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395_0 | Broca's area, or the Broca area (, also , ), is a region in the frontal lobe of the dominant hemisphere, usually the left, of the brain with functions linked to speech production.
Language processing has been linked to Broca's area since Pierre Paul Broca reported impairments in two patients. They had lost the ability to speak after injury to the posterior inferior frontal gyrus (pars triangularis) (BA45) of the brain. Since then, the approximate region he identified has become known as Broca's area, and the deficit in language production as Broca's aphasia, also called expressive aphasia. Broca's area is now typically defined in terms of the pars opercularis and pars triangularis of the inferior frontal gyrus, represented in Brodmann's cytoarchitectonic map as Brodmann area 44 and Brodmann area 45 of the dominant hemisphere. |
395_1 | Functional magnetic resonance imaging (fMRI) has shown language processing to also involve the third part of the inferior frontal gyrus the pars orbitalis, as well as the ventral part of BA6 and these are now often included in a larger area called Broca's region.
Studies of chronic aphasia have implicated an essential role of Broca's area in various speech and language functions. Further, fMRI studies have also identified activation patterns in Broca's area associated with various language tasks. However, slow destruction of Broca's area by brain tumors can leave speech relatively intact, suggesting its functions can shift to nearby areas in the brain.
Structure |
395_2 | Broca's area is often identified by visual inspection of the topography of the brain either by macrostructural landmarks such as sulci or by the specification of coordinates in a particular reference space. The currently used Talairach and Tournoux atlas projects Brodmann's cytoarchitectonic map onto a template brain. Because Brodmann's parcelation was based on subjective visual inspection of cytoarchitectonic borders and also Brodmann analyzed only one hemisphere of one brain, the result is imprecise. Further, because of considerable variability across brains in terms of shape, size, and position relative to sulcal and gyral structure, a resulting localization precision is limited. |
395_3 | Nevertheless, Broca's area in the left hemisphere and its homologue in the right hemisphere are designations usually used to refer to the triangular part of inferior frontal gyrus (PTr) and the opercular part of inferior frontal gyrus (POp). The PTr and POp are defined by structural landmarks that only probabilistically divide the inferior frontal gyrus into anterior and posterior cytoarchitectonic areas of 45 and 44, respectively, by Brodmann's classification scheme.
Area 45 receives more afferent connections from the prefrontal cortex, the superior temporal gyrus, and the superior temporal sulcus, compared to area 44, which tends to receive more afferent connections from motor, somatosensory, and inferior parietal regions. |
395_4 | The differences between area 45 and 44 in cytoarchitecture and in connectivity suggest that these areas might perform different functions. Indeed, recent neuroimaging studies have shown that the PTr and Pop, corresponding to areas 45 and 44, respectively, play different functional roles in the human with respect to language comprehension and action recognition/understanding.
In women, Broca's area is about 20% larger than in men.
Functions
Language comprehension |
395_5 | For a long time, it was assumed that the role of Broca's area was more devoted to language production than language comprehension. However, there is evidence to demonstrate that Broca's area also plays a significant role in language comprehension. Patients with lesions in Broca's area who exhibit agrammatical speech production also show inability to use syntactic information to determine the meaning of sentences. Also, a number of neuroimaging studies have implicated an involvement of Broca's area, particularly of the pars opercularis of the left inferior frontal gyrus, during the processing of complex sentences. Further, functional magnetic resonance imaging (fMRI) experiments have shown that highly ambiguous sentences result in a more activated inferior frontal gyrus. Therefore, the activity level in the inferior frontal gyrus and the level of lexical ambiguity are directly proportional to each other, because of the increased retrieval demands associated with highly ambiguous |
395_6 | content. |
395_7 | There is also specialisation for particular aspects of comprehension within Broca's area. Work by Devlin et al. (2003) showed in a repetitive transcranial magnetic stimulation (rTMS) study that there was an increase in reaction times when performing a semantic task under rTMS aimed at the pars triangularis (situated in the anterior part of Broca's area). The increase in reaction times is indicative that that particular area is responsible for processing that cognitive function. Disrupting these areas via TMS disrupts computations performed in the areas leading to an increase in time needed to perform the computations (reflected in reaction times). Later work by Nixon et al. (2004) showed that when the pars opercularis (situated in the posterior part of Broca's area) was stimulated under rTMS there was an increase in reaction times in a phonological task. Gough et al. (2005) performed an experiment combining elements of these previous works in which both phonological and semantic tasks |
395_8 | were performed with rTMS stimulation directed at either the anterior or the posterior part of Broca's area. The results from this experiment conclusively distinguished anatomical specialisation within Broca's area for different components of language comprehension. Here the results showed that under rTMS stimulation: |
395_9 | Semantic tasks only showed a decrease in reaction times when stimulation was aimed at the anterior part of Broca's area (where a decrease of 10% (50 ms) was seen compared to a no-TMS control group)
Phonological tasks showed a decrease in reaction times when stimulation was aimed at the posterior part of Broca's area (where a decrease of 6% (30 ms) was seen compared to control)
To summarise, the work above shows anatomical specialisation in Broca's area for language comprehension, with the anterior part of Broca's area responsible for understanding the meaning of words (semantics) and the posterior part of Broca's area responsible for understanding how words sound (phonology). |
395_10 | Action recognition and production
Recent experiments have indicated that Broca's area is involved in various cognitive and perceptual tasks. One important contribution of Brodmann's area 44 is also found in the motor-related processes. Observation of meaningful hand shadows resembling moving animals activates frontal language area, demonstrating that Broca's area indeed plays a role in interpreting action of others. An activation of BA 44 was also reported during execution of grasping and manipulation.
