... More »
Authentically Irish - the people, the cuisine, the BEER! It is not fake - and that's why I love it here.
Nice Pub Love all musicz
Since the beginning of time men have fought for stuff. Honor. Women. Countries. Kingdoms. Men like fighting. Though they might not support kicking the crap out of someone to make a point, they will watch. They chanted in the school yard when Billy the bully used to beat up nerdy Norman for his lunch money, and they still chant. So, want to meet a manç Head to the Playwright anytime they broadcast a pay-per-view boxing match -- schedule available online. You might have to fork over... More »
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Get Living Without's FREE Recipe of the Week
Delicious allergy-friendly recipes for you and your family
House Call
Oct/Nov 2012 Issue
No time for homemade? These commercial insect repellants use natural ingredients.
Bug Band
(sprays, wipes, wrist bands)
Burts Bees
(Natural Insect Repellent)
Emerson Ecologics
(Bugs Be Gone)
LA Fresh
(insect repellent wipes)
Sallye Ander
(No Bite Me Cream)
Essential Oils
Different essential oils repel different insects.
■ Cinnamon: mosquitoes
■ Citronella: mosquitoes,
■ Eucalyptus: mosquitoes, ticks, lice
■ Geranium: mosquitoes, ticks, lice
■ Orange: fleas
Pure essential oils are available at most natural food stores. Before using, check with your physician and test a tiny amount on a small patch of skin.
Bug Busters
Repel insects with natural ingredients
Most commercial bug sprays contain harsh, synthetic chemicals that can irritate those who are sensitive. Fortunately, effective insect control is possible using safer, non-toxic products.
You can make your house and yourself less attractive to flying and biting pests by keeping your home and yard clean and by dressing in light colors when you're outside. (Insects use dark hues to locate their targets). Avoid using products perfumed with fruity or floral scents, as bugs are attracted to these. Instead, use scents that bugs don't like, such as lemon or cinnamon.
Citronella Sold in candles, incense, lotions and oils, citronella exudes a lemony aroma that repels insects. Add a few drops of essential citronella oil to your favorite sunscreen or body lotion. Purchase a citronella-scented geranium plant and place it near your favorite outdoor chair or table.
Cloves Ants are repelled by the smell of cloves. Purchase clove oil or make your own by soaking a few clove buds in a small amount of natural oil for several hours or overnight. Dab this scented oil around your kitchen counter and wherever else you spot ants.
Coffee Used coffee grounds repulse ants. Sprinkle old grounds around your plants.
Eucalyptus Flies and mosquitoes hate the scent of eucalyptus. Purchase it as tea tree oil at natural food stores or your pharmacy. Mix a few drops with 1 cup of water and spray around your home and garden to eliminate flying pests.
Mint The scent of mint wards off ants and flies. Tuck small bunches of fresh mint into your flower arrangements (fresh lavender and basil work, too). Brew some strong mint tea and use it as a natural insect repellent spray. Fresh basil and bay leaves can also be brewed into an anti-bug spray.
For bug bites, old-fashioned remedies are safe and helpful: Make a paste of baking soda (or cornstarch), water and a little lemon juice (or vinegar) for a bee or wasp sting.* Relieve the itch of insect bites with egg white, if tolerated, applied to the skin or rub the juice of a freshly broken rhubarb stalk over the bite.
*Allergic anaphylactic reaction to insect sting should be treated immediately with epinephrine and a trip to the emergency room.
Natural Insect Repellent
Make your own natural repellent by diluting essential oils in a light, natural oil or a mild
10-20 drops essential oil (see list above right)
¼ cup sunflower oil or almond oil (if tolerated) or witch hazel
1. Mix essential oil (or a combination) with light oil or witch hazel.
2. Pour mixture into a clean container. Spray or dab onto exposed skin or clothing.
Janice Cox, author of Natural Beauty at Home (Henry Holt and Company), lives in Medford, Oregon.
Comments (1)
What an adorable girl!!! :)
Posted by: Kimberly K B | August 27, 2012 9:00 PM Report this comment


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Oh my stars. Kris Murray. Does this name ring a bell? She was one of our unforgettable video contest winners last year and if she ever decides to NOT enter, I'll head to Alberta, Canada and go knocking on her door. If you missed last year's video, catch it here. Pure awesomeness in documenting the everyday.
Kris seriously needs to be my next door neighbor. I don't know her personally, but I love her. I love how she documents. I love how you can tell she loves her role as a wife and mother without trying to paint it as some rosy journey. In her own words:
As soon as I heard this song by Go Fish Guys, I could just imagine my life as a music video to the song and wanted to get started on it so bad! But, I am a procrastinator and only seem to be motivated by urgency. So, I kept putting it off and onto the back burner ONLY until I read about the 12 Videos of Christmas contest. BOOM! Urgency! Instantly motivated. And I got 'er done! I love a good contest, but I also need a kick in the pants when it comes to making sure I take time to document my BLESSED, beautiful life!
Tags: 12 videos of christmas


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Leptin | |||||||||
Structure of the obese protein leptin-E100.[1] |
Identifiers | |||||||||
Symbol | Leptin | ||||||||
Pfam | PF02024 | ||||||||
Pfam clan | CL0053 | ||||||||
InterPro | IPR000065 | ||||||||
SCOP | 1ax8 | ||||||||
SUPERFAMILY | 1ax8 | ||||||||
Leptin (Greek λεπτός (leptos) meaning "thin") is a 16-kDa protein hormone that plays a key role in regulating energy intake and expenditure, including appetite and hunger, metabolism, and behavior. It is one of the most important adipose-derived hormones.[2] Leptin functions by binding to the leptin receptor. The Ob(Lep) gene (Ob for obese, Lep for leptin) is located on chromosome 7 in humans.[3]
Contents |
The effects of leptin were observed by studying mutant obese mice that arose at random within a mouse colony at the Jackson Laboratory in 1950.[4] Subsequent work by Douglas Coleman at the Jackson Laboratory indicated that the ob gene encoded a hormone regulating body weight and that a second mutation, also causing obesity, the db/db gene, encoded the receptor for this hormone. Both ob and db mice were morbidly obese and ate voraciously. Ultimately, several strains of laboratory mice have been found to be homozygous for single-gene mutations that cause them to become obese, and they fall into two classes: "ob/ob", those having mutations in the gene for the protein hormone leptin, and "db/db", those having mutations in the gene that encodes the receptor for leptin. When ob/ob mice are treated with injections of leptin, they lose their excess fat and return to normal body weights. Leptin itself was co-discovered in 1994 by Jeffrey M. Friedman, Rudolph Leibel and their research teams at the Rockefeller University together with Douglas L. Coleman through the study of such mice.[3][5][6][7][8][9] While a dispute over the attribution of the discovery has been documented in published literature such as the Ellen Ruppel Shell's The Hungry Gene, Dr. Friedman won the Time Magazine, Best of Science in 1994 and the Albert Lasker Basic Medical Research Award in 2010 for his discovery of leptin.[5][6]
Human leptin is a protein of 167 amino acids. It is manufactured primarily in the adipocytes of white adipose tissue, and the level of circulating leptin is proportional to the total amount of fat in the body.
In addition to white adipose tissue—the major source of leptin—it can also be produced by brown adipose tissue, placenta (syncytiotrophoblasts), ovaries, skeletal muscle, stomach (the lower part of the fundic glands), mammary epithelial cells, bone marrow, pituitary, and liver.[10]
Leptin has also been discovered to be synthesized from gastric chief cells and P/D1 cells in the stomach.[11]
Leptin acts on receptors in the hypothalamus of the brain, where it inhibits appetite
- counteracting the effects of neuropeptide Y (a potent feeding stimulant secreted by cells in the gut and in the hypothalamus)
- counteracting the effects of anandamide (another potent feeding stimulant that binds to the same receptors as THC)
- promoting the synthesis of α-MSH, an appetite suppressant.
