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Leptin (from Greek λεπτός leptos, "thin" or "light" or "small") is a hormone predominantly made by adipose cells and its primary role is likely to regulate long-term energy balance.

As one of the major signals of energy status, leptin levels influence appetite, satiety, and motivated behaviors oriented towards the maintenance of energy reserves (e.g., feeding, foraging behaviors).

The amount of circulating leptin correlates with the amount of energy reserves, mainly triglycerides stored in adipose tissue. High leptin levels are interpetred by the brain that energy reserves are high, whereas low leptin levels indicate that energy reserves are low, in the process adapting the organism to starvation through a variety of metabolic, endocrine, neurobiochemical, and behavioral changes.

Leptin is coded for by the LEP gene. Leptin receptors are expressed by a variety of brain and peripheral cell types. These include cell receptors in the arcuate and ventromedial nuclei, as well as other parts of the hypothalamus and dopaminergic neurons of the ventral tegmental area, consequently mediating feeding.

Although regulation of fat stores is deemed to be the primary function of leptin, it also plays a role in other physiological processes, as evidenced by its many sites of synthesis other than fat cells, and the many cell types beyond hypothalamic cells that have leptin receptors. Many of these additional functions are yet to be fully defined.

In obesity, a decreased sensitivity to leptin occurs (similar to insulin resistance in type 2 diabetes), resulting in an inability to detect satiety despite high energy stores and high levels of leptin. A synonym for LEP is OB (for obese).

Effects

Predominantly, the "energy expenditure hormone" leptin is made by adipose cells, and is thus labeled fat cell-specific. In the context of its effects, the short describing words central, direct and primary are not used interchangeably. In regard to the hormone leptin, central vs peripheral refers to the hypothalamic portion of the brain vs non-hypothalamic location of action of leptin; direct vs indirect refers to whether there is no intermediary, or there is an intermediary in the mode of action of leptin; and primary vs secondary is an arbitrary description of a particular function of leptin.

Location of action The central location of action (effect) of the fat cell-specific hormone leptin is the hypothalamus, a part of the brain, which is a part of the central nervous system. Non-hypothalamic targets of leptin are referred to as peripheral targets. There is a different relative importance of central and peripheral leptin interactions under different physiologic states, and variations between species.

Mode of action Leptin acts directly on leptin receptors in the cell membrane of different types of cells in the human body in particular, and in vertebrates in general. The leptin receptor is found on a wide range of cell types. It is a single-transmembrane-domain type I cytokine receptor, a special class of cytokine receptors. Further, leptin interacts with other hormones and energy regulators, indirectly mediating the effects of: insulin, glucagon, insulin-like growth factor, growth hormone, glucocorticoids, cytokines, and metabolites.

Function The primary function of the hormone leptin is the regulation of adipose tissue mass through central hypothalamus mediated effects on hunger, food energy use, physical exercise and energy balance. Outside the brain, in the periphery of the body, leptin's secondary functions are: modulation of energy expenditure, modulation between fetal and maternal metabolism, and that of a permissive factor in puberty, activator of immune cells, activator of beta islet cells, and growth factor.

Central nervous system
In vertebrates, the nervous system consists of two main parts, the central nervous system (CNS) and the peripheral nervous system (PNS). The primary effect of leptins is in the hypothalamus, a part of the central nervous system. Leptin receptors are expressed not only in the hypothalamus but also in other brain regions, particularly in the hippocampus. Thus some leptin receptors in the brain are classified as central (hypothalamic) and some as peripheral (non-hypothalamic).

As scientifically known so far, the general effects of leptin in the central nervous system are:
Deficiency of leptin has been shown to alter brain proteins and neuronal functions of obese mice which can be restored by leptin injection.
Leptin receptor signaling in the hippocampus enhances learning and memory. Treatment with leptin has been shown to enhance learning and memory in animal models.
In humans, low circulating plasma leptin has been associated with cognitive changes associated with anorexia, depression, and Alzheimer's Disease.
Studies in transgenic mouse models of Alzheimer's disease have shown that chronic administration of leptin can ameliorate brain pathology and improve cognitive performance, by reducing b-amyloid and hyperphosphorylated Tau, two hallmarks of Alzheimer's pathology.

Generally, leptin is 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.

Increased levels of melatonin causes a downregulation of leptin, however, melatonin also appears to increase leptin levels in the presence of insulin, therefore causing a decrease in appetite during sleeping. Partial sleep deprivation has also been associated with decreased leptin levels.

Mice with type 1 diabetes treated with leptin or leptin plus insulin, compared to insulin alone had better metabolic profiles: blood sugar did not fluctuate so much; cholesterol levels decreased; less body fat formed.

Hypothalamus
Leptin acts on receptors in the lateral hypothalamus to inhibit hunger and the medial hypothalamus to stimulate satiety.
In the lateral hypothalamus, leptin inhibits hunger by
counteracting the effects of neuropeptide Y, a potent hunger promoter secreted by cells in the gut and in the hypothalamus
counteracting the effects of anandamide, another potent hunger promoter that binds to the same receptors as THC
In the medial hypothalamus, leptin stimulates satiety by
promoting the synthesis of α-MSH, a hunger suppressant
Thus, a lesion in the lateral hypothalamus causes anorexia (due to a lack of hunger signals) and a lesion in the medial hypothalamus causes excessive hunger (due to a lack of satiety signals).
This appetite inhibition is long-term, in contrast to the rapid inhibition of hunger 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 hunger and resulting obesity. Fasting or following a very-low-calorie diet lowers leptin levels.
Leptin levels change more when food intake decreases than when it increases. The dynamics of leptin due to an acute change in energy balance may be related to appetite and eventually, to food intake rather than fat stores.

 It controls food intake and energy expenditure by acting on receptors in the mediobasal hypothalamus.

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 to the hypothalamus which produces a feeling of satiety. Moreover, leptin signals may make it easier for people to resist the temptation of foods high in calories.

Leptin receptor activation inhibits neuropeptide Y and agouti-related peptide (AgRP), and activates α-melanocyte-stimulating hormone (α-MSH). The NPY neurons are a key element in the regulation of hunger; 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 α-MSH receptor are linked to obesity in humans.

Leptin interacts with six types of receptors (Ob-Ra–Ob-Rf, or LepRa-LepRf), which in turn are encoded by a single gene, LEPR. Ob-Rb is the only receptor isoform that can signal intracellularly via the JAK-STAT and MAPK signal transduction pathways, and is present in hypothalamic nuclei.

Once leptin has bound to the Ob-Rb receptor, it activates the stat3, which is phosphorylated and travels to the nucleus to effect changes in gene expression, one of the main effects being the down-regulation of the expression of endocannabinoids, responsible for increasing hunger. In response to leptin, receptor neurons have been shown to remodel themselves, changing the number and types of synapses that fire onto them.

Circulatory system
The role of leptin/leptin receptors in modulation of T cell activity and the innate immune system was shown in experimentation with mice. It modulates the immune response to atherosclerosis, of which obesity is a predisposing and exercise a mitigating factor.

Exogenous leptin can promote angiogenesis by increasing vascular endothelial growth factor levels.

Hyperleptinemia produced by infusion or adenoviral gene transfer decreases blood pressure in rats.

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.

Fetal lung
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.

Reproductive system

Ovulatory cycle
In mice, and to a lesser extent in humans, leptin is required for male and female fertility. 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. Leptin levels outside an ideal range may have a negative effect on egg quality and outcome during in vitro fertilization. Leptin is involved in reproduction by stimulating gonadotropin-releasing hormone from the hypothalamus.

Pregnancy
The placenta produces leptin. Leptin levels rise during pregnancy and fall after childbirth. Leptin is also expressed in fetal membranes and the uterine tissue. Uterine contractions are inhibited by leptin. Leptin plays a role in hyperemesis gravidarum (severe morning sickness of pregnancy), in polycystic ovary syndrome and hypothalamic leptin is implicated in bone growth in mice.

Lactation
Immunoreactive leptin has been found in human breast milk; and leptin from mother's milk has been found in the blood of suckling infant animals.

Puberty
Leptin along with kisspeptin controls the onset of puberty. High levels of leptin, as usually observed in obese females, can trigger neuroendocrine cascade resulting in early menarche. This may eventually lead to shorter stature as oestrogen secretion starts during menarche and causes early closure of epiphyses.

Bone
Leptin's role in regulating bone mass was identified in 2000. Leptin can affect bone metabolism via direct signalling from the brain. Leptin decreases cancellous bone, but increases cortical bone. This "cortical-cancellous dichotomy" may represent a mechanism for enlarging bone size, and thus bone resistance, to cope with increased body weight.

Bone metabolism can be regulated by central sympathetic outflow, since sympathetic pathways innervate bone tissue. 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. Leptin binds to its receptors in the hypothalamus, where it acts through the sympathetic nervous system to regulate bone metabolism. Leptin may also act directly on bone metabolism via a balance between energy intake and the IGF-I pathway. There is a potential for treatment of diseases of bone formation - such as impaired fracture healing - with leptin.

Immune system
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, 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. Circulating leptin seems to affect the HPA axis, suggesting a role for leptin in stress response. Elevated leptin concentrations are associated with elevated white blood cell counts in both men and women.

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. While leptin is associated with body fat mass, the size of individual fat cells, and overeating, 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. 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. High leptin levels have been also demonstrated in patients with COVID-19 pneumonia.

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 the ability of fat cells 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. (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.) Furthermore, plasma leptin concentrations have been observed to gradually increase when acipimox is administered to prevent lipolysis, concurrent hypocaloric dieting and weight loss notwithstanding. Such findings appear to demonstrate high caloric loads in excess of storage rate capacities of fat cells 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.

Leptin increases the production of leukocytes via actions on the hematopoietic niche, a pathway that is more active in sedentary mice and humans when compared to individuals which are physically active.

Location of gene and structure of hormone
The Ob(Lep) gene (Ob for obese, Lep for leptin) is located on chromosome 7 in humans. Human leptin is a 16-kDa protein of 167 amino acids.

Mutations
A human mutant leptin was first described in 1997, and subsequently six additional mutations were described. All of those affected were from Eastern countries; and all had variants of leptin not detected by the standard immunoreactive technique, so leptin levels were low or undetectable. The most recently described eighth mutation reported in January 2015, in a child with Turkish parents, is unique in that it is detected by the standard immunoreactive technique, where leptin levels are elevated; but the leptin does not turn on the leptin receptor, hence the patient has functional leptin deficiency. These eight mutations all cause extreme obesity in infancy, with hyperphagia.

Nonsense
A nonsense mutation in the leptin gene that results in a stop codon and lack of leptin production was first observed in mice. In the mouse gene, arginine-105 is encoded by CGA and only requires one nucleotide change to create the stop codon TGA. The corresponding amino acid in humans is encoded by the sequence CGG and would require two nucleotides to be changed to produce a stop codon, which is much less likely to happen.

Frameshift
A recessive frameshift mutation resulting in a reduction of leptin has been observed in two consanguineous children with juvenile obesity. A 2001 study of 13 people with a heterozygous frameshift mutation known as delta-G133 found that they had lower blood leptin levels than controls. There was an increased rate of obesity in these individuals, with 76% having a BMI of over 30 compared to 26% in the control group.

Polymorphisms
A Human Genome Equivalent (HuGE) review in 2004 looked at studies of the connection between genetic mutations affecting leptin regulation and obesity. They reviewed a common polymorphism in the leptin gene (A19G; frequency 0.46), three mutations in the leptin receptor gene (Q223R, K109R and K656N) and two mutations in the PPARG gene (P12A and C161T). They found no association between any of the polymorphisms and obesity.

A 2006 study found a link between the common LEP-2548 G/A genotype and morbid obesity in Taiwanese aborigines, but a 2014 meta-analysis did not, however, this polymorphism has been associated with weight gain in patients taking antipsychotics.

The LEP-2548 G/A polymorphism has been linked with an increased risk of prostate cancer, gestational diabetes, and osteoporosis.

Other rare polymorphisms have been found but their association with obesity are not consistent.

Transversion
A single case of a homozygous transversion mutation of the gene encoding for leptin was reported in January 2015. It leads to functional leptin deficiency with high leptin levels in circulation. The transversion of (c.298G → T) changed aspartic acid to tyrosine at position 100 (p.D100Y). The mutant leptin could neither bind to nor activate the leptin receptor in vitro, nor in leptin-deficient mice in vivo. It was found in a two-year-old boy with extreme obesity with recurrent ear and pulmonary infections. Treatment with metreleptin led to "rapid change in eating behavior, a reduction in daily energy intake, and substantial weight loss."

Sites of synthesis
Leptin is produced primarily in the adipocytes of white adipose tissue. It also is produced by brown adipose tissue, placenta (syncytiotrophoblasts), ovaries, skeletal muscle, stomach (the lower part of the fundic glands), mammary epithelial cells, bone marrow, gastric chief cells and P/D1 cells.

Blood levels
Leptin circulates in blood in free form and bound to proteins.

Physiologic variation
Leptin levels vary exponentially, not linearly, with fat mass. Leptin levels in blood are higher between midnight and early morning, perhaps suppressing appetite during the night. The diurnal rhythm of blood leptin levels may be modified by meal-timing.

In specific conditions
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 plays a critical role in the adaptive response to starvation.
 Leptin level is decreased after short-term fasting (24–72 hours), even when changes in fat mass are not observed.
 Serum level of leptin is reduced by sleep deprivation.
 Leptin levels are paradoxically increased in obesity.
 Leptin level is increased by emotional stress.
 Leptin level is chronically reduced by physical exercise training.
 Leptin level is decreased by increases in testosterone levels and increased by increases in estrogen levels.
 Leptin level is increased by insulin.
 Leptin release is increased by dexamethasone.
 In obese patients with obstructive sleep apnea, leptin level is increased, but decreased after the administration of continuous positive airway pressure. In non-obese individuals, however, restful sleep (i.e., 8–12 hours of unbroken sleep) can increase leptin to normal levels.

In mutations
All known leptin mutations except one are associated with low to undetectable immunoreactive leptin blood levels. The exception is a mutant leptin reported in January 2015 which is not functional, but is detected with standard immunoreactive methods. It was found in a massively obese -year-old boy who had high levels of circulating leptin which had no effect on leptin receptors, so he was functionally leptin-deficient.

Role in disease

Obesity

Although leptin reduces appetite as a circulating signal, obese individuals generally exhibit a higher circulating concentration of leptin than normal weight individuals due to their higher percentage body fat. These people show resistance to leptin, similar to resistance of insulin in type 2 diabetes, with the elevated levels failing to control hunger and modulate their weight. A number of explanations have been proposed to explain this. An important contributor to leptin resistance is changes to leptin receptor signalling, particularly in the arcuate nucleus, however, deficiency of, or major changes to, the leptin receptor itself are not thought to be a major cause. Triglycerides crossing the blood brain barrier (BBB) can induce leptin and insulin resistance in the hypothalamus. Triglycerides can also impair leptin transport across the BBB.

Studies on leptin cerebrospinal fluid (CSF) levels provide evidence for the reduction in leptin crossing the BBB and reaching obesity-relevant targets, such as the hypothalamus, in obese people. In humans it has been observed that the ratio of leptin in the CSF compared to the blood is lower in obese people than in people of a normal weight. The reason for this may be high levels of triglycerides affecting the transport of leptin across the BBB or due to the leptin transporter becoming saturated. Although deficits in the transfer of leptin from the plasma to the CSF is seen in obese people, they are still found to have 30% more leptin in their CSF than lean individuals. These higher CSF levels fail to prevent their obesity. Since the amount and quality of leptin receptors in the hypothalamus appears to be normal in the majority of obese humans (as judged from leptin-mRNA studies), it is likely that the leptin resistance in these individuals is due to a post leptin-receptor deficit, similar to the post-insulin receptor defect seen in type 2 diabetes.

When leptin binds with the leptin receptor, it activates a number of pathways. Leptin resistance may be caused by defects in one or more parts of this process, particularly the JAK/STAT pathway. Mice with a mutation in the leptin receptor gene that prevents the activation of STAT3 are obese and exhibit hyperphagia. The PI3K pathway may also be involved in leptin resistance, as has been demonstrated in mice by artificial blocking of PI3K signalling. The PI3K pathway also is activated by the insulin receptor and is therefore an important area where leptin and insulin act together as part of energy homeostasis. The insulin-pI3K pathway can cause POMC neurons to become insensitive to leptin through hyperpolarization.

Leptin is known to interact with amylin, a hormone involved in gastric emptying and creating a feeling of fullness. When both leptin and amylin were given to obese, leptin-resistant rats, sustained weight loss was seen. Due to its apparent ability to reverse leptin resistance, amylin has been suggested as possible therapy for obesity.

It has been suggested that the main role of leptin is to act as a starvation signal when levels are low, to help maintain fat stores for survival during times of starvation, rather than a satiety signal to prevent overeating. Leptin levels signal when an animal has enough stored energy to spend it in pursuits besides acquiring food. This would mean that leptin resistance in obese people is a normal part of mammalian physiology and possibly, could confer a survival advantage. Leptin resistance (in combination with insulin resistance and weight gain) is seen in rats after they are given unlimited access to palatable, energy-dense foods. This effect is reversed when the animals are put back on a low-energy diet. This also may have an evolutionary advantage: allowing energy to be stored efficiently when food is plentiful would be advantageous in populations where food frequently may be scarce.

A fad diet, the Rosedale diet is based on ideas about how leptin might affect weight. It is based on unsound science and marketed with unevidenced claims of health benefits.

Role in osteoarthritis with obesity

Obesity and osteoarthritis
Osteoarthritis and obesity are closely linked. Obesity is one of the most important preventable factors for the development of osteoarthritis.

Originally, the relationship between osteoarthritis and obesity was considered to be exclusively biomechanically based, according to which the excess weight caused the joint to become worn down more quickly. However, today we recognise that there is also a metabolic component which explains why obesity is a risk factor for osteoarthritis, not only for weight-bearing joints (for example, the knees), but also for joints that do not bear weight (for example, the hands). Consequently, it has been shown that decreasing body fat lessens osteoarthritis to a greater extent than weight loss per se. This metabolic component related with the release of systemic factors, of a pro-inflammatory nature, by the adipose tissues, which frequently are critically associated with the development of osteoarthritis.

Thus, the deregulated production of adipokines and inflammatory mediators, hyperlipidaemia, and the increase of systemic oxidative stress are conditions frequently associated with obesity which can favour joint degeneration. Furthermore, many regulation factors have been implicated in the development, maintenance and function, both of adipose tissues, as well as of the cartilage and other joint tissues. Alterations in these factors can be the additional link between obesity and osteoarthritis.

Leptin and osteoarthritis
Adipocytes interact with other cells through producing and secreting a variety of signalling molecules, including the cell signalling proteins known as adipokines. Certain adipokines can be considered as hormones, as they regulate the functions of organs at a distance, and several of them have been specifically involved in the physiopathology of joint diseases. In particular, there is one, leptin, which has been the focus of attention for research in recent years.

The circulating leptin levels are positively correlated with the Body Mass Index (BMI), more specifically with fatty mass, and obese individuals have higher leptin levels in their blood circulation, compared with non-obese individuals. In obese individuals, the increased circulating leptin levels induce unwanted responses, that is, reduced food intake or losing body weight does not occur as there is a resistance to leptin (ref 9). In addition to the function of regulating energy homeostasis, leptin carries out a role in other physiological functions such as neuroendocrine communication, reproduction, angiogenesis and bone formation. More recently, leptin has been recognised as a cytokine factor as well as with pleiotropic actions also in the immune response and inflammation. For example, leptin can be found in the synovial fluid in correlation with the body mass index, and the leptin receptors are expressed in the cartilage, where leptin mediates and modulates many inflammatory responses that can damage cartilage and other joint tissues. Leptin has thus emerged as a candidate to link obesity and osteoarthritis and serves as an apparent objective as a nutritional treatment for osteoarthritis.

As in the plasma, the leptin levels in the synovial fluid are positively correlated with BMI. The leptin of the synovial fluid is synthesised at least partially in the joint and may originate in part in the circulation. Leptin has been shown to be produced by chondrocytes, as well as by other tissues in the joints, including the synovial tissue, osteophytes, the meniscus and bone. An infrapatellar fat pad located extrasynovially within the knee joint is also adjacent to the synovial membrane and cartilage, and has recently been highly appreciated as an important source of leptin, as well as other adipokines and mediators which contribute to the pathogenesis of osteoarthritis

The risk of suffering osteoarthritis can be decreased with weight loss. This reduction of risk is related in part with the decrease of the load on the joint, but also in the decrease of fatty mass, the central adipose tissue and the low-level inflammation associated with obesity and systemic factors.

This growing evidence points to leptin as a cartilage degradation factor in the pathogenesis of osteoarthritis, and as a potential biomarker in the progression of the disease, which suggests that leptin, as well as regulation and signalling mechanisms, can be a new and promising target in the treatment of osteoarthritis, especially in obese patients.

Obese individuals are predisposed to developing osteoarthritis, not only due to the excess mechanical load, but also due to the excess expression of soluble factors, that is, leptin and pro-inflammatory cytokines, which contribute to joint inflammation and cartilage destruction. As such, obese individuals are in an altered state, due to a metabolic insufficiency, which requires specific nutritional treatment capable of normalising the leptin production and reducing the systematic low-level inflammation, in order to reduce the harmful impact of these systematic mediators on the joint health.

There are nutritional supplements and pharmacological agents capable of directing these factors and improving both conditions.

Therapeutic use

Leptin

Leptin was approved in the United States in 2014 for use in congenital leptin deficiency and generalized lipodystrophy.

Analog metreleptin

An analog of human leptin metreleptin (trade names Myalept, Myalepta) was first approved in Japan in 2013, and in the United States in February 2014 and in Europe in 2018. In the US it is indicated as a treatment for complications of leptin deficiency, and for the diabetes and hypertriglyceridemia associated with congenital or acquired generalized lipodystrophy. In Europe based on EMA, metreleptin should be used in addition to diet to treat lipodystrophy, where patients have loss of fatty tissue under the skin and build-up of fat elsewhere in the body such as in the liver and muscles. The medicine is used in adults and children above the age of 2 years with generalised lipodystrophy (Berardinelli-Seip syndrome and Lawrence syndrome); and in adults and children above the age of 12 years with partial lipodystrophy (including Barraquer-Simons syndrome), when standard treatments have failed.