This appetite inhibition is long-term, in contrast to the rapid inhibition of eating by cholecystokinin (CCK) and the slower suppression of hunger between meals mediated by PYY3-36. The absence of leptin (or its receptor) leads to uncontrolled food intake and resulting obesity. Several studies have shown fasting or following a very-low-calorie diet (VLCD) lowers leptin levels.[12] In the short-term, leptin might be an indicator of energy balance. This system is more sensitive to starvation than to overfeeding; leptin levels change more when food intake decreases than when it increases.[13] The dynamics of leptin due to an acute change in energy balance may be related to appetite and eventually to food intake. Although this is a new hypothesis, some data already supports it.[14][15]
Controversy is ongoing regarding the regulation of leptin by melatonin during the night. One research group suggested increased levels of melatonin caused a downregulation of leptin.[16] However, in 2004, Brazilian researchers found melatonin to increase leptin levels in the presence of insulin, therefore causing a decrease in appetite during sleeping.[17] Still other researchers in Belgium found partial sleep deprivation to be associated with decreased leptin levels [18]
Mice with type 1 diabetes treated with leptin alone or in conjunction with insulin did better (blood sugar did not fluctuate as much; cholesterol levels decreased; less body fat formed) than those treated with insulin alone, raising the prospect of a new treatment for diabetes.[19]
Adiposity signal[edit]
To date, only leptin and insulin are known to act as adiposity signals. In general,
- Leptin circulates at levels directly proportional to body fat.
- It enters the central nervous system in proportion to its plasma concentration.
- Its receptors are found in brain neurons involved in regulating energy intake and expenditure.
- It controls food intake and energy expenditure by acting on receptors in the mediobasal hypothalamus.[20]
Interaction with amylin[edit]
Coadministration of two neurohormones known to have a role in body weight control, amylin (produced by beta cells in the pancreas) and leptin (produced by fat cells), results in sustained, fat-specific weight loss in a leptin-resistant animal model of obesity.[21]
Leptin binds to neuropeptide Y (NPY) neurons in the arcuate nucleus in such a way as to decrease the activity of these neurons. Leptin signals the brain that the body has had enough to eat, producing a feeling of satiety. Moreover, this fullness hormone may make it easier for people to resist the temptation of foods high in calories.[22]
Circulating leptin levels give the brain input regarding energy storage, so it can regulate appetite and metabolism. Leptin works by inhibiting the activity of neurons that contain neuropeptide Y (NPY) and agouti-related peptide (AgRP), and by increasing the activity of neurons expressing α-melanocyte-stimulating hormone (α-MSH). The NPY neurons are a key element in the regulation of appetite; small doses of NPY injected into the brains of experimental animals stimulates feeding, while selective destruction of the NPY neurons in mice causes them to become anorexic. Conversely, α-MSH is an important mediator of satiety, and differences in the gene for the receptor at which α-MSH acts in the brain are linked to obesity in humans.
A very small group of humans possesses homozygous mutations for the leptin gene, leading to a constant desire for food and resulting in severe obesity. This condition can be treated somewhat successfully by the administration of recombinant human leptin.[23][24] However, extensive clinical trials using recombinant human leptin as a therapeutic agent for treating obesity in humans have been inconclusive because only the most obese subjects who were given the highest doses of exogenous leptin produced statistically significant weight loss. Large and frequent doses are needed to provide only modest benefit because of leptin's low circulating half-life, low potency, and poor solubility. Furthermore, these injections caused some participants to drop out of the study due to inflammatory responses of the skin at the injection site. Some of these problems can be alleviated by a form of leptin called Fc-leptin, which takes the Fc fragment from the immunoglobulin gamma chain as the N-terminal fusion partner and follows it with leptin. This Fc-leptin fusion has been experimentally proven to be highly soluble, more biologically potent, and contain a much longer serum half-life. As a result, this Fc-leptin was successfully shown to treat obesity in both leptin-deficient and normal mice, although studies have not been undertaken on human subjects. This makes Fc-leptin a potential treatment for obesity in humans after more extensive testing.[25][26][27]
Circulatory system[edit]
The role of leptin/leptin receptors in modulation of T cell activity in immune system was shown in experimentation with mice. It modulates the immune response to atherosclerosis, of which obesity is a predisposing factor.[28]
Exogenous leptin can promote angiogenesis by increasing vascular endothelial growth factor levels.
In some epidemiological studies, hyperleptinemia is considered as a risk factor. However, a few animal experiments demonstrated systemic hyperleptinemia produced by infusion or adenoviral gene transfer decreases blood pressure in rats.[29][30]
Lung surfactant activity[edit]
In fetal lung, leptin is induced in the alveolar interstitial fibroblasts ("lipofibroblasts") by the action of PTHrP secreted by formative alveolar epithelium (endoderm) under moderate stretch. The leptin from the mesenchyme, in turn, acts back on the epithelium at the leptin receptor carried in the alveolar type II pneumocytes and induces surfactant expression, which is one of the main functions of these type II pneumocytes.[31]
In mice, leptin is also required for male and female fertility. It has a lesser effect in humans. In mammals such as humans, ovulatory cycles in females are linked to energy balance (positive or negative depending on whether a female is losing or gaining weight) and energy flux (how much energy is consumed and expended) much more than energy status (fat levels). When energy balance is highly negative (meaning the woman is starving) or energy flux is very high (meaning the woman is exercising at extreme levels, but still consuming enough calories), the ovarian cycle stops and females stop menstruating. Only if a female has an extremely low body fat percentage does energy status affect menstruation. Some studies have indicated leptin levels outside an ideal range can have a negative effect on egg quality and outcome during in vitro fertilization.[32]
The body's fat cells, under normal conditions, are responsible for the constant production and release of leptin. This can also be produced by the placenta.[33] Leptin levels rise during pregnancy and fall after parturition (childbirth). Leptin is also expressed in fetal membranes and the uterine tissue. Uterine contractions are inhibited by leptin.[34]
Leptin plays a role in hyperemesis gravidarum (severe morning sickness of pregnancy),[35] in polycystic ovary syndrome[36] and hypothalamic leptin is implicated in bone growth.[37] It has been shown that high levels of Leptin, as usually observed in obese females, can trigger neuroendocrine cascade resulting in early menarche.[38] This may eventually lead to shorter stature as oestrogen secretion starts during menarche and causes early closure of epiphyses.
Effects on bone[edit]
Leptin's ability to regulate bone mass was first recognized in 2000.[39] Leptin can affect bone metabolism via direct signalling from the brain, and although leptin acts to reduce cancellous bone, it conversely increases cortical bone. A number of theories have been put forward concerning the cortical-cancellous dichotomy, including a recent theory suggesting increased leptin during obesity may represent a mechanism for enlarging bone size and thus bone resistance to cope with increased body weight.[40]
Bone metabolism is under direct control of the brain, so nerve fibres are present in bone tissue.[41] A number of brain-signalling molecules (neuropeptides and neurotransmitters) have been found in bone, including adrenaline, noradrenaline, serotonin, calcitonin gene-related peptide, vasoactive intestinal peptide and neuropeptide Y.[41][42] This evidence supports a direct signalling system between the brain and bone with accumulating evidence suggesting that these molecules are directly involved in the regulation of bone metabolism. Leptin, once released from fat tissue, can cross the blood–brain barrier and bind to its receptors in the brain, where it acts through the sympathetic nervous system to regulate bone metabolism.[43] In addition to its effects through the brain, leptin may act directly on cells in the bone to regulate bone metabolism. In reality, leptin probably signals to bone on multiple levels, with local and systemic checks and balances impacting the final outcome.[citation needed] As a result, the clinical utility of leptin for treatment of bone diseases remains open, but ongoing research may yet provide much-needed therapies for stimulating bone formation.