The National Health Service in England will commission metreleptin treatment for all with congenital leptin deficiency regardless of age beginning on April 1, 2019.

Research
Leptin is currently being evaluated as a potential target for the treatment of anorexia nervosa. It is hypothesized that the gradual loss of body fat mass, and more specifically the ensuing low leptin levels, escalate the preexisting drive for thinness into an obsessive-compulsive-like and addictive-like state. It was shown that short-term metreleptin treatment of patients with anorexia nervosa had rapid on-set of beneficial cognitive, emotional, and behavioral effects. Among other things, depression, drive for activity, repetitive thoughts of food, inner restlessness, and weight phobia decreased rapidly. Whether metreleptin (or another leptin analogue) is a suitable treatment for anorexia nervosa is currently unknown. Potential side effects are weight loss and the development of anti-metreleptin antibodies.

History
The leptine was discovered by Jeffrey Friedman in 1994 after several decades of research conducted by others institutions since 1950 on obese mouse models

Identification of the encoding gene
In 1949, a non-obese mouse colony being studied at the Jackson Laboratory produced a strain of obese offspring, suggesting that a mutation had occurred in a hormone regulating hunger and energy expenditure. Mice homozygous for the so-called ob mutation (ob/ob) ate voraciously and were massively obese. In the 1960s, a second mutation causing obesity and a similar phenotype was identified by Douglas Coleman, also at the Jackson Laboratory, and was named diabetes (db), as both ob/ob and db/db were obese. In 1990 Rudolph Leibel and Jeffrey M. Friedman reported mapping of the db gene.

Consistent with Coleman's and Leibel's hypothesis, several subsequent studies from Leibel's and Friedman's labs and other groups confirmed that the ob gene encoded a novel hormone that circulated in blood and that could suppress food intake and body weight in ob and wild type mice, but not in db mice.

In 1994, Friedman's laboratory reported the identification of the gene. In 1995, Jose F. Caro's laboratory provided evidence that the mutations in the mouse ob gene did not occur in humans. Furthermore, since ob gene expression was increased, not decreased, in human obesity, it suggested resistance to leptin to be a possibility. At the suggestion of Roger Guillemin, Friedman named this new hormone "leptin" from the Greek lepto meaning thin. Leptin was the first fat cell-derived hormone (adipokine) to be discovered.

Subsequent studies in 1995 confirmed that the db gene encodes the leptin receptor, and that it is expressed in the hypothalamus, a region of the brain known to regulate the sensation of hunger and body weight.

Recognition of scientific advances
Coleman and Friedman have been awarded numerous prizes acknowledging their roles in discovery of leptin, including the Gairdner Foundation International Award (2005), the Shaw Prize (2009), the Lasker Award, the BBVA Foundation Frontiers of Knowledge Award and the King Faisal International Prize, Leibel has not received the same level of recognition from the discovery because he was omitted as a co-author of a scientific paper published by Friedman that reported the discovery of the gene. The various theories surrounding Friedman's omission of Leibel and others as co-authors of this paper have been presented in a number of publications, including Ellen Ruppel Shell's 2002 book The Hungry Gene.

The discovery of leptin also is documented in a series of books including Fat: Fighting the Obesity Epidemic by Robert Pool, The Hungry Gene by Ellen Ruppel Shell, and Rethinking Thin: The New Science of Weight Loss and the Myths and Realities of Dieting by Gina Kolata. Fat: Fighting the Obesity Epidemic and Rethinking Thin: The New Science of Weight Loss and the Myths and Realities of Dieting review the work in the Friedman laboratory that led to the cloning of the ob gene, while The Hungry Gene draws attention to the contributions of Leibel.

See also
 Ghrelin
 NAPEs
 Teleost leptins

References

External links
Leptin: Your brain, appetite and obesity by the British Society of Neuroendocrinology
Leptin by Colorado State University – last updated 1998
Leptin at 3Dchem.com, description and structure diagrams

Leptin receptor agonists
Peptide hormones
Mutated genes
Obesity


text:
Hos prins Wilhelm och prinsessan Maria är en svensk dokumentärfilm från 1911.

Filmen skildrar Prins Wilhelm, hertig av Södermanland och Maria Pavlovna av Ryssland vid Oakhill på Djurgården i Stockholm där prinsessan ses rida. Filmen var den första i en serie filmer av Biograf AB Victoria som skildrade svenska kungligheter i mer privata sammanhang. Premiären ägde rum den 7 mars 1911 på Brunkebergsteatern i Stockholm.

Referenser

Svenska dokumentärfilmer
Svenska stumfilmer
Svenska kortfilmer
Filmer 1911
Svartvita filmer
Stockholm på film
Svenska 1910-talsfilmer

redpajama_set_name: RedPajamaWikipedia


text:
La Liga Leumit 1979-1980 è stata la 39ª edizione della massima serie del campionato israeliano di calcio.

Presero parte al torneo 16 squadre, che si affrontarono in un girone all'italiana con partite di andata e ritorno. Per ogni vittoria si assegnavano due punti e per il pareggio un punto.

Le ultime tre classificate sarebbero state retrocesse in Liga Artzit, dalla quale sarebbero state promosse le prime tre classificate.

Il torneo fu vinto, per la quarta volta, dal Maccabi Netanya.

Capocannoniere del torneo fu David Lavi, del Maccabi Netanya, con 18 goal.

Squadre partecipanti

Classifica finale

Verdetti
  Maccabi Netanya campione di Israele 1979-1980
  Hakoah Ramat Gan, Beitar Tel Aviv e Beitar Gerusalemme retrocessi in Liga Artzit 1980-1981
  Hapoel Rishon LeZion, Hapoel Gerusalemme e Hapoel Ramat Gan promossi in Liga Leumit 1980-1981

Collegamenti esterni

Calcio nel 1979
Calcio nel 1980
Campionato israeliano di calcio


text:
Joseph Louis, comte de Luppé, né le  à Corbère (Basses-Pyrénées) et mort le  à Paris, est un homme politique français.

Biographie

Joseph-Louis de Luppé était le fils de Gaston, marquis de Luppé (1802-1880) et d'Armandine d'Angosse (1809-1853).

Louis de Luppé était propriétaire de domaines agricoles dans les Pyrénées-Atlantiques et fit partie du conseil général de ce département de 1871 à 1880.

Il se présenta pour la première fois aux élections législatives du  dans la première circonscription (Pau), mais il n'obtint que  voix contre  au républicain Marcel Barthe. Après la dissolution de la Chambre, il fut élu dans la même  circonscription le  par  voix contre  au député sortant. Mais l'élection fut invalidée et Louis de Luppé fut battu le  par  voix contre  à Marcel Barthe.

Le , inscrit sur la liste conservatrice des Basses-Pyrénées, Louis de Luppé devint élu de ce département, quatrième sur cinq. Il prit place sur les bancs de la droite avec laquelle il vota en particulier contre la loi sur l'enseignement primaire, contre la nouvelle loi militaire, contre le rétablissement du scrutin d'arrondissement, contre les poursuites contre trois députés membres de la Ligue des patriotes, contre le projet de loi Lisbonne restrictif de la liberté de la presse, contre les poursuites contre le général Boulanger.

Il ne remplit pas d'autre mandat parlementaire.

Son épouse, Louise de Rivière (1844-1897), périt dans l'incendie du Bazar de la Charité.

Notes et références

Voir aussi

Bibliographie

 Diane de Maynard, La descendance de Jean-Paul, marquis d'Angosse (1732-1798), Paris, éd. Christian, 1998.

Articles connexes
 Familles subsistantes de la noblesse française

Liens externes

Naissance en septembre 1837
Naissance dans les Basses-Pyrénées
Député des Basses-Pyrénées (Troisième République)
Décès en novembre 1912
Décès dans le 7e arrondissement de Paris
Décès à 75 ans


text:
Le Auckland Art Gallery Toi o Tāmaki (en français « musée d'art d'Auckland ») est un musée d'art situé à Auckland, en Nouvelle-Zélande. Créé en 1887, c'est le plus grand musée d'art de la Nouvelle-Zélande. Le musée se trouve au coin de la rue Wellesley et Kitchener, en face de la bibliothèque municipale.

Les portraits de dignitaires maoris peints par l'artiste Charles Frederick Goldie font partie de la collection permanente.

Directeurs du musée

Notes et références

Liens externes

 Site web officiel du musée

Musée en Nouvelle-Zélande
Musée fondé en 1887
Auckland


text:
La chiesa di Sant'Agostino è una chiesa di Cantiano consacrata a Sant'Agostino. Ubicata poco distante dalle mura castellane, era in passato dedicata a santa Caterina d'Alessandria ed era pertinenza del Monastero di Fonte Avellana. La costruzione dell'edificio, risalente ai primi del Duecento mostra ancora la sua struttura romanica esterna con una facciata primitiva ancora intatta, un paramento murario dal sapiente contrasto cromatico dei conci policromi disposti a fasce alternate, nel quale si apre il magnifico portale romanico dai capitelli guarniti da bassorilievi fitomorfici stilizzati. Il fianco destro lungo la via Mazzini è corso da lesene e presenta alcune monofore da fastigio trilobato. Nel 1272 fu concessa all'Ordine degli Agostiniani, per secoli affidatari dell'educazione della gioventù di Cantiano che vi costruiscono un annesso convento, oggi sede del Museo. Centro dell'edificio conventuale è il porticato chiostro della fine del Duecento. All'interno della chiesa, ad un'unica navata, vi si conservano importanti dipinti ed affreschi tra i quali: un affresco del secolo XV raffigurante la Madonna con Bambino tra Santa Monica e San Nicola da Tolentino riconducibile alla scuola di Gentile da Fabriano, un crocefisso ligneo del 1400, la "Madonna della Cintura" del XVI secolo, attribuita ad Antonio Viviani detto "il Sordo" allievo del Barocci; una Concezione della Beata Vergine Maria di Giovanni Dionigi da Cagli datata 1535, una Pietà umbra del secolo XVI e Cristo con Apostoli e Pie Donne della scuola di Virgilio Nucci da Gubbio (1547-1621); inoltre nell'abside originaria sono visibili tracce di affresco raffigurante Sant'Agostino e la Vergine del Soccorso, databili al XIII secolo.

Agostino
Cantiano


text:
Weniamin Weniaminowitsch Alexandrow (; * 18. April 1937 in Moskau, Russische SFSR; † 6. November 1991 ebenda) war ein sowjetischer Eishockeyspieler.

In der sowjetischen Liga erzielte er insgesamt 345 Tore in 400 Spielen. Er spielte von 1955 bis 1969 für den HK ZSKA Moskau und gewann zehnmal den sowjetischen Meistertitel (1956, 1958–61, 1963–66 & 1968). 1963 war er mit 53 Toren der Top-Scorer der Liga.

Für die Sowjetische Eishockeynationalmannschaft spielte er von 1957 bis 1968. Hier erzielte er 119 Tore in 161 Spielen und gewann die Eishockey-Weltmeisterschaft in den Jahren 1963, 1964, 1965, 1966, 1967 und 1968. Zunächst bildete er mit Alexander Almetow und Konstantin Loktew eine überaus leistungsstarke Sturmreihe. Später dann mit Boris Michailow und Wladimir Petrow, hier wurde er dann durch Waleri Charlamow abgelöst.

Später war er als Trainer für HK ZSKA Moskau, SKA Sankt Petersburg und den bulgarischen Club ZSKA Sofia tätig.

1963 wurde er für seine Verdienste mit der Aufnahme in die Russische und sowjetische Hockey Hall of Fame und 2007 in die IIHF Hall of Fame geehrt.

Auszeichnungen
 Goldmedaille bei den Eishockey-Weltmeisterschaften 1963, 1964, 1965, 1966, 1967 und  1968
 Goldmedaille bei den Eishockey-Europameisterschaften  1963, 1964, 1965, 1966, 1967 und 1968
 Goldmedaille bei den Olympischen Winterspielen 1964 und  1968
 Bronzemedaille bei den Olympischen Winterspielen 1960

Weblinks

 Infos bei peoples.ru (russ.)

Eishockeynationalspieler (Sowjetunion)
Eishockeyspieler (HK ZSKA Moskau)
Eishockeytrainer (Sowjetunion)
Eishockeytrainer (HK ZSKA Moskau)
Eishockeytrainer (SKA Sankt Petersburg)
Eishockeytrainer (Bulgarien)
Olympiasieger (Eishockey)
Olympiateilnehmer (Sowjetunion)
Teilnehmer der Olympischen Winterspiele 1960
Teilnehmer der Olympischen Winterspiele 1964
Teilnehmer der Olympischen Winterspiele 1968
Weltmeister (Eishockey)
Europameister (Eishockey)
Sowjetischer Meister (Eishockey)
Mitglied der IIHF Hall of Fame
Verdienter Meister des Sports der UdSSR und Russlands im Eishockey
Sowjetbürger
Russe
Geboren 1937
Gestorben 1991
Mann


text:
Jona Efoloko (* 23. September 1999 in Kinshasa, DR Kongo) ist ein britischer Leichtathlet kongolesischer Herkunft, der in den Kurzsprintdisziplinen an den Start ging. Mit der Staffel konnte er 2022 Europameister werden und zudem die Bronzemedaille bei den Weltmeisterschaften in Eugene gewinnen.

Leben
Jona Efoloko wurde in der kongolesischen Hauptstadt Kinshasa geboren. Er besuchte das Loreto College in Manchester, wobei er mittels eines Stipendiums des Talented Athlete Scholarship Scheme unterstützt wurde. 2018 schloss er das College mit der Hochschulreife ab. Parallel zu seiner Schulausbildung betrieb er zunächst die Sportarten Fußball und Rugby Union. Während eines Schulwettkampfes wurde sein Sprintpotenzial entdeckt, so dass er 2013 mit der Leichtathletik begann.

Sportliche Laufbahn
Bereits seinen ersten Wettkampf bei den britischen Schulmeisterschaften konnte er in der Altersklasse U15 siegreich über 200 Meter bestreiten. 2014 gewann er in derselben Altersklasse bei den englischen Hallenmeisterschaften jeweils über 60 und 200 Meter die Goldmedaille. 2016 gewann er in der Halle und in der Freiluft in der nächsthöheren Altersklasse U17 jeweils die nationalen Meistertitel über 60, 100 und 200 Meter. Auch 2016 konnte er im Frühjahr zunächst bei den U17-Hallenmeisterschaften Englischer Meister über 60 und 200 Meter werden. Im Laufe der Saison steigerte er seine 100-Meter-Bestzeit auf 10,59 s. Über 200 Meter lief er 21,45 s und konnte damit im Sommer bei den U18-Europameisterschaften in Tiflis an den Start gehen. Zunächst erreichte er das Halbfinale, in dem er eine neue Bestzeit lief. Im anschließenden Finale steigerte er sich auf 21,15 s und konnte damit den Europameistertitel gewinnen. Ein Jahr später qualifizierte er sich über 200 Meter für die U20-Europameisterschaften in Grosseto. Auch dort erreichte er das Finale, in dem er die Silbermedaille gewinnen konnte. 2018 wurde Efoloko mit neuer Bestzeit von 20,79 s englischer U20-Meister. Damit war er für die U20-Weltmeisterschaften im finnischen Tampere qualifiziert. Auch dort konnte er in den einzelnen Läufen neue Bestzeiten aufstellen. Im Finale lief er mit 20,48 s seine persönliche 200-Meter-Bestzeit und gewann damit den Weltmeistertitel.

2019 schaffte er es nicht die 200 Meter unter 21 Sekunden zu absolvieren. Fortan trat er vermehrt mit der Staffel an. Im Sommer nahm er mit der 4-mak-100-Meter-Staffel an den U23-Europameisterschaften in Gävle teil. Die Staffel konnte in das Finale einziehen, wobei es ihr darin nicht gelang, das Rennen zu beenden. 2020 belegte Efoloko den vierten Platz über 200 Meter bei den britischen Meisterschaften. 2021 gewann er über 200 und über 100 Meter jeweils die Bronzemedaille bei den britischen Meisterschaften. Dabei steigerte er seine 100-Meter-Bestzeit auf 10,30 s und wurde in der Folge vom Nationalen Olympischen Komitee als Reserveläufer für die Sprintstaffel berücksichtigt. Zu einem Einsatz bei den Olympischen Sommerspielen in Tokio kam es schließlich nicht. 2022 steigerte er sich in Florida auf 10,27 s über 100 Meter. Dort in den USA nahm er im Sommer an seinen ersten Weltmeisterschaften teil. Im Vorlauf noch geschont, startete er im Finale als Startläufer für die britische Sprintstaffel, mit der er schließlich die Bronzemedaille gewinnen konnte. Einen Monat später gewann er mit der englischen Sprintstaffel bei den Commonwealth Games in Birmingham. Nur wenige Wochen später trat er auch bei den Europameisterschaften in München an und gehörte dort zum britischen Quartett, das sich im Finale den Europameistertitel sichern konnte.

Wichtige Wettbewerbe

Persönliche Bestleistungen
Freiluft
 100 m: 10,27 s, 16. April 2022, Gainesville
 200 m: 20,48 s, 13. Juli 2018, Tampere

Halle
 60 m: 6,65 s, 22. Januar 2022, Manchester
 200 m: 21,13 s, 16. Februar 2022, Sheffield

Weblinks

Einzelnachweise

100-Meter-Läufer (Vereinigtes Königreich)
4-mal-100-Meter-Staffel-Läufer (Vereinigtes Königreich)
Europameister (4-mal-100-Meter-Staffel, Leichtathletik)
Teilnehmer an den Commonwealth Games (England)
Brite
Kongolese (Demokratische Republik Kongo)
Geboren 1999
Mann


text:
Zagorsekia is an extinct Eocene genus of bryozoan. It formed erect colonies of bifurcating branches, which were a few millimeters long and  sometimes terminated in mushroom-like capitula covered in numerous holes that would have contained autozooids. Branches had multiple annulations along their length, which were also covered in large autozooidal apertures and smaller kenozooidal apertures. The genus was discovered in Chatham Island, New Zealand.

References

Prehistoric bryozoan genera


text:
Fizești este un sat în comuna Pui din județul Hunedoara, Transilvania, România. Se află în partea de sud a județului, în Depresiunea Hațeg.

Imagine

Note

Fizești, Pui


text:
Partition es una película de 2007 dirigida por Vic Sarin, escrita por Patricia Finn y Vic Sarin, y protagonizada por Jimi Mistry y Kristin Kreuk.

Argumento

Margaret Stillwell (Neve Campbell) y su hermano son británicos viviendo en La India. El hermano de Margaret, un joven soldado, es enviado a una misión junto a su amigo Gian Singh (Jimi Mistry). Stillwell muere en combate y al volver, Gian decide dejar el ejército y volver a su aldea. En ese momento, el país estaba pasando por un momento difícil momento: tras retirarse los británicos, el conflicto entre hindúes y musulmanes por el territorio, crecía. Cientos de musulmanes se iban exiliados a Pakistán. Un día, mientras familias musulmanas enteras caminaban hacia Pakistán, fueron brutalmente atacadas por hindúes. La joven Naseem (Kristin Kreuk) logra escapar y se esconde, perdiendo de vista a sus padres y sus dos hermanos, sin ver el momento en que su padre es asesinado. Gian encuentra a Naseem escondida y decide ayudarla y llevarla a su casa. Mientras tanto, el conflicto entre hindúes y musulmanes era cada vez mayor, tras el ataque por parte de los hindúes, un tren repleto de hindúes provenientes de Pakistán llegó a La India sin sobrevivientes, todos habían sido masacrados por los musulmanes como venganza. Gian sabe que debe mantener a Naseem escondida, ya que, por ser musulmana, en su pueblo no iba a ser bien recibida. Un día mientras Gian trabajaba en el campo, alguien descubre a Naseem, a través de un hueco en una puerta, y todo el pueblo le exige a Gian que la entregue, pero él se niega. Gian pide ayuda a Margaret para encontrar a la familia de Naseem. Gian y Naseem se enamoran, se casan y tienen un hijo. Cuando Margaret consigue información sobre la familia de Naseem, va a visitarlos y les da la noticia de que están vivos. Naseem decide ir a Pakistán por un mes a reencontrarse con ellos. Pero tres meses después, Gian no tiene noticias de ella. Ninguna de sus cartas habían tenido respuesta y su preocupación aumentaba. Naseem, que estaba en la casa de su familia, con su madre y sus dos hermanos, no había recibido ninguna carta. Su familia intentaba mantenerla sin contacto con Gian porque no aprobaban que se haya casado con un hindú. Cuando Naseem encuentra las cartas de Gian escondidas, se enfurece y decide irse. Al mismo tiempo, acusa a su familia de retenerla con pretextos para alejarla de su esposo. Naseem no consigue irse, su hermano mayor la encierra con tal de impedir que vuelva a la India. Gian decide ir a buscarla, pero le advierten que para entrar a Pakistán tiene que ser musulmán, de lo contrario no es posible cruzar la frontera. Entonces Gian se convierte al islam para poder ir a recuperar a su esposa. Una vez allá, después de un viaje complicado junto a su hijo, Gian se encuentra en un hotel con Margaret y un amigo, periodista, que están dispuestos a ayudarlo. Gian llega a la casa de la familia de Naseem, ella lo ve e intenta correr a abrazarlo, pero sus hermanos lo impiden, golpean a Gian y hacen que se vaya. Gian no quiere volver a La India sin Naseem, pero el periodista amigo de Margaret le aconseja que se vaya de Pakistán con su hijo, ya que corrían peligro. Mientras Gian va hacia la estación de trenes para volver a su país, con su hijo, Margaret y el periodista, la madre de Naseem recapacita y la deja escapar para que vuelva con Gian y su hijo. Naseem llega a la misma estación, ve a su hijo y después a Gian, ambos se abrazan fuerte en un puente sobre las vías, sin saber que los hermanos de Naseem habían ido a buscarla. De repente, el hermano mayor los separa y empieza a golpear a Gian, la pelea termina cuando Gian cae del puente y muere. Naseem llora desesperada, pero gracias a Margaret logra subir al tren con su hijo y escapar de sus hermanos. Finalmente, Naseem y su hijo se van con Margaret a vivir a Inglaterra.