Leptin receptors are expressed not only in the hypothalamus but also in other brain regions, particularly in the hippocampus. Deficiency of leptin has been shown to alter brain proteins and neuronal functions of obese mice which can be restored by leptin injection.[44] In humans, low circulating plasma leptin has been associated with cognitive changes associated with anorexia, depression, HIV and the development of Alzheimer's disease.[45] Studies in transgenic mouse models of Alzheimer's disease have shown that chronic administration of leptin can ameliorates brain pathology and improve cognitive performance.[46] At the cellular level, the mechanism of leptin action involves reducing b-amyloid and hyperphosphorylated Tau,[47][48] two hallmarks of Alzheimer's pathology.
Clinical significance[edit]
Leptin has traditionally been regarded as a link between present fat storage, food intake, and energy expenditure. Leptin playing a role in the long term regulation of energy balance. This link originally arose from animal research findings, but its application to describing human systems has since been challenged.[49] In humans, many instances are seen where Leptin dissociates from the strict role of communicating nutritional status between body and brain and no longer correlates with body fat levels:
- Leptin level is decreased after short-term fasting (24–72 hours), even when changes in fat mass are not observed.[50]
- In obese patients with obstructive sleep apnea, leptin level is increased, but decreased after the administration of continuous positive airway pressure.[51][52] In non-obese individuals, however, restful sleep (i.e., 8–12 hours of unbroken sleep) can increase leptin to normal levels.
- Serum level of leptin is reduced by sleep deprivation.[53][54] However, a recent study showed that sleep deprivation was linked with higher levels of leptin.
- Leptin level is increased by perceived emotional stress.[55]
- Leptin level is decreased or increased by increases in testosterone or estrogen level, respectively.[56]
- Leptin level is chronically reduced by physical exercise training.[57]
Inflammatory marker[edit]
Factors that acutely affect leptin levels are also factors that influence other markers of inflammation, e.g., testosterone, sleep, emotional stress, caloric restriction, and body fat levels. While it is well-established that leptin is involved in the regulation of the inflammatory response,[58][59][60] it has been further theorized that leptin's role as an inflammatory marker is to respond specifically to adipose-derived inflammatory cytokines.
In terms of both structure and function, leptin resembles IL-6 and is a member of the cytokine superfamily.[1][59][61] Circulating leptin seems to affect the HPA axis, suggesting a role for leptin in stress response.[62] Elevated leptin concentrations are associated with elevated white blood cell counts in both men and women.[63]
Similar to what is observed in chronic inflammation, chronically elevated leptin levels are associated with obesity, overeating, and inflammation-related diseases, including hypertension, metabolic syndrome, and cardiovascular disease. However, while leptin is associated with body fat mass, the size of individual fat cells, and the act of overeating, it is interesting that it is not affected by exercise (for comparison, IL-6 is released in response to muscular contractions). Thus, it is speculated that leptin responds specifically to adipose-derived inflammation.[64] Leptin is a pro-angiogenic, pro-inflammatory and mitogenic factor, the actions of which are reinforced through crosstalk with IL-1 family cytokines in cancer.[65]
Taken as such, increases in leptin levels (in response to caloric intake) function as an acute pro-inflammatory response mechanism to prevent excessive cellular stress induced by overeating. When high caloric intake overtaxes fat cells' ability to grow larger or increase in number in step with caloric intake, the ensuing stress response leads to inflammation at the cellular level and ectopic fat storage, i.e., the unhealthy storage of body fat within internal organs, arteries, and/or muscle. The insulin increase in response to the caloric load provokes a dose-dependent rise in leptin, an effect potentiated by high cortisol levels.[66] (This insulin-leptin relationship is notably similar to insulin's effect on the increase of IL-6 gene expression and secretion from preadipocytes in a time- and dose-dependent manner.)[67] Furthermore, plasma leptin concentrations have been observed to gradually increase when acipimox is administered to prevent lipolysis, concurrent hypocaloric dieting and weight loss notwithstanding.[68] Such findings appear to demonstrate high caloric loads in excess of fat cells' storage rate capacities lead to stress responses that induce an increase in leptin, which then operates as an adipose-derived inflammation stopgap signaling for the cessation of food intake so as to prevent adipose-derived inflammation from reaching elevated levels. This response may then protect against the harmful process of ectopic fat storage, which perhaps explains the connection between chronically elevated leptin levels and ectopic fat storage in obese individuals.
Obesity and leptin resistance[edit]
Although leptin reduces appetite as a circulating signal, obese individuals generally exhibit an unusually high circulating concentration of leptin.[69] These people are said to be resistant to the effects of leptin, in much the same way that people with type 2 diabetes are resistant to the effects of insulin. The sustained high concentrations of leptin from the enlarged adipose stores implies leptin desensitization. The pathway of leptin control in obese people might be flawed at some point, so the body does not adequately receive the satiety feeling subsequent to eating.
Some researchers attempted to explain the failure of leptin to prevent obesity in modern humans as a metabolic disorder, possibly caused by a specific nutrient or a combination of nutrients not present or uncommon in the prehistoric diet. Some proposed "villain" nutrients include lectins[70] and fructose.[71]
A signal-to-noise ratio theory has been proposed to explain the phenomenon of leptin resistance.[49] In healthy individuals, baseline leptin levels are between 1 and 5 ng/dl in men and 7 and 13 ng/dl in women.[49] A large intake of calories triggers a leptin response that reduces hunger, thereby preventing an overload of the inflammatory response induced by caloric intake. In obese individuals, the leptin response to caloric intake is theorized to be blunted due to chronic, low-grade hyperleptinemia, depressing the signal-to-noise ratio such that acute leptin responses have less of a physiological effect on the body.
Although leptin resistance is sometimes described as a metabolic disorder that contributes to obesity, similar to the way insulin resistance is sometimes described as a metabolic disorder that has the potential to progress into type 2 diabetes, it is not certain that it is true in most cases. The mere fact that leptin resistance is extremely common in obese individuals suggests it may simply be an adaptation to excess body weight. The major physiological role of leptin is suggested to be not as a "satiety signal" to prevent obesity in times of energy excess, but as a "starvation signal" to maintain adequate fat stores for survival during times of energy deficit,[72][73] and leptin resistance in overweight individuals is the standard feature of mammalian physiology, which possibly confers a survival advantage.[74]
A different form of leptin resistance (in combination with insulin resistance and weight gain) easily arises in laboratory animals (such as rats), as soon as they are given unlimited (ad libitum) access to palatable, energy-dense foods,[75] and it is reversed when these animals are put back on low energy-density chow.[76] That, too, may have an evolutionary advantage: "the ability to efficiently store energy during periods of sporadic feast represented a survival advantage in ancestral societies subjected to periods of starvation."[77] The combination of two mechanisms (one, which temporarily suspends leptin action when presented with excess of high-quality food, and the other, which blunts the processes that could drive the body weight back to "normal"), could explain the current obesity epidemic without invoking any metabolic disorders or "villain" nutrients.
Although the notion of obesity as a state of 'leptin resistance' has become ingrained in the minds of many researchers, some observations do not directly support this contention. For example, the work of Rudolph Leibel at Columbia University has shown that, in both obese and lean individuals, leptin injections do not reduce body mass. Despite the lack of response in obese and lean subjects, there is little argument that lean subjects are also leptin-resistant; hence, whether obese subjects are in fact resistant to leptin remains to be empirically demonstrated. This finding also underscores the notion that the brain is not designed to respond to increased leptin by decreasing food intake; rather, as discussed above, lack of leptin acts as a signal to increase food intake. Indeed, Leibel's work has shown that the decreases in serum leptin that occur post-weight-loss constitute a state of leptin deficiency, which drives increased appetite. As such, leptin injections in weight-reduced patients can prevent the increases in appetite and thereby allow patients to maintain weight loss. These studies therefore demonstrate that leptin treatment may be a useful strategy to treat obesity in humans, if not by driving weight loss directly then by allowing weight loss (as a result of diet and exercise) to be more readily maintained.