Elenco
Jimi Mistry ... Gyan Singh
Kristin Kreuk ... Naseem Khan
Neve Campbell ... Margaret Stilwell
John Light ... Walter Hankins
Irrfan Khan ... Avtar
Madhur Jaffrey ... Shanti Singh
Arya Babbar ... Akbar Khan
Lushin Dubey ... Mumtaz
Chenier Hundal ... Zakir Khan
Jesse Moss ... Andrew Stilwell
Jaden Rain ... Vijay Singh

Nominaciones
2008 Genie Award for Best Achievement in Cinematography - Nominada
2007 Leo Award por mejor cinematografía en un Drama - Nominada
2007 Leo Award por mejor dirección en un Drama - Nominada
2007 Leo Award por mejor guion en un Drama - Nominada (con Patricia Finn)

Referencias


text:
La seconda edizione di Jevrobačennja (, "Eurovisione") è stata organizzata dall'emittente radiotelevisiva ucraina Nacional'na Teleradiokompanija Ukraïny (NTU) per selezionare il rappresentante nazionale all'Eurovision Song Contest 2007 ad Helsinki.

La vincitrice è stata Vjerka Serdjučka con Danzing.

Organizzazione
L'emittente ucraina Nacional'na Teleradiokompanija Ukraïny (NTU) ha confermato la partecipazione dell'Ucraina all'Eurovision Song Contest 2007 il 19 gennaio 2006. La ricerca del rappresentante nazionale è iniziata il mese successivo con una selezione interna; tuttavia, citando difficoltà nella scelta, NTU ha annunciato di avere optato per il ritorno di una selezione pubblica, per la seconda volta con il nome Jevrobačennja.

La competizione si è tenuta in un'unica serata il 9 marzo 2007 e ha visto otto artisti, divenuti poi sette, sfidarsi per la possibilità di rappresentare l'Ucraina all'Eurovision Song Contest 2007.

Giuria
La giuria è stata composta da:

 Vitalij Dokalenko, direttore generale per NTU;
 Jan Tabačnyk, compositore;
 Svjatoslav Vloch, presidente del World DanceSport Federation;
 Oksana Novyc'ka, vicepresidente della Confederazione dei designer e stilisti dell'Ucraina;
 Olena Mozgova, direttrice della sezione intrattenimento per NTU.

Partecipanti e risultati
NTU ha aperto la possibilità di inviare proposte per la competizione dal 24 gennaio al 10 febbraio 2007. Una giuria composta da cinque membri ha selezionato gli 8 finalisti per la finale televisiva, tra le 18 proposte ricevute, annunciati il 13 febbraio 2007.

Nonostante inizialmente figurasse nella lista dei partecipanti, Vitalij Kozlovs'kyj ha annunciato il suo ritiro il successivo 22 febbraio, citando il suo disappunto riguardo il tipo di format utilizzato per la selezione nazionale.

Finale
La finale si è tenuta presso gli studi televisivi di NTU di Kiev. Lo show è stato presentato da Timur Mirošnyčenko e Marija Orlova, ed è stato trasmesso su Peršyj Nacional'ni.

Durante la serata si sono esibiti come ospiti Iryna Bilyk, Natalija Mohylevs'ka, Oleksandr Ponomar'ov e Tina Karol', rappresentanti dell'Ucraina all'Eurovision Song Contest 2003 e 2006, ed alcuni rappresentanti dell'Eurovision Song Contest 2007: Kaldun (Bielorussia), Olivia Lewis (Malta), The Jet Set (Polonia) ed i Todomondo (Romania).

Vjerka Serdjučka è stata proclamata vincitrice trionfando sia nel televoto che nel voto della giuria.

Controversie
La vittoria di Vjerka Serdjučka, un personaggio en travesti, generò accese polemiche di diversi media e vari esponenti politici nazionali. Taras Čornovil, esponente del Partito delle Regioni, ha dichiarato in merito: «Credo che alcuni dei nostri stimati esperti abbiano visto quei "bei ragazzi finlandesi" vestiti da mostri, ma non abbiano capito che c'è una subcultura e una pseudocultura. Quei mostri fanno parte della loro subcultura, che ha il diritto di esistere; ma tutti questi ermafroditi non sono mai stati accettati da nessuna parte. Perciò penso che questo sarà un grave fattore di imbarazzo e il mondo ci vedrà come dei completi idioti».

Ulteriori accuse sono state poste al testo del brano Danzing; infatti al suo interno è presente la parola "Lasha Tumbai", che richiama foneticamente alla frase "Russia, Goodbye" (in italiano: "Russia, addio"), facendo presumibilmente riferimento alla Rivoluzione arancione avvenuta in Ucraina dal 22 novembre 2004 al 23 gennaio 2005. In un'intervista gestita dall'emittente russa Prevyj kanal, Serdjučka ha dichiarato che tale parola sia in realtà un espressione proveniente dalla lingua mongola per indicare la panna montata o il frappé; tuttavia molte personalità di origine mongola hanno confermato che tale espressione sia inesistente all'interno della loro lingua. In un'ulteriore intervista l'artista ha successivamente dichiarato che in realtà sia priva di significato, scelta solo per il bisogno di una rima per la composizione musicale. In occasione della manifestazione europea il titolo del brano è stato ribattezzato come Dancing Lasha Tumbai.

Note

Voci correlate

 Eurovision Song Contest 2007
 Ucraina all'Eurovision Song Contest

Eurovision Song Contest 2007


text:
Massy ist eine Commune déléguée in der französischen Gemeinde La Vineuse sur Fregande mit  Einwohnern (Stand: ) im Département Saône-et-Loire in der Region Bourgogne-Franche-Comté.

Zum 1. Januar 2017 wurde die Gemeinde Massy mit der Nachbargemeinden Donzy-le-National, La Vineuse und Vitry-lès-Cluny zur Commune nouvelle La Vineuse sur Fregande vereinigt. Sie gehörte zum Arrondissement Mâcon und war Teil des Kantons Cluny.

Geografie
Massy liegt etwa fünf Kilometer nordnordwestlich von Cluny.

Bevölkerungsentwicklung

Sehenswürdigkeiten
 romanische Kirche Saint-Denis aus dem 11. Jahrhundert, Monument historique seit 1991

Weblinks

Ort in Bourgogne-Franche-Comté
Commune déléguée im Département Saône-et-Loire
Gemeindeauflösung 2017
Weinbauort in Frankreich
La Vineuse sur Fregande


text:
Anthony Kelly CBE FRS (25 January 1929 — 3 June 2014) was a British materials scientist.

Career
He joined the Crystallography Research Group in the Cavendish Laboratory in 1950, after completing his physics undergraduate degree at the University of Reading. In the 50s, he held positions at the University of Illinois, the University of Birmingham, and Northwestern University, before returning to Cambridge in 1959 as lecturer in the department of metallurgy.

In 1967, he moved to the National Physical Laboratory, where he worked first in the Division of Inorganic and Metallic Structure, and then in the Materials Group as deputy director. Whilst still involved with NPL, he served an extensive period as Vice Chancellor of the University of Surrey from 1975 to 1994. He returned to Cambridge in 1994 as a distinguished research fellow in the Department of Materials Science.

He was elected Fellow of the Royal Society in 1973, Fellow of the Royal Academy of Engineering in 1979.

References

1929 births
2014 deaths
Fellows of the Royal Society
Fellows of the Royal Academy of Engineering
Materials scientists and engineers


text:
La Fabrique de ciment Vigier, à Péry, été fondée en 1890 par Georgine Vigier, veuve de Robert Vigier. En 2021, l'entreprise, qui fait partie du groupe Vicat, occupe 750 collaborateurs et produit plus de 500 000 tonnes de ciment par an.

Chronologie

 1871 Robert Vigier produit à Luterbach (SO) du ciment Portland. Il est le premier à le faire en Suisse.
 1884 Création de l'entreprise Vigier Cement AG à Deitingen
 1890 La cimenterie de Luterbach installe une succursale dans la cluse de Reuchenette pour profiter de la proximité du calcaire et de la marne présents de la chaîne du Jura
 1897 Vigier renforce ses installations de production par de nouvelles machines mues par l'électricité.
 1910 Création du cartel des ciments Portland
 1994 Un glissement de terrain empêche l'exploitation à long terme du nouveau site d'extraction de Châtel, dans la cluse de Rondchâtel.
 1995 Le statut de succursale est changé en société anonyme sous le nom de Ciment Vigier SA. William A. de Vigier siège au Conseil d'administration.
 2000 Ciments Vigier SA reprend les activités cimentières de la société Brodtbeck SA Lausen.
 2001  Vigier est racheté par le groupe français Vicat.
 2002 La cimenterie exploite une nouvelle carrière au lieu-dit « La Tscharner », sur le territoire communal de La Heutte.
 2011 Acquisition de la société Beton AG Basel.

Notes et références

Liens externes

 Ciment Vigier Site internet
 Groupe Vicat Site internet

Entreprise du bâtiment ayant son siège en Suisse
Producteur de ciment
Entreprise ayant son siège dans le canton de Berne
Jura bernois


text:
Elbio Maximiliano Álvarez Wallace (born 13 June 1994) is a Uruguayan professional footballer who plays as midfielder.

Club career
Álvarez was born in Montevideo, Uruguay. On 29 January 2015, the former Peñarol player, joined Portuguese champions S.L. Benfica, along with countryman Jonathan Rodríguez, being assigned to the reserve team. On 15 March 2015, he debuted for Benfica B as a substitute in an away win at Farense (0–3) in Segunda Liga.

Honours
Uruguay
FIFA U-17 World Cup: Runner-up 2011

References

External links

1994 births
Living people
Footballers from Montevideo
Uruguayan footballers
Association football midfielders
Peñarol players
S.L. Benfica B players
Liga Portugal 2 players
Uruguay youth international footballers
Uruguayan expatriate footballers
Expatriate footballers in Portugal
Uruguayan expatriate sportspeople in Portugal


text:
Quercus frainetto — вид рослин з родини Букові (Fagaceae); поширений у Європі й Туреччині.

Опис
Це велике листопадне дерево до 35 м заввишки. Крона округла. Міцний стовбур до 2 м у діаметрі. Кора борозниста, світло-сіра. Гілочки блідо-коричнево-зелені, злегка запушені. Листки 10–25 × 8–15 см, скупчені на кінчику гілочок; овальні, більш-менш довгасті; верхівки округлої форми (з часто трьома маленькими часточками); глибоко вирізані, з 7–10 часточками з кожного боку; блискучі темно-зелені, трохи шорсткі зверху й сіруваті, запушені знизу; ніжка листка волосиста, 0.2–1.2 см. Чоловічі квітки зібрані в 5–8 см сережки, повислі, золотисто-коричневі. Жолудь 2 см завдовжки; укладений на 1/3–1/2 в чашечку; дозріває через 1 рік.

Середовище проживання
Поширений у центральній і центрально-південній Європі, а також у Туреччині; також культивується.

Має низьку толерантність до посухи та високих температур і вимагає добре политих ґрунтів. Зростає в листяних лісах.

Використання
Традиційно використовується на дрова й деревину й випасається худобою.

Загрози й охорона
Сільськогосподарські практики в півострівній Італії вплинули на розповсюдження цього виду, який колись був безперервним, але зараз фрагментарно через тривалий людський порушення рослинності. Дерева також сприйнятливі до зміни кліматичних умов і чутливі до посухи та морозів. У Греції виду загрожує велика експлуатація деревини й деградації ділянок. Гібридизація з Quercus virgiliana (та потенційно іншими видами дуба) є додатковою загрозою.

В Червоній книзі Угорщини має статус DD через невизначену належність до рідної чи нерідної флори. У Червоній книзі Словаччини має статус VU. Відомий із 77 колекцій ex situ у ботанічних садах по всьому світу.

Галерея

Примітки

frainetto
Флора Європи
Флора Туреччини
Рослини, описані 1815


text:
(6042) Cheshirecat ist ein marsbahnstreifender Asteroid des Hauptgürtels, der am 23. November 1990 von den japanischen Astronomen Akira Natori und Takeshi Urata an der JCPM Yakiimo Station (IAU-Code 885) in Shimizu in der Präfektur Shizuoka entdeckt wurde.

Der Asteroid wurde am 9. Februar 1999 nach der Figur der Cheshire Cat (Grinsekatze) aus dem Kinderbuch Alice im Wunderland des britischen Schriftstellers Lewis Carroll benannt.

Siehe auch
 Liste der Asteroiden

Weblinks
 Asteroid Cheshirecat: Discovery Circumstances gemäß dem Minor Planet Center der Internationalen Astronomischen Union bei dem Harvard-Smithsonian Center for Astrophysics, Cambridge, USA
 Asteroid Cheshirecat in der Small-Body Database des Jet Propulsion Laboratory der NASA bei dem California Institute of Technology, Pasadena, USA

Hauptgürtelasteroid unter 50 km Durchmesser


text:
Alias Boston Blackie (1942) is the third in a series of fourteen Columbia Pictures "B" movies starring Chester Morris as Boston Blackie. It was preceded by Meet Boston Blackie, Confessions of Boston Blackie and followed by Boston Blackie Goes Hollywood. Once again, Blackie is suspected of committing a crime, in this instance of helping a prisoner escape.

Plot
In the Christmas spirit, Boston Blackie (Chester Morris) decides to entertain the inmates at his old "alma mater" by bringing a variety show headed by clown Roggi McKay (George McKay). Roggi drops one of his showgirls, Eve Sanders (Adele Mara), as she has already visited her prisoner brother, Joe Trilby (Larry Parks), the maximum allowed number of times that month. However, Blackie kindheartedly lets her tag along.

Inspector Farraday (Richard Lane) and Detective Joe Mathews (Walter Sande) unexpectedly join the group on the bus, just to keep an eye on Blackie. When Joe manages to escape from the prison, by tying Roggi up and putting on his costume and makeup, Farraday suspects Blackie helped him.

Blackie heads to Eve's apartment. Sure enough, Joe shows up soon afterward. Joe claims he is innocent and that Duke Banton and someone named Steve got him to drive them to the crime scene without telling him why. When the robbery was foiled, they fled, leaving him behind. Now he wants to kill the pair, regardless of the consequences. Joe takes Blackie's suit and ties him up. Eve eventually arrives and frees him.

Blackie and his sidekick "the Runt" (George E. Stone) head to Duke Banton's place, but arrive too late and find only a dead body. Then Joe enters. He claims he did not kill Banton. When the police surround the building, Blackie has Joe switch places with Banton after Farraday has examined the corpse. The "body" is taken away in an ambulance. Blackie is taken into custody, but manages to victimize Detective Mathews, putting on his uniform to get away.

From information provided by Jumbo Madigan (Cy Kendall), Blackie figures out that the other robber was taxi driver Steve Caveroni (Paul Fix). He has Eve pose as a fare to lure Caveroni to Banton's hotel room. Caveroni feels he is in control of the situation as he has a gun, so Blackie has little trouble getting him to confess he killed his partner (Banton was trying to flee, leaving Caveroni to take the blame) and that Joe is innocent. Farraday and his policemen eavesdrop through the door. Once he realizes he is trapped, Caveroni makes a break for it, but is shot dead.

Cast

Lloyd Bridges plays the uncredited bus driver.

References

External links

1942 films
1940s Christmas films
1940s crime films
American black-and-white films
Columbia Pictures films
American Christmas films
Films directed by Lew Landers
American crime films
Boston Blackie films
1940s American films


text:
Andoni Ortuzar Arruabarrena (Abanto i Ciérvana, 13 de juliol de 1962), és un periodista i polític espanyol pertanyent al Partit Nacionalista Basc (PNB), exdirector de EITB, membre del Parlament Basc i des de 2013, president del Partit Nacionalista Basc.

Biografia
Andoni Ortuzar va néixer el 13 de juliol de 1962 en la localitat biscaïna de Sanfuentes, Abanto i Ciérvana, en la Zona Minera (Biscaia). Va estudiar "ciències de la informació", branca periodisme, en la Universitat del País Basc. Quan va acabar la carrera va entrar com a redactor en Ràdio Popular de Bilbao i, posteriorment, el 1981 en el diari Deia on es va mantenir fins a 1987. En Deia va ser responsable de les Seccions de Laboral i Euskadi-Política. Militant del sindicat ELA va pertànyer al comitè d'empresa d'aquest mitjà arribant a ser president d'aquest.

Activitat política
Al setembre de 1987 va abandonar Deia i es va incorporar al Departament de Presidència, Justícia i Desenvolupament del Govern Basc com a assessor encarregant-se de la prefectura de premsa i de les relacions internacionals. Al febrer de 1991 va ser nomenat Assessor de Comunicació i Difusió en la Secretaria de la Presidència i assignat a la llavors acabada de crear Secretaria General d'Acció Exterior. Des de 1992 va exercir el lloc de Coordinador d'aquesta Secretaria, amb responsabilitats directes en la preparació de missions institucionals basques a l'exterior i la programació de les visites oficials a Euskadi de personalitats i mandataris estrangers.

El gener de 1995, dins d'un nou gabinet de govern, va ocupar el lloc de Secretari General d'Acció Exterior, sota la dependència directa del lehendakari.

Ha tingut també les responsabilitats de President del Consell Assessor Basc de Cooperació al Desenvolupament, Vicepresident del Consell Assessor amb les Col·lectivitats Basques i membre de la Comissió Bilateral Euskadi-Estat per a Assumptes Europeus.

Al juliol de 1999 és nomenat director general d'Euskal Irrati Telebista (la ràdio i televisió pública basca), càrrec que va mantenir fins a gener de 2008 quan va ser nomenat president del Bizkai Buru Batzar del PNB, l'òrgan de direcció d'aquest partit a Biscaia, en substitució d'Iñigo Urkullu.

El març de 2009 recull l'acta de membre del grup parlamentari Euzko Abertzaleak-Nacionalistes Bascos en el Parlament Basc, càrrec que ocupa fins al 31 de gener de 2012.

El 12 de gener de 2013 és elegit President del Euzkadi Buru Batzar del PNB, càrrec que va revalidar en el marc de l'Assemblea General del PNB celebrada en Iruñea els dies 13 i 14 de febrer de 2016.

Referències

Polítics biscaïns
Alumnes de la Universitat del País Basc
Militants del Partit Nacionalista Basc


text:
Pengzhou (彭州 ; pinyin : Péngzhōu) est une ville de la province du Sichuan en Chine. C'est une ville-district placée sous la juridiction administrative de la ville sous-provinciale de Chengdu.

Démographie
La population du district était de  en 1999.

Personnalités

 Chen Daojun a publié un article le  sur le site China E-Weekly réclamant l'arrêt de usine pétrochimique de Pengzhou située à 40 km de Chengdu. Il a été arrêté le , pour "tentative de subversion du pouvoir de l'Etat", car il aurait participé à un rassemblement dénonçant des risques environnementaux.

Notes et références

Voir aussi

Liens externes
  Site gouvernemental
  Page descriptive

Ville dans la province du Sichuan
Chengdu


text:
Daegu-Gyeongbuk or Taegu-Kyŏngbuk (대구경북, 大邱慶北) is the compound word of Daegu and Gyeongbuk (formally Gyeongsangbuk-do), and indicates both administrative regions in South Korea. The region usually forms the similar political, economic, and cultural area. Daegu is an independent city from Gyeongsangbuk-do and has the same administrative status with its mother province. Both have their separate local governments reporting directly to the national government.

In addition to the foremost city Daegu, there are many cities in this region including Pohang the major port and steel industrial city, Gumi the electronics industrial city, Gyeongju and Andong as the historic cities.

With a population of 5.1 million, the region has about one tenth of South Korea's population and GDP. It also has the country's third largest metropolitan area centering the Daegu city.

History

Historically, the region was the birthplace of the Silla Kingdom. With Gyeongju as the capital, it first unified the Korean Peninsula and prospered for about thousand years. It left a number of remains around the city, which are listed as a World Heritage Site by UNESCO.

In the Goryeo and Joseon Dynasty, it formed the northern half of Gyeongsang-do. Its name is from Gyeong of Gyeongju and Sang of Sangju, the two largest cities at that time. In the latter part of Joseon, it became home to the Korean Confucianism. Many cultural assets can be seen throughout the region including Andong. The Hahoe village of Andong and Yangdong village of Gyeongju are designated as the World heritages. From around the time, Daegu became the commercial center of the region. The provincial capital moved to Daegu in 1601.

The current boundary of the region was first defined with the name of Gyeongsangbuk-do in 1896, the year when Gyeongsang-do was divided into Gyeongsangbuk-do and Gyeongsangnam-do. It had the largest population in the country until its division in 1981, when Daegu separated from Gyeongsangbuk-do. After more than four hundred years at Daegu, Gyeongsangbuk-do's provincial office moved to Andong in 2016.

References

Geography of Daegu
Geography of North Gyeongsang Province


text:
Санкт Вит () е град в Югоизточна Белгия, окръг Вервие на провинция Лиеж. Населението му е около 9200 души (2006).

Външни препратки
 www.st.vith.be

Градове в Белгия
Общини в провинция Лиеж


text:
El Premi Nacional de Literatura Dramàtica (en castellà: Premio Nacional de Literatura Dramática) és un premi literari que atorga anualment el Ministeri d'Educació, Cultura i Esports d'Espanya des de l'any 1992.

Premia a la millor obra en la modalitat de litaratura dramàtica escrita per un autor espanyol, en qualsevol de les llengües oficials de l'Estat, entre totes les obres d'aquest gènere publicades a Espanya l'any anterior. Està dotat amb 20.000 euros.