Interactions with fructose[edit]
The consumption of high amounts of fructose is suggested to cause leptin resistance and elevated triglycerides in rats. The rats consuming the high-fructose diet subsequently ate more and gained more weight than controls when fed a high-fat, high-calorie diet.[71][78][79] These studies, however, did not control against other monosaccharides or polysaccharides, therefore leptin resistance may be a result of a diet that contains high saccharide indices (soda, candy, and other foods with easily liberated sugar).[citation needed]
Leptin and weight regain[edit]
Dieters who lose weight experience a drop in levels of circulating leptin. This drop causes reversible decreases in thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increases in muscle efficiency and parasympathetic tone. The result is that a person who has lost weight has a lower basal metabolic rate than an individual at the same weight who has never lost weight; these changes are leptin-mediated, homeostatic responses meant to reduce energy expenditure and promote weight regain. Many of these changes are reversed by peripheral administration of recombinant leptin to restore pre-diet levels.[80]
A decline in levels of circulating leptin also changes brain activity in areas involved in the regulatory, emotional, and cognitive control of food intake that are reversed by administration of leptin.[80]
Mechanism of action[edit]
Leptin interacts with six types of receptors (Ob-Ra–Ob-Rf, or LepRa-LepRf), that in turn are encoded by a single gene, LEPR.[81] Ob-Rb is the only receptor isoform that can signal intracellularly via the Jak-Stat and MAPK signal transduction pathways,[82] and is present in hypothalamic nuclei.[83]
Whether leptin can cross the blood–brain barrier to access receptor neurons is unknown, because the blood–brain barrier is attenuated in the area of the median eminence, close to where the NPY neurons of the arcuate nucleus are located. Leptin is generally thought to enter the brain at the choroid plexus, where the intense expression of a form of leptin receptor molecule could act as a transport mechanism.
Once leptin has bound to the Ob-Rb receptor, it activates the stat3, which is phosphorylated and travels to the nucleus to presumably effect changes in gene expression. One of the main effects on gene expression is the down-regulation of the expression of endocannabinoids, responsible for increasing appetite.[citation needed] Other intracellular pathways are activated by leptin, but less is known about how they function in this system. In response to leptin, receptor neurons have been shown to remodel themselves, changing the number and types of synapses that fire onto them.
Leptin action is recognized to be more decentralized than previously assumed. In addition to its endocrine action at a distance (from adipose tissue to brain), leptin also acts as a paracrine mediator.[10]
Recently, leptin microinjections into the nucleus of the solitary tract (NTS) have been shown to elicit sympathoexcitatory responses, and potentiate the cardiovascular responses to activation of the chemoreflex.[84]
An analog of human leptin, metreleptin, is under investigation for the treatment of diabetes and/or hypertriglyceridemia, in patients with rare forms of lipodystrophy, syndromes characterized by abnormalities in adipose tissue distribution, and severe metabolic abnormalities. Amylin Pharmaceuticals, the drug's developer, has received orphan drug designation for metreleptin from the US Food and Drug Administration (FDA) Office of Orphan Products Development, as well as fast track designation for this indication. In a three-year study of metreleptin in patients with lipodystrophy organized by the National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health, metreleptin treatment was associated with a significant decrease in blood glucose (A1c decreased from 9.4% at baseline to 7.0% at study end) and triglyceride concentration (from 500 mg/dl at baseline to 200 mg/dl at study end).[85] The Juvenile Diabetes Research Foundation has also partnered with Amylin Pharmaceuticals and researchers at the University of Texas Southwestern Medical Center to study whether metreleptin can be used to improve the treatment of type 1 diabetes.[86]
See also[edit]
- ^ a b Zhang F, Basinski MB, Beals JM, Briggs SL, Churgay LM, Clawson DK, DiMarchi RD, Furman TC, Hale JE, Hsiung HM, Schoner BE, Smith DP, Zhang XY, Wery JP, Schevitz RW (May 1997). "Crystal structure of the obese protein leptin-E100". Nature 387 (6629): 206–9. doi:10.1038/387206a0. PMID 9144295.
- ^ Brennan AM, Mantzoros CS (June 2006). "Drug Insight: the role of leptin in human physiology and pathophysiology--emerging clinical applications". Nat Clin Pract Endocrinol Metab 2 (6): 318–327. doi:10.1038/ncpendmet0196. PMID 16932309.
- ^ a b GreGreen ED, Maffei M, Braden VV, Proenca R, DeSilva U, Zhang Y, Chua SC Jr, Leibel RL, Weissenbach J, Friedman JM (August 1995). "The human obese (OB) gene: RNA expression pattern and mapping on the physical, cytogenetic, and genetic maps of chromosome 7". Genome Res. 5 (1): 5–12. doi:10.1101/gr.5.1.5. PMID 8717050.
- ^ Ingalls AM, Dickie MM, Snell GD (December 1950). "Obese, a new mutation in the house mouse". J. Hered. 41 (12): 317–8. PMID 14824537.
- ^ a b Shell E (January 1, 2002). "Chapter 4: On the Cutting Edge". The Hungry Gene: The Inside Story of the Obesity Industry. Atlantic Monthly Press. ISBN 978-1422352434.
- ^ a b Shell E (January 1, 2002). "Chapter 5: Hunger". The Hungry Gene: The Inside Story of the Obesity Industry. Atlantic Monthly Press. ISBN 978-1422352434.
- ^ Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (December 1994). "Positional cloning of the mouse obese gene and its human homologue". Nature 372 (6505): 425–432. doi:10.1038/372425a0. PMID 7984236.
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|lay summary=
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Further reading[edit]
- Torday JS, Sun H, Wang L, Torres E, Sunday ME, Rubin LP (March 2002). "Leptin mediates the parathyroid hormone-related protein paracrine stimulation of fetal lung maturation". Am. J. Physiol. Lung Cell Mol. Physiol. 282 (3): L405–10. PMC 2942763. PMID 11839533.
- Torday JS, Rehan VK (July 2002). "Stretch-stimulated surfactant synthesis is coordinated by the paracrine actions of PTHrP and leptin". Am. J. Physiol. Lung Cell Mol. Physiol. 283 (1): L130–5. doi:10.1152/ajplung.00380.2001 (inactive 2010-08-06). PMID 12060569.
- Dubey L, Hesong Z (2006). "Role of leptin in atherogenesis". Exp Clin Cardiol 11 (4): 269–75. PMC 2274849. PMID 18651016.
- Friedman JM, Halaas JL (1998). "Leptin and the regulation of body weight in mammals". Nature 395 (6704): 763–770. doi:10.1038/27376. PMID 9796811.
- Prolo P, Wong ML, Licinio J (1999). "Leptin". Int. J. Biochem. Cell Biol. 30 (12): 1285–1290. doi:10.1016/S1357-2725(98)00094-6. PMID 9924798.
- Heshka JT, Jones PJ (2001). "A role for dietary fat in leptin receptor, OB-Rb, function". Life Sci. 69 (9): 987–1003. doi:10.1016/S0024-3205(01)01201-2. PMID 11508653.
- Janeckova R (2002). "The role of leptin in human physiology and pathophysiology". Physiological research / Academia Scientiarum Bohemoslovaca 50 (5): 443–59. PMID 11702849.
- Lee DW, Leinung MC, Rozhavskaya-Arena M, Grasso P (2002). "Leptin and the treatment of obesity: its current status". Eur. J. Pharmacol. 440 (2–3): 129–139. doi:10.1016/S0014-2999(02)01424-3. PMID 12007531.
- Al-Daghri N, Bartlett WA, Jones AF, Kumar S (2002). "Role of leptin in glucose metabolism in type 2 diabetes". Diabetes, obesity & metabolism 4 (3): 147–155. doi:10.1046/j.1463-1326.2002.00194.x. PMID 12047393.
- Sabath Silva EF (2002). "[Leptin]". Rev. Invest. Clin. 54 (2): 161–5. PMID 12053815.
- Thomas T, Burguera B (2003). "Is leptin the link between fat and bone mass?". J. Bone Miner. Res. 17 (9): 1563–1569. doi:10.1359/jbmr.2002.17.9.1563. PMID 12211425.
- Kraemer RR, Chu H, Castracane VD (2002). "Leptin and exercise". Exp. Biol. Med. (Maywood) 227 (9): 701–8. PMID 12324651.
- Waelput W, Brouckaert P, Broekaert D, Tavernier J (2003). "A role for leptin in the systemic inflammatory response syndrome (SIRS) and in immune response". Current drug targets. Inflammation and allergy 1 (3): 277–289. doi:10.2174/1568010023344634. PMID 14561193.
- Stenvinkel P, Pecoits-Filho R, Lindholm B (2004). "Leptin, ghrelin, and proinflammatory cytokines: compounds with nutritional impact in chronic kidney disease?". Advances in renal replacement therapy 10 (4): 332–345. doi:10.1053/j.arrt.2003.08.009. PMID 14681862.
- Cohen P, Ntambi JM, Friedman JM (2004). "Stearoyl-CoA desaturase-1 and the metabolic syndrome". Curr. Drug Targets Immune Endocr. Metabol. Disord. 3 (4): 271–280. doi:10.2174/1568008033340117. PMID 14683458.
- Sahu A (2004). "Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance". Frontiers in neuroendocrinology 24 (4): 225–253. doi:10.1016/j.yfrne.2003.10.001. PMID 14726256.
- Elefteriou F, Karsenty G (2004). "[Bone mass regulation by leptin: a hypothalamic control of bone formation]". Pathol. Biol. 52 (3): 148–153. doi:10.1016/j.patbio.2003.05.006. PMID 15063934.
- Blüher S, Mantzoros CS (2004). "The role of leptin in regulating neuroendocrine function in humans". J. Nutr. 134 (9): 2469S–2474S. PMID 15333744.
- Farooqi S, O'Rahilly S (2007). "Genetics of obesity in humans". Endocr. Rev. 27 (7): 710–18. doi:10.1210/er.2006-0040. PMID 17122358.
- Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, Ohannesian JP, Marco CC, McKee LJ, Bauer TL (February 1996). "Serum immunoreactive-leptin concentrations in normal-weight and obese humans". N. Engl. J. Med. 334 (5): 292–5. doi:10.1056/NEJM199602013340503. PMID 8532024.
External links[edit]
- Leptin in a bulletin by the Howard Hughes Medical Institute (HHMI)
- Leptin: Your brain, appetite and obesity by the British Society of Neuroendocrinology
- Leptin/ghrelin and their role in obesity from hungerhormones.com, a weight control website
- Leptin by Colorado State University
- Leptin at 3Dchem.com, description and structure diagrams
Wikimedia Commons has media related to: Leptin |


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Release Notes: This release adds support for the Shenzhou and Wildfire STM32 boards, a new granule-based allocator for DMA memory management, and new devices drivers for the ENC28J60 and Windbond W25 FLASH. New applications include a UDP network discovery tool and an XML RPC server. Two critical bugfixes are also included which affect FAT and networking performance. Upgrading to version 6.22 is recommended for these changes.
Release Notes: This release adds verified kernel build support. In this (optional) buildmode, NuttX is built as a monolithic kernel. NuttX is built as a separate kernel mode "blob", and the applications are built as a separate user mode "blob". Extended platform support includes support for the WaveShare Open1788 (NXP LPC1788) with the LCD frame-buffer driver, SDRAM, and DMA SD card support, and support for the Kinetis L Cortex-M0+ family and a (minimal) port for the Freedom KL25Z board. Architecture support for the STMicro STM32F4727/737 has been added.
Release Notes: This release adds support for the Cortex-M0 family, and for the nuvonTon NuTiny-SDK-NUC120 in particular. The STM32 support has been extended to include the F3 family and the STM32F3discovery board. Also included is support for the Cortex-M3 LPC1788 and WaveShare Open1788 board.
Release Notes: This release includes a major restructuring of OS data structures in order to support some new, standard OS interfaces. Numerous other changes and several important bugfixes are also included.
Release Notes: This release adds several new core OS features including address environments (aka "Processes"), support for a PATH variable, and a native Windows build. In addition, platform support support is now available for the the ZiLOG z180 (via the P112), STM32 F100 high density boards, and additional ARM board support. Several additional features and important bugfixes are included.
Release Notes: This is the 90th release of NuttX. It adds support for the uClibc++ implementation of the C++ standard library and the standard math library as derived from the Rhombus OS. uClibc++ is released as a separate, installable add-on component, due to the differences in licensing from NuttX. This release also adds support for ELF modules which may be loaded from a filesystem, dynamically linked to the base NuttX code, and executed from RAM. New drivers include drivers for the MAX11802 touchscreen and for the STM32 /dev/random.
A tool for securing DNS communications between a client and a DNS resolver.


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In This Presentation: - The Qualified Mortgage (QM) Rule - Small Creditor QM Proposal - The Ability-to-Repay (ATR) Rule: What It Says and What It Means - Liability for Failure to Comply with the ATR and QM...more
4/16/2013 - Ability-to-Repay CFPB Disparate Impact Fair Lending HUD Lenders Loans Mortgages Qualified Mortgage Rule Safe Harbors Underwriting
Originally published in BNA's Banking Report, 100 BBR 617 on 04/02/2013. Overall Trends & Outlook - In 2012, the federal banking agencies, including the Federal Deposit Insurance Corporation (''FDIC''), Office...more
4/4/2013 - Anti-Money Laundering CFPB Enforcement Actions Fair Lending FCRA FDIC FinCEN Mortgage Reform OCC OFAC Unfair or Deceptive Trade Practices
The U.S. Department of Housing and Urban Development ("HUD") issued a final rule ("Rule") on February 8, 2013, which provides additional support to potential government and private plaintiffs seeking to challenge "facially...more
2/15/2013 - Burden of Proof Burden-Shifting Discriminatory Effects Rule Disparate Impact FHA HUD Legally Sufficient Justification
The U.S. Consumer Financial Protection Bureau (the "Bureau") has released a proposal (the "Proposal") to amend the Bureau's recently issued final rules (the "Rules") on the definition of a qualified mortgage ("QM") and the...more
2/15/2013 - Ability-to-Repay Additional Classes of QM CFPB Exemptions Mortgages Qualified Mortgage Rule Rebuttable Presumption Threshold Safe Harbors
Congress in the Dodd-Frank Act responded to concerns about the quality of mortgage loans by establishing incentives for lenders to seek to ensure that borrowers had the ability to repay mortgage loans made to them. In...more
1/16/2013 - Ability-to-Repay Borrowers CFPB Damages Dodd-Frank Foreclosure Lenders Loans Mortgages Penalties Qualified Mortgage Rule Rebuttable Presumptions Safe Harbors TILA
The U.S. Department of Treasury (Treasury) recently issued a report that reviewed the implementation of Treasury guidelines for streamlining distressed homeowners' communications with mortgage lenders. The Treasury...more
12/4/2012 - Mortgages Servicing Policies Treasury
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Marine 107


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International Indian Treaty Council
International Indian Treaty Council
If you haven't already, please connect with Treaty Council on Facebook: http://lnk.ms/f94sc
International Indian Treaty Council, San Francisco, California. 7,692 likes &###xb7; 51 talking about this &###xb7; 10 were here.
International Indian Treaty Council
uploaded a new photo
- DISSTRICK1 year ago
Hey, just stoppin by to show sum luv on ur page. By the way, we just uploaded a track from our new album "That's What SHE Said" plus 9 tracks from our 1st album. You should check 'em out and tell us what you think. You won't "regret" it.
- 1 year ago
- bayareauk2 years ago
On this Earth Day all our thoughts are supposed to be directed at saving the planet.~~
For late April, its hot...the traffic has been bad with all the peeps
trying to get out of the city for the long weekend. Nobody
working today (Good Friday) so its been pretty quite for those
of us who didn't seek out of town sunshine fun. Enjoy your days
off. (Don't forget to recycle) - ♪ *~~*Bella*~~* ♪2 years agoGoodmorning :-)
But you, when you pray, enter into your room. And shutting your door, pray to your Father in secret; and your Father who sees in secret shall reward you openly. Mat 6:6
My voice You shall hear in the morning, O LORD; in the morning I will direct my prayer to You, and I will look up. Psa 5:3
After this manner therefore pray ye...