Guanyadors
 1992: Francisco Nieva, per El manuscrito encontrado en Zaragoza
 1993: Alfonso Sastre, per Jenofa Juncal
 1994: José María Rodríguez Méndez, per El pájaro solitario
 1995: Josep Maria Benet i Jornet, per E.R.
 1996: Sergi Belbel, per Morir
 1997: Manuel Lourenzo, per Veladas indecentes
 1998: Jerónimo López Mozo, per Ahlán
 1999: Agustín García Calvo, per Baraja del rey don Pedro
 2000: Domingo Miras, per Una familia normal; Gente que prospera
 2001: Jesús Campos García, per Naufragar en Internet
 2002: Ignacio Amestoy, per Cierra bien la puerta
 2003: Fernando Arrabal, per Carta de amor (como un suplicio chino)
 2004: José Sanchis Sinisterra, per Terror y miseria en el primer franquismo
 2005: Alberto Miralles, per Metempsicosis
 2006: Santiago Martín Bermúdez, per Las gradas de San Felipe y empeño de la lealtad
 2007: Rubén Ruibal, per Limpeza de sangue
 2008: Miguel Romero Esteo, per Pontifical
 2009: Paco Bezerra, per Dentro de la tierra
 2010: Lluïsa Cunillé, per Aquel aire infinito
 2011: José Ramón Fernández, per La colmena científica o el café de Negrín
 2012: Angélica Liddell, per La casa de la fuerza
 2013: Juan Mayorga per La lengua en pedazos
 2014: Manuel Calzada Pérez, per El Diccionario.
 2015: Laila Ripoll i Mariano Llorente, per El triángulo azul
 2016: Lola Blasco, per Siglo mío, bestia mía.
 2017: Alfredo Sanzol, per La respiración.
 2018: Yolanda García Serrano, per ¡Corre!.
 2019: Alberto Conejero, per La geometría del trigo.
 2020: Guillem Clua, per Justícia.
 2021: Pablo Remón Magaña, per Doña Rosita, anotada.
 2022: Josep Maria Miró i Coromina, per El cos més bonic que s'haurà trobat mai en aquest lloc.

Referències

Enllaços externs
 www.mcu.es - Premi Nacional de Literatura Dramàtica


text:
The Nome–Council Highway is a highway that runs for  between the communities of Council and Nome in the Nome Census Area of the Unorganized Borough in the U.S. state of Alaska. The road travels east from Nome, following the shore of the Bering Sea until it reaches the ghost town of Solomon. From there, the route travels northeast through the interior of the Seward Peninsula before it terminates on the south bank of the Niukluk River, south of Council. One of three highways traveling from Nome to surrounding communities, the highway is disconnected from the rest of the Alaska Highway System. The route is unpaved for its entire length and becomes impassable for automobiles in the winter outside of a short portion immediately outside of Nome. The portion of the road between Nome and Solomon is part of the Iditarod Trail and the highway passes several historic sites associated with the trail and the area's gold mining history.

The route began as a collection of informal trails connecting Nome with mining communities established on the peninsula at the beginning of the 20th century. In 1906, the Alaska Road Commission constructed a wagon road along most of the length of the trails from Nome to Council. Because of the value of the gold coming from the Council area, this road quickly became the main artery for the region and the Road Commission spent significant amounts of money improving and maintaining the route into the 1930s. However, the road had fallen below state standards by the 1960s and 70s and projects were undertaken to update the highway and replace river-crossing ferries with bridges. The road has been studied since the 1950s as part of a potential Fairbanks-Nome Highway; the expected cost of such a project has consistently prevented any development.

Route description

The Nome–Council Highway begins at a T intersection with Nome Bypass Road and Front Street; the former route travels north from the intersection and forms a partial loop around the main built-up area of Nome, while the latter extends westward from the intersection along the Nome seawall into the city. The highway travels southeastward from this intersection, parallel to the Bering Sea. For the first mile, the route passes East End Park Ponds to the north, a city park which contains the Swanberg Dredge and is an important point for bird migration. After approximately , the highway intersects Kougarok Road, another state highway, which travels  northward to the Kougarok River south of the community of Taylor. After milepost 2, the road bends northeastward around the mouth of the Nome River. On the east bank of the river, the route intersects West Fork Road, East Fork Road, and Fort Davis Road, all of which lead to the former site of Fort Davis, a U.S. Army facility operated during the Nome Gold Rush. The area now hosts scattered houses and fishing huts. The roadway returns to following the coastline for a few miles, before it bends and continues slightly inland. Along this stretch, the highway passes a few quarries. Between miles 12 and 14, the road again follows the shore, traveling around Cape Nome, a large headland.

Historic sites
There are four important landmarks that are listed in the United States National Register of Historic Places within the Nome Census Area.

|}

Major intersections

References

External links

State highways in Alaska
Transportation in Unorganized Borough, Alaska
Nome, Alaska
Nome Census Area, Alaska
Gold rush trails and roads


text:
Oudeuil ist eine französische Gemeinde mit  Einwohnern (Stand ) im Département Oise in der Region Hauts-de-France. Die Gemeinde liegt im Arrondissement Beauvais und ist Teil der Communauté de communes de la Picardie Verte und des Kantons  Grandvilliers.

Geographie
Die agrarisch geprägte Gemeinde liegt im Tal des Bachs Herperie rund neun Kilometer südsüdwestlich von Crèvecœur-le-Grand und drei Kilometer östlich des Tals des Petit Thérain. Sie wird von der seit dem Ende der 1980er Jahre bis Saint-Omer-en-Chaussée stillgelegten, aber bis Crèvecœur-le-Grand als Industriegleis erhaltenen, sonst abgebauten Bahnstrecke von Amiens nach Beauvais durchzogen. Zu Oudeuil gehören die Ortsteile Grand Oudeuil und Ribeauville sowie das Gehöft Coullemogne.

Einwohner

Verwaltung
Bürgermeister (maire) ist seit 2008 Philippe Sys.

Sehenswürdigkeiten
 Pfarrkirche Saint-Martin mit romanischem Chor und Taufe aus der Wende vom 12. zum 13. Jahrhundert
 Ruinen des mittelalterlichen Schlosses

Einzelnachweise

Weblinks

 Monuments historiques (Objekte) in Oudeuil in der Base Palissy des französischen Kultusministeriums

Ort in Hauts-de-France


text:
This is a list of contestants who have appeared on the British television show Britain & Ireland's Next Top Model. Contestants compete against each other to become the next British and Irish top model. They are judged by model Abigail Clancy (previously Lisa Butcher, Lisa Snowdon, and Elle Macpherson) and her panel of judges to win a modeling contract with Models 1, a cover and/or spread in a magazine, and a cosmetics campaign. The series first aired in 2005 and as of 2017, there have been twelve
"cycles" that have aired. In its twelve years running, twelve models have been crowned Britain's Next Top Model: Lucy Ratcliffe, Lianna Fowler, Lauren McAvoy, Alex Evans, Mecia Simson, Tiffany Pisani, Jade Thompson, Letitia Herod, Lauren Lambert, Chloe Keenan, Olivia Wardell & Ivy Watson.

Contestants

1 Originally from Hungary
2 Originally from Nigeria
3 Originally from Serbia
4 Originally from Russia/Latvia
5 Originally from Lithuania
6 Originally from Jamaica
7 Originally from France
8 Originally from The Congo/Ukraine
9 Originally from St. Lucia

Notes
 Contestant's ages are at the time of the season's filming.

References

Britain and Ireland's Next Top Model contestants

Lists of British people
Lists of models


text:
Oecobius is een  spinnengeslacht uit de familie der spiraalspinnen (Oecobiidae).

Het geslacht omvat de volgende soorten.

Soorten
 Oecobius achimota Shear & Benoit, 1974
 Oecobius aculeatus Wunderlich, 1987
 Oecobius affinis O. P.-Cambridge, 1872
 Oecobius agaetensis Wunderlich, 1992
 Oecobius albipunctatus O. P.-Cambridge, 1872
 Oecobius alhoutyae Wunderlich, 1995
 Oecobius amboseli Shear & Benoit, 1974
 Oecobius annulipes Lucas, 1846
 Oecobius ashmolei Wunderlich, 1992
 Oecobius beatus Gertsch & Davis, 1937
 Oecobius bracae Shear, 1970
 Oecobius brachyplura (Strand, 1913)
 Oecobius brachyplura demaculata (Strand, 1914)
 Oecobius caesaris Wunderlich, 1987
 Oecobius cambridgei Wunderlich, 1995
 Oecobius camposi Wunderlich, 1992
 Oecobius cellariorum (Dugès, 1836)
 Oecobius chiasma Barman, 1978
 Oecobius civitas Shear, 1970
 Oecobius concinnus Simon, 1893
 Oecobius culiacanensis Shear, 1970
 Oecobius cumbrecita Wunderlich, 1987
 Oecobius depressus Wunderlich, 1987
 Oecobius dolosus Wunderlich, 1987
 Oecobius doryphorus Schmidt, 1977
 Oecobius eberhardi Santos & Gonzaga, 2008
 Oecobius erjosensis Wunderlich, 1992
 Oecobius fortaleza Wunderlich, 1992
 Oecobius fuerterotensis Wunderlich, 1992
 Oecobius furcula Wunderlich, 1992
 Oecobius gomerensis Wunderlich, 1979
 Oecobius hayensis Wunderlich, 1992
 Oecobius hidalgoensis Wunderlich, 1992
 Oecobius hierroensis Wunderlich, 1987
 Oecobius hoffmannae Jiménez & Llinas, 2005
 Oecobius idolator Shear & Benoit, 1974
 Oecobius iguestensis Wunderlich, 1992
 Oecobius incertus Wunderlich, 1995
 Oecobius infierno Wunderlich, 1987
 Oecobius interpellator Shear, 1970
 Oecobius isolatoides Shear, 1970
 Oecobius isolatus Chamberlin, 1924
 Oecobius juangarcia Shear, 1970
 Oecobius lampeli Wunderlich, 1987
 Oecobius latiscapus Wunderlich, 1992
 Oecobius linguiformis Wunderlich, 1995
 Oecobius longiscapus Wunderlich, 1992
 Oecobius machadoi Wunderlich, 1995
 Oecobius maculatus Simon, 1870
 Oecobius marathaus Tikader, 1962
 Oecobius marcosensis Wunderlich, 1992
 Oecobius maritimus Wunderlich, 1987
 Oecobius minor Kulczynski, 1909
 Oecobius nadiae (Spassky, 1936)
 Oecobius navus Blackwall, 1859
 Oecobius navus hachijoensis Uyemura, 1965
 Oecobius palmensis Wunderlich, 1987
 Oecobius pasteuri Berland & Millot, 1940
 Oecobius paulomaculatus Wunderlich, 1995
 Oecobius persimilis Wunderlich, 1987
 Oecobius petronius Simon, 1890
 Oecobius piaxtla Shear, 1970
 Oecobius pinoensis Wunderlich, 1992
 Oecobius przewalskyi Hu & Li, 1987
 Oecobius pseudodepressus Wunderlich, 1992
 Oecobius putus O. P.-Cambridge, 1876
 Oecobius rhodiensis Kritscher, 1966
 Oecobius rioensis Wunderlich, 1992
 Oecobius rivula Shear, 1970
 Oecobius rugosus Wunderlich, 1987
 Oecobius selvagensis Wunderlich, 1995
 Oecobius sheari Benoit, 1975
 Oecobius similis Kulczynski, 1909
 Oecobius sombrero Wunderlich, 1987
 Oecobius tadzhikus Andreeva & Tyschchenko, 1969
 Oecobius tasarticoensis Wunderlich, 1992
 Oecobius teliger O. P.-Cambridge, 1872
 Oecobius templi O. P.-Cambridge, 1876
 Oecobius tibesti Shear & Benoit, 1974
 Oecobius trimaculatus O. P.-Cambridge, 1872
 Oecobius unicoloripes Wunderlich, 1992

Spiraalspinnen


text:
Space Escape mit dem Untertitel S.O.S. – Schlangenalarm (englischer Originaltitel: Mole Rats in Space) ist ein kooperatives Brettspiel des kanadischen Spieleautoren Matt Leacock für zwei bis vier Personen. Das Spiel baut auf dem klassischen Brettspiel Schlangen und Leitern auf und erschien 2017 bei dem Verlag Peaceable Kingdom, 2018 wurde es in einer deutschen Version bei Game Factory veröffentlicht. Bei dem Spiel übernehmen die Spieler ein Team von Nacktmullen, die auf einer Raumstation ihre Rettungskapsel erreichen müssen, nachdem Schlangen eingedrungen sind.