Our Father which art in heaven, Hallowed be thy name. Thy kingdom come. Thy will be done in earth, as it is in heaven. Give us this day our daily bread. And forgive us our trespassess, as we forgive those who trespass against us. And lead us not into temptation, but deliver us from evil: For thine is the kingdom, and the power, and the glory, forever. Amen. Mt 6.9-13
In Yahshua/Jesus
Love always,
~Bella - A2 years ago
bonjour. comme je ne peux pas vous envoyer de mail, je vous écris ici :
vous avez mis mon adresse Facebook par deux fois sur "activités"....il y a "16heures"
beaucoup de personnes se sont connectées et cela a engendré des problèmes sur ma page...
pourquoi avez vous fait cela? - A2 years ago
- ♪ *~~*Bella*~~* ♪2 years ago
But the Comforter, which is the Holy Spirit, whom the Father will send
in my name, he shall teach you all things, and bring all things
to your remembrance, whatsoever I have said unto you. – John 14:26
Love always,
~Bella - 2 years ago
- ♪ *~~*Bella*~~* ♪2 years ago
Have a great rest of the week to you and yours..
Love always,
Bella - ♪ *~~*Bella*~~* ♪2 years ago
Psalm 1
1Blessed is the man that walketh not in the counsel of the ungodly, nor standeth in the way of sinners, nor sitteth in the seat of the scornful.2But his delight is in the law of the LORD; and in his law doth he meditate day and night.3And he shall be like a tree planted by the rivers of water, that bringeth forth his fruit in his season; his leaf also shall not wither; and whatsoever he doeth shall prosper.4The ungodly are not so: but are like the chaff which the wind driveth away.5Therefore the ungodly shall not stand in the judgment, nor sinners in the congregation of the righteous.6For the LORD knoweth the way of the righteous: but the way of the ungodly shall perish.
Love always,
A View of the United Nations Permanent Forum on Indigenous Issues
Latest Blog Entries
- Nov 16, 2009 5:47 AM Preliminary findings by the UN Special Rapporteur on the Right to Adequate Housing R. Rolnik
- Nov 16, 2009 5:36 AM The Rights of Indigenous Peoples, Drinking Water and the Impacts of Pesticides", 12/05/09
- Nov 16, 2009 5:30 AM Annual Sunrise Gathering on Alcatraz Island, San Francisco, 11/26/09
- Oct 23, 2009 4:30 AM United Nations Press Release 20 October 2009, "UN housing expert makes first visit to the US"
- Oct 13, 2009 10:34 PM Taino News - Filmmakers Reconsider Columbus Share
About me:
The International Indian Treaty Council (IITC) is an organization of Indigenous Peoples from North, Central, South America, the Caribbean and the Pacific working for the Sovereignty and Self Determination of Indigenous Peoples and the recognition and protection of Indigenous Rights, Treaties, Traditional Cultures and Sacred Lands.
* To seek, promote and build participation of Indigenous Peoples in the United Nations (UN) and its specialized agencies, as well as other international forums.
* To seek international recognition for Treaties and Agreements between Indigenous Peoples and Nation-States.
* To support the human rights, self-determination and sovereignty of Indigenous Peoples; to oppose colonialism in all its forms, and its effects upon Indigenous Peoples.
* To build solidarity and relationships of mutual support among Indigenous Peoples of the world.
* To disseminate information about Indigenous Peoples' human rights issues, struggles, concerns and perspectives.
* To establish and maintain one or more organizational offices to carry out IITC's information dissemination, networking and human rights programs.
* Implementation of an effective plan of action for the 2nd International Decade of the World's Indigenous Peoples.
* Implementation of the U.N. Declaration on the Rights of Indigenous Peoples and adoption of a strong Declaration on the Rights of Indigenous Peoples at the Organization of American States.
2. Responding to threats and violations of Indigenous Peoples' rights including:
* Sovereignty, Self-Determination & Free Prior Informed Consent.
* Health & Environmental impacts of nuclear and toxic contamination, mining, drilling, dams, deforestation and climate change.
* Food Sovereignty & Subsistence Rights.
* Racism & Racial Discrimination.
* Violations of Treaty, Land & Water Rights.
* Cultural Rights, Sacred sites, Religious Freedom & Traditional Knowledge.
* Indigenous Women & Children's rights.
* Economic Globalization & "free trade".
* Militarism and military repression.
3. Human Rights Training, Capacity-building and Mentorship.
4. Communications, Outreach, Networking and Alliance Building.
The International Indian Treaty Council Information Office
The Redstone Building
2940 16th Street, Suite 305
San Francisco, CA 94103-3664
Phone: (415) 641-4482
Fax: (415) 641-1298
Postal Address
456 N. Alaska Street
Palmer, AK 99645
Phone: (907) 745-4482
Fax: (907) 745-4484
Administration Email: email to email@example.com
The IITC was founded in 1974 at a gathering by the American Indian Movement in Standing Rock, South Dakota attended by more than 5000 representatives of 98 Indigenous Nations.
The Declaration of Continuing Independence, Standing Rock South Dakota, June 1974 (PDF)
The symbol of the sacred pipe uniting the hemisphere was chosen for the IITC by the elders to represent the common bonds of spirituality, ties to the land and respect for traditional cultures common to all Indigenous Peoples.
The IITC supports grassroots Indigenous struggles through information dissemination, networking, coalition building, technical assistance, organizing and facilitating the effective participation of traditional Peoples in local, regional, national and international forums, events and gatherings.
In 1977, the IITC became the first organization of Indigenous Peoples to be reorganized as a Non-Governmental Organization (NGO) with Consultative Status to the United Nations Economic and Social Council. The IITC focuses on building Indigenous Peoples' participation in key U.N. fora such as the Commission on Human Rights, the Working Group on Indigenous Populations, the Sub-Commission on Prevention of Discrimination and Protection of Minorities, the Conference of the Parties to the Convention on Biological Diversity, UNESCO and the Commission on Sustainable Development. In recent years, IITC has also participated in the International Labor Organization (ILO), U.N. World Conferences, the International Union for the Conservation of Nature (IUCN) and the World Archeological Congress to systematically address concerns vital to Indigenous Peoples.
The IITC submits testimony, documentation and formal complaints to these fora as well as to the U.N. Center for Human Rights and the Organization of American States (OAS), to redress grievances, increase awareness and impact the development of international standards protecting the rights and survival of Indigenous Peoples.
The IITC also focuses on dissemination of information regarding the U.N. and opportunities for involvement to grassroots Indigenous communities, and works to educate and build awareness about Indigenous struggles among non-Indigenous Peoples and organizations.
Who I'd like to meet:
- Status: Single
- Here for: Networking
- Ethnicity: Native American
- Zodiac Sign: Pisces


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Everything you need to know about City Winery: wine, wine, wine, cheese, wine. This massive (21,000 square feet!), Mediterranean-styled wine bar and music venue offers patrons a "Build-a-Barrel" special, which involves selecting crimson-colored grapes from the Olsen Family Vineyard, investing in an American Oak barrel, and then aging your own Pinot Noir. As for the menu, your meal of choice is dictated by one of the 500 varieties of wine available. Equally eclectic artists perform in front of stacked wine barrels; private parties dine among fruit-smelling, wine-making equipment downstairs; main-area guests access a tap that pumps up home-brewed ruby goodness straight from the cellar.
If you're looking for Hayes Carll, the singer-songwriter who was Americana before Americana was selling out the Garden and the Barclays, your best bet is to check either the Texas clubs where the 37-year-old first made his name or the top ten of... More »
Ex-Foreigner singer Lou Gramm has survived a lot -- a rare brain tumor, all the usual rock 'n' roll excesses, a feud with ex-bandmate Mick Jones, his old band continuing to tour with a karaoke singer ... More »
According to a lyric on Ready for Confetti, Texas-based country singer Robert Earl Keen's latest album, "Real cowboys say the party never ends and the road goes on and on." Maybe he's just trying to make himself out to be a real cowboy, but the... More »
Monday, January 7th The Harmony of Beer and Cheese: If you're sick of pairing cheese with wine, Murray's Cheese is offering a beer and cheese pairing class for $75. The experts at Murray's say to pa... More »
Bluegrass elder Del McCoury, 73, offers a mainline connection to the sound's origins in Bill Monroe's Blue Grass Boys, whom he joined for a while in 1963. This short tour teams the guitarist with Sam Bush, the mandolin king of modern bluegrass... More »
To mutilate an old adage, wine doesn't sophisticate people. People sophisticate people. So why does every wine bar in New York seem to pipe in that glassy, thin, innocuous piano pop, that nü-elevator nonsense? Is it supposed to add to the soi-adult atmosphere? City Winery, the intimate new wine space in Tribeca, seems to have solved the music crisis: They book live acts several times a week, with excellent taste in the city's indie scene. Brilliant Canadian classical-popster Patrick... More »
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Issue Overview
Cloud Development Digest - June 2012, Issue 3Until now, most cloud applications have been developed in desktop environments, but cloud integrated development environments (IDEs) may be poised to upset the status quo. The question is, can cloud IDEs provide greater value to developers than local IDEs? Access >>>
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What's Inside
Vendors aim to get cloud app development off the ground
by Adam Riglian
Plenty of application development is done for the cloud, but little is done in it. Cloud IDE vendors are trying to change that.
Vendors aim to get cloud app development off the ground
by Adam Riglian
Trust in OAuth speeds app development
by Adam Riglian
OAuth, a standard that allows for communication between applications, has sped application development and contributed to the application explosion of the past few years.
Cloud computing trends, cloud strategy begins to emerge
by Jason Tee and Cameron McKenzie
As cloud computing trends continue to evolve, more enterprises are beginning to dabble in cloud-based development environments and cloud strategies are becoming more predominate with early adopters.
Trust in OAuth speeds app development
by Adam Riglian
More Premium Content Accessible For Free
Up, up and away: Java app development heads to the cloud
With all the hype surrounding cloud computing, everyone is eager to see how the cloud "revolution" will play out. And while a "paradigm shift" might ...
Private cloud blueprints and guidelines in the boardroom
To enjoy the flexibility and resource savings of a private cloud, you need to know where to begin with building one. In this issue of Cloud ...
Cloud architecture key to leveraging cloud-based services
This first issue of Cloud Development Digest, geared for Java developers, features the following three articles: "Java Platform as a Service ...


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Most active posts
- Yes, lying really is intrinsically evil posted on May 16, 2013
- About the Followers of the Way blog posted on October 27, 2008
- The Holy Father's prayer intentions – May 2013 posted on May 1, 2013
Recent posts
- Yes, lying really is intrinsically evil
- The Holy Father's prayer intentions – May 2013
- Easter joy: the remedy to disunity & loneliness
- Happy Easter!
- The Holy Father's prayer intentions – April 2013
- Waiting
- (2013) Palm Sunday: Gazing upon the cross
- The Holy Father's prayer intentions – March 2013
- Lenten lessons
- Judging others
- Heaven's joys help us prepare for life's sorrows
- The Holy Father's prayer intentions – February 2013
- Plenty of challenges, but not a few graces too!
- Confession: the beginning of abortion's end
- Just for fun!
Blogs of Note:
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Pulse 2.0
May 18, 2013
In a fight over the value of Chrysler, Fiat and the United Automobile Workers union are $6 billion apart, the Deal Professor writes.
May 07, 2013, TuesdayAcross the country, businesses have recovered while the public sector has struggled, and Detroit may be the most extreme example of a city's dual fates diverging.
March 5, 2013, TuesdayTop executives at firms that received taxpayer bailouts during the financial crisis received generous government-approved compensation packages, a Treasury watchdog said.
January 29, 2013, TuesdayAlly agreed on Wednesday to sell its European and Latin American businesses, as well as a share of a joint venture in China, to G.M.'s financial arm for about $4.2 billion.
November 21, 2012, WednesdayIn exchange, the government of President Francois Hollande will demand fewer job cuts, changes in governance and a seat on the troubled carmaker's board.
October 24, 2012, WednesdayEven Wentzville, Mo., where a new General Motors plant is under construction, is expected to favor Mitt Romney, who opposed saving the automaker.
September 15, 2012, SaturdayThe Treasury Department's plan to sell a big chunk of its A.I.G. holdings is a big step in unwinding one of the most controversial bailouts of the financial crisis. But there are still plenty of other rescue programs to dismantle.
September 10, 2012, MondayA "super PAC" founded by the Koch brothers goes after President Obama on so-called green spending.
April 26, 2012, ThursdayIn search of a federal loan to build its cars at a plant in Delaware, Fisker is trying to re-establish its credibility as an independent automaker with cutting-edge technology.
April 04, 2012, WednesdayIn search of a federal loan to build its cars at a plant in Delaware, Fisker is trying to re-establish its credibility as an independent automaker with cutting-edge technology.
April 4, 2012, WednesdaySEARCH 375 ARTICLES ABOUT THE AUTO INDUSTRY BAILOUT:
Major events in the automakers' decline and rescue efforts.
Amid plant closings and buyouts, a few workers hold onto their jobs as G.M.'s once-huge complex in Flint, Mich., fades away.
The smallest of the three American automakers has been known for its innovations and for its brushes with insolvency.
Michigan may take over the finances of Pontiac, a town tied to the struggling auto industry, in the next few days.
CNBC coverage of Senate testimony by Alan R. Mulally, chief executive of Ford, about the carmaker's desire for government assistance.
CNBC coverage of Senate testimony by Rick Wagoner, chief executive of General Motors, about the carmaker's desire for government assistance.
CNBC coverage of Senate testimony by Robert L. Nardelli, chief executive of Chrysler, about the carmaker's desire for government assistance.


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Campus Life
My North Park
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Office of Diversity Home
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Contact Us
Office of Diversity
What's New?
Diversity Events
The Office of Diversity and Intercultural Programs offers a number of signature events to the internal and external communities. Some of our most popular events include our
Student Diversity Leadership Conference
, hosting the annual
Chicago Latino Film Festival
, the Dr. Martin Luther King Jr. Commemorative Program and Service Day, and our
Multicultural Awards Banquet
. For more information about all of our events and programs, visit the
Collaboratory for Urban and Intercultural Learning
or choose one of the options below.
For more details, click on the title of each event.
Full North Park University Calendar


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President Andrew Slade called the meeting of the Duluth Public Library Board to order at 4:30 p.m. on Tuesday, November 25, 2008.
Present: L. Benson Johnson, J. Brissett, D. Casperson, D. D'Allaird,
V. Katz, P. Markert, A. Slade, P. Spooner, M. Watson, J. Sheriff
Excused: R. Zurn
Approval of Minutes from Library Board meeting
The Library Board minutes of the October 28, 2008, meeting were
approved as distributed.
A. Friends of the Duluth Public Library - P. Markert
Friends are collaborating with UMD and others on the Northeast
Minnesota Book Awards (NEMBA), including $540 in financial support.
Friends also co-sponsored a Duluth poet laureate event on November
1 and will support an upcoming exhibit, "Lewis and Clark
and the Indian Country: The Native American Perspective,"
at UMD. They are advertising for a new board member with proficiency
in public relations.
B. Directors' Report - J. Sheriff, R. Zurn
Old Business
Bylaws revision: Proposed changes were discussed. Discussion will
be reflected in revision to be sent to Board at least 10 days
before next meeting. Vote will take place on January 27, 2009.
Coffee shop: Board discussed startup costs, economic issues, pluses and minuses of public/private collaboration, space considerations, and other factors. There was hesitancy to pursue, especially at the time. If pursued, a small cart seems to be only viable option at this time. Casperson raised question about what impact light rail might have on coffee shops near the library if Depot is remodeled related to such services.