Thema und Ausstattung
Bei dem Spiel handelt sich um ein kooperatives Spiel, bei dem die Spieler ein Team von Nacktmullen auf einer Raumstation zu ihrer Rettungskapsel bringen müssen, nachdem Schlangen eingedrungen sind. Wie bei anderen vollständig kooperativen Spielen können die Mitspieler nur gemeinsam gewinnen oder verlieren.

Das Spielmaterial besteht neben der Spieleanleitung aus:
 einem Spielplan, auf dem die Raumstation mit ihren fünf Ebenen abgebildet ist, die jeweils über Leitern und Rohre verbunden sind,
 vier Nacktmullfiguren in vier Farben,
 vier Erste-Hilfe-Koffer mit jeweils einer Portion Antiserum in den vier Spielerfarben,
 12 Schlangentoken in vier Farben,
 12 Ausrüstungstoken,
 ein Kartenset mit 46 Karten für die Bewegungen der Nacktmulle und der Schlangen,
 ein Umschlag mit Challenge-Karten.

Spielweise
Zur Spielvorbereitung wird das Spielfeld in die Spielmitte gelegt und jeder Spieler wählt eine Spielerfarbe. Er bekommt die passende Figur und den Erste-Hilfe-Koffer. Die Figuren werden auf das jeweils entsprechende Startfeld platziert. Auf die vier farbigen Schlangenfelder werden jeweils die entsprechenden Schlangentoken abgelegt und die Ausrüstungstoken kommen auf die dafür vorgesehenen Felder. Die Karten werden gemischt und jeder Spieler bekommt eine Karte, die restlichen Karten bilden den Nachziehstapel.

 Karte spielen
 Nacktmullaktion durchführen
 Schlangenaktion durchführen
 Karte nachziehen

Beginnend mit einem Startspieler spielen die Mitspieler reihum im Uhrzeigersinn. Jeder Spieler spielt, wenn er an der Reihe ist, seine Karte aus und führt die darauf abgebildete Nacktmull- und Schlangenaktion durch. Der Zug beginnt mit dem Nacktmull, der entsprechend der angegebenen Anzahl von Schritten gezogen wird und dabei alle Leitern und Röhren auf dem Weg ignoriert. Trifft der Nacktmull auf eine Schlange, wird er gebissen und muss zurück zu seinem Startfeld und seinen Erste-Hilfe-Koffer abgeben. Wird er zum zweiten Mal gebissen, stirbt er und das Team verliert das Spiel. Endet der Zug des Nacktmulls auf einem Ausrüstungsgegenstand, darf er diesen aufnehmen. Endet der Zug auf einer Leiter, steigt der Nacktmull auf die nächste Ebene. Endet der Zug auf einer Röhre, fällt der Nacktmull hinab bis zum Ende der Röhre oder aus dem Raumschiff hinaus. Nach dem Nacktmull wird die Schlange gezogen. Endet deren Zug auf einer Leiter, zieht die Schlange ebenfalls auf die nächste Ebene, und endet er auf einer Röhre, fällt auch die Schlange hinab bis zum Ende der Röhre oder aus dem Raumschiff hinaus. Nach dem Zug wird die Karte abgelegt und eine neue gezogen.

Die Spieler müssen gemeinsam versuchen, mit den vier Nacktmullen alle vier Ausrüstungsgegenstände einzusammeln und dann mit allen Figuren in die Rettungskapsel zu kommen, bevor
 ein Nacktmull zwei Mal von einer Schlange gebissen wurde,
 ein Nacktmull durch eine Röhre aus dem Schiff befördert wird,
 eine Schlange in die Rettungskapsel klettert oder
 ein Spieler keine Karte mehr spielen kann und damit die verfügbare Zeit verstrichen ist.
Gelingt ihnen dies, haben sie das Spiel gewonnen.

Entwicklung und Rezeption

Das Spiel Mole Rats in Space wurde von dem kanadischen Spieleautoren Matt Leacock entwickelt und 2017 bei dem Verlag bei dem Verlag Peaceable Kingdom auf Englisch veröffentlicht. Im deutschsprachigen Raum wurde es zu den Internationalen Spieltagen 2017 vorgestellt, 2018 erschien es unter dem Namen Space Escape bei dem Verlag Game Factory. Das Spiel selbst basiert auf dem klassischen Brettspiel Schlangen und Leitern und setzt diese Motive entsprechend auch ein. Der Autor ist bekannt für zahlreiche kooperative Spiele, darunter die ausgezeichneten Spiele Pandemie und Die verbotene Insel.

Belege

Weblinks
 Spielanleitung Mole Rats in Space

 Mole Rats in Space auf der Website von Matt Leacock
 Mole Rats in Space, Review bei opinionatedgamers.com

Spiel 2017
Brettspiel
Science-Fiction-Spiel


text:
Zykovo () is a rural locality (a village) in Fominskoye Rural Settlement, Gorokhovetsky District, Vladimir Oblast, Russia. The population was 2 as of 2010.

Geography
Zykovo is located 35 km southwest of Gorokhovets (the district's administrative centre) by road. Prosye is the nearest rural locality.

References

Rural localities in Gorokhovetsky District


text:
Чинку () — село у повіті Брашов в Румунії. Адміністративний центр комуни Чинку.

Село розташоване на відстані 193 км на північний захід від Бухареста, 68 км на північний захід від Брашова, 133 км на південний схід від Клуж-Напоки.

Населення
За даними перепису населення 2002 року у селі проживали  особи.

Національний склад населення села:

Рідною мовою назвали:

Примітки

Села повіту Брашов


text:
Bijou Thaangjam (born Thangjam Biju Singh) is an Indian actor, lyricist, art director, chef and entrepreneur. He is of Meitei descent originally from Imphal, Manipur. He was one of the contestants on the reality cooking competition MasterChef India 2. He is known for his role in the film Mary Kom and Shivaay.

Masterchef India
Bijou Thaangjam competed on the Star Plus reality cooking competition, Masterchef India. He was one of the Top 50 contestants of Masterchef India 2011.

Career
Bijou Thaangjam first appeared as a contestant on the reality cooking competition MasterChef India 2. He later debuted as an actor and a lyricist in Omung Kumar's Mary Kom (film) (2014) starring Priyanka Chopra as Mary Kom.

He played the role 'Kancha' in Shivaay (2016) which is a Hindi film directed and produced by Ajay Devgan.

He was also seen in successful films like Jagga Jasoos, Paltan, Happy Phirr Bhag Jayegi, Vodka Diaries, III Smoking Barrels and Penalty.

He also debuted as an Art Director in III Smoking Barrels which earned him a nomination for Best Art Director in Prag Cine Awards 2018.

He has also worked in films like Om The Battle Within and Rocketry: The Nambi Effect which is set for commercial release later in 2022.

Beside films, he acted in web series for various companies like ALT Balaji where he worked in a series The Test Case (web series). Apart from that, he was seen in Netflix show Typewriter directed by Sujoy Ghosh and Bi-Lingual Webseries Kark Rogue for Zee5 and Flesh (web series) for Eros Now.

In 2021 he was seen in a Sony Liv web series Love J Action, Disney+ Hotstar's 1962: The War In The Hills and TVF Original TVF Aspirants.

Filmography

Television

Web series

Producer filmography

Awards and Nominations

References

External links

Male actors from Manipur
Indian chefs
Meitei people
Living people
1986 births
People from Imphal


text:
O esporte no interior paulista é comandado pela Secretaria de Esporte, Lazer e Turismo do estado de São Paulo (SELT-SP).

Sua maior competição é o Jogos Abertos do Interior "Horácio Baby Barioni", geralmente realizados em novembro.

E ainda realiza em julho os Jogos Regionais em 8 regiões esportivas do estado.

Os melhores colocados nos Jogos Regionais garantem vaga nos Jogos Abertos do Interior, e os melhores colocados nos Jogos Abertos do Interior se classificam para os Jogos Abertos Brasileiros.

Os Jogos são responsáveis pela revelação de vários talentos esportivos.

Ligações externas

Esporte do estado de São Paulo


text:
The governor of New Hampshire has a term of two years; the officeholder can seek reelection. The original title was president of New Hampshire. It was changed to "governor" during the term of Josiah Bartlett, though the office itself remained the same.

The longest-serving governor in state history is Federalist John Taylor Gilman, who served as governor for 14 years (albeit nonconsecutive), from 1794 to 1805 and from 1813 to 1816.

List of governors and presidents
The last of the colonial governors of New Hampshire fled in 1775.

 Parties

Succession

Notes

See also
 List of colonial governors of New Hampshire
 New Hampshire
 Province of New Hampshire

Lists of state governors of the United States
Governors
Governors


text:
Het Junioren Wereldkampioenschap Oriëntatielopen (Junior World Orientering Championships - JWOC) werd voor het eerst gehouden in 1990. Met uitzondering van 1994 werd het kampioenschap elk jaar gehouden.

Het eerste jaar waren er maar twee afstanden: een individuele wedstrijd en een estafette. Een jaar later werd de korte afstand toegevoegd en in 2006 de sprint.

De huidige afstanden tijdens de kampioenschappen zijn:

 Estafette
 Lange afstand - voorheen klassiek
 Middellange afstand - voorheen korte afstand
 Sprint

Gaststeden

Klassiek/Lang
Deze afstand werd van 1990 tot en met 2003 Klassiek genoemd. Vanaf 2004 wordt het Lange afstand genoemd.

Mannen

Vrouwen

Kort/Middellange afstand
De korte afstand werd gehouden van 1991 tot en met 2003, daarna werd de afstand vervangen door de middellange afstand.

Mannen

Vrouwen

Sprint
Deze afstand werd voor het eerst gelopen in 2006.

Mannen

Vrouwen

Estafette

Mannen

Vrouwen

Externe links en referenties
Resultaten JWOC, International Oriëntatieloop Federatie
Hongaarse database met resultaten van alle jaren

JWOC
Junior World Orientering Championships 1995
Junior World Orientering Championships 2000
Junior World Orientering Championships 2002
Junior World Orientering Championships 2005
Junior World Orientering Championships 2006
Junior World Orientering Championships 2007
Junior World Orientering Championships 2008
Junior World Orientering Championships 2009

Wereldkampioenschap oriëntatieloop