New Business
Watson asked if Board has ever sent thank you letters to staff
who retire. Board has not but agreed to do it in future. Watson
volunteered to send card on Board's behalf to 2008 retiree Karen
Casperson reported that potential Duluth federally-funded stimulus
projects were discussed on a radio program, and he asked for information.
Explanation: A project list is in development stage to be submitted
to the United States Conference of Mayors for promotion purposes.
Preliminary list includes a library "winter garden,"
the design of which would enclose the Plaza area. The list is
not final. Zurn requested that the renovation/replacement of the
library's heating and cooling system be placed on the list. The
Board supports this recommendation. There will be an update at
the January Board meeting.
The meeting adjourned at 5:45 p.m.
The next meeting will be on Tuesday, January 27 at 4:30 p.m. in the Library's Conference Room.


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Divine Liturgy and the Sacraments of the Church
The previous column left off with "Not only could Catherine of Genoa be quoted but Sts. Ambrose, Augustine, Gregory of Nyssa and a host of other masters of the spiritual life who are unsparing in their description of the pains of purgatory." Picking up the thread, we continue on. Let us be clear. Sin and pain go together as cause and effect. Had there been no sin in the world, there would be no pain. Absolutely speaking we have only one choice. As sinners we must either suffer here on earth or, even though we die in the grace of God, suffer in purgatory.
But there is one more choice. What is that? If we receive the sacrament of Anointing before bodily death, we can deserve to enter heaven immediately without the purgatorial sufferings that we had deserved. No human language can exaggerate the importance of being anointed before we enter eternity. This sacrament has the power of bringing us immediately in to the presence of God for whom we were made.
How fitting is it then to conclude this segment on the sacrament of Anointing with thanksgiving and gratitude for Jesus' instituting such a marvelous sacrament.
Lord Jesus, we are deeply grateful for your institution of the sacrament of Anointing. It is your divine will that all of us will die in body as the price we have to pay for our sins. However, it is also by your divine grace that we can see you face to face the moment you call us into eternity. If we are anointed by your sacrament of mercy, we may hope to be received in your divine arms, provided our hearts are totally detached from every creature here on earth and totally united with your Sacred Heart. Amen.
May God bless each and every one of you as we celebrate the birth of our Saviour, Jesus the Christ, the Word become Incarnate on Christmas Day.
Next week, we will chart new waters and seek new horizons in this column. Stay tuned.
Divine Liturgy and the Sacraments of the Church
As of late the Sacraments of Penance and Anointing have been explored in this column. However, do we ever take into consideration of laying the groundwork, if you will, by preparing ourselves to receive the sacraments worthily. St. Ignatius of Loyola stressed in the spiritual life that we should make a daily examination of conscience and even better, if possible, twice daily an examination of conscience.
As one reads the Spiritual Exercises of St. Ignatius, we may be overwhelmed by the minute detail of his treatment of what this saint calls the particular examination of conscience. At the same time, he is careful to provide, "Some Notes on Scruples."
It is very important, therefore, that each of us form a clear and correct conscience. This means that we cultivate a sensitive judgment which is alert to the least offense against the Divine will and, at the same time, protect ourselves against the wiles and ways of the devil. "The enemy," says St. Ignatius, "considers carefully whether one has a lax or a delicate conscience. If one has a delicate conscience, the devil seeks to make it excessively sensitive in order to disturb and upset it more easily. Thus, if he sees that one will not consent to mortal sin or venial sin, or even to the appearance of deliberate sin, since he cannot cause him to fall in a matter that appears sinful, he strives to make the soul judge that there is a sin, for example in a word or passing thought, where there is no sin."
It is valuable to reflect on this tactic of the devil before we offer some practical norms for making our daily examination of conscience. Why? Because otherwise, we are liable to overlook the importance of a daily inventory of our moral conduct for fear of becoming scrupulous.
There is such a thing as growing in prudent sensitivity of conscience, without becoming a victim of the "enemy" as St. Ignatius likes to name him. This may be set down as a general principle, for those who are sincerely striving to do the will of God: It is characteristic of God and His angels, when they act upon the soul, to give true happiness and spiritual joy and to banish all the sadness and disturbances which are caused by the enemy.
It is characteristic of the devil to fight against such happiness and consolation by proposing improper reasonings, subtleties, and continual deceptions. What are we to conclude from this? That the more zealous we are in trying to please God, the more He will give us a deep interior peace of soul.
To be continued....
Divine Liturgy and the Sacraments of the Church
As promised in last week's column we are picking up the thread and will weave our way through the warp and weft of the Church's teaching on the efficacy of the sacrament of Anointing to heal the human body.
It is a defined article of the Catholic faith that Anointing sometimes produces the restoration of bodily health even in persons who were at the point of death. It is not coincidental that St. James distinguishes between two effects of this sacrament, one effect is to save a sick person and "raise him up." The other effect is to forgive a sinner who is estranged from God.
Moreover, as we have seen, the new ritual for administering Anointing distinguishes between receiving grace from the Holy Spirit and being "raised up." In other words, the primary purpose of Anointing is to receive divine grace. But another purpose is to heal the body.
What is the Church's teaching on the efficacy of this sacrament to heal the human body? This effect is not produced directly in a miraculous manner. Rather Anointing indirectly influences the body through its healing of the human soul. We know on faith that, had there been no sin, there would had been no bodily sickness or death. Consequently, while the soul is being healed the body benefits accordingly.
One important proviso must be added. In God's providence, this sacrament restores bodily health conditionally. The condition is that the healing of the body is of spiritual benefit to the soul. Anointing of persons who are expected to die has frequently, even regularly, restored these people to bodily health.
To be emphasized, however, is that this is not the primary purpose of Anointing. As instituted by Christ, the main reason is to restore persons in grave bodily sickness to divine grace if they are estranged from God by mortal sin, to give them the courage they need in their passage from time into eternity, and, depending on their dispositions, to remove much, or even all, of the penalties which they may still deserve for their sins they have committed. The more fervent their resignation to the divine will and the more deeply they love God, their purgatory is correspondingly lessened or may even be totally removed as their immortal souls leave their mortal bodies.
Next week's column will look at anointing and purgatory. To be continued....


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Desserts are a super easy food to take to any potluck or family gathering because there are so many options to choose from and they are sure to be hit with everyone. However, sometimes it is a little time consuming to make something homemade and if you are like me, most of the time don't taste anywhere near as good as a store bought dessert.
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by James Dunne – The CREative Department
As a kid visiting NYC in the 80's, I was always fascinated by the graffiti covering subway cars and buildings. However, by the time I moved here as a young adult in 2001, the city had been cleaned up. Â I was on Davis Street in LIC this morning, and happened upon one of the last graffiti-covered blocks I know of. Â As LIC has now been as part of the Hunters Point Subdistrict Rezoning, these buildings (in their current form) may not be around for much longer:


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After how many lessons did you do manoeuvres?
For discussion relating to any and all aspects of learning to drive from finding an instructor to passing the test. Get advice, tips and support from other fellow learners.
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Re: After how many lessons did you do manoeuvres?(Original post by JustDisturbia)
Hey all
Basically I was wondering,after how many lessons did you start doing your manoeuvres ? I've had about 11/12 lessons- more than capable driver and I haven't done any. My instructor said I should be doing my test by July though?:s I have a feeling he might be milking me of my money because on my 2nd lesson he said i was quite advanced so he wouldn't "have me too long". Thoughts?
So I just politely but firmly said that I feel ready to do the manoeuvres, can we do some next lesson? And we did. Done them all now. He's quite sheepish at times, but he knows who's boss
So basically, just ask your instructor, tell them you feel ready. -
Re: After how many lessons did you do manoeuvres?
In Poland we have different system of driving lessons. I had been only 15 minutes for the first time in car and my instructor told me to drive out from manouvering area But it makes sense because I think people learn faster when they are under pressure on my second hour I had perpendicular(?) park and turing back on road