Speech-associated gestures
It has been speculated that because speech-associated gestures could possibly reduce lexical or sentential ambiguity, comprehension should improve in the presence of speech-associated gestures. As a result of improved comprehension, the involvement of Broca's area should be reduced. |
395_11 | Many neuroimaging studies have also shown activation of Broca's area when representing meaningful arm gestures. A recent study has shown evidence that word and gesture are related at the level of translation of particular gesture aspects such as its motor goal and intention. This finding helps explain why, when this area is defective, those who use sign language also suffer from language deficits. This finding, that aspects of gestures are translated in words within Broca's area, also explains language development in terms of evolution. Indeed, many authors have proposed that speech evolved from a primitive communication that arose from gestures. (See below.)
Speaking without Broca's area |
395_12 | Damage to Broca's area is commonly associated with telegraphic speech made up of content vocabulary. For example, a person with Broca's aphasia may say something like, "Drive, store. Mom." meaning to say, "My mom drove me to the store today." Therefore, the content of the information is correct, but the grammar and fluidity of the sentence is missing. |
395_13 | The essential role of the Broca's area in speech production has been questioned since it can be destroyed while leaving language nearly intact. In one case of a computer engineer, a slow-growing glioma tumor was removed. The tumor and the surgery destroyed the left inferior and middle frontal gyrus, the head of the caudate nucleus, the anterior limb of the internal capsule, and the anterior insula. However, there were minimal language problems three months after removal and the individual returned to his professional work. These minor problems include the inability to create syntactically complex sentences including more than two subjects, multiple causal conjunctions, or reported speech. These were explained by researchers as due to working memory problems. They also attributed his lack of problems to extensive compensatory mechanisms enabled by neural plasticity in the nearby cerebral cortex and a shift of some functions to the homologous area in the right hemisphere. |
395_14 | Clinical significance
Stuttering
A speech disorder known as stuttering is seen to be associated with underactivity in Broca's area.
Aphasia
Aphasia is an acquired language disorder affecting all modalities such as writing, reading, speaking, and listening and results from brain damage. It is often a chronic condition that creates changes in all areas of one's life.
Expressive aphasia vs. other aphasias
Patients with expressive aphasia, also known as Broca's aphasia, are individuals who know "what they want to say, they just cannot get it out". They are typically able to comprehend words, and sentences with a simple syntactic structure (see above), but are more or less unable to generate fluent speech. Other symptoms that may be present include problems with fluency, articulation, word-finding, word repetition, and producing and comprehending complex grammatical sentences, both orally and in writing. |
395_15 | This specific group of symptoms distinguishes those who have expressive aphasia from individuals with other types of aphasia. There are several distinct "types" of aphasia, and each type is characterized by a different set of language deficits. Although those who have expressive aphasia tend to retain good spoken language comprehension, other types of aphasia can render patients completely unable to understand any language at all, unable to understand any spoken language (auditory verbal agnosia), whereas still other types preserve language comprehension, but with deficits. People with expressive aphasia may struggle less with reading and writing (see alexia) than those with other types of aphasia. Although individuals with expressive aphasia tend to have a good ability to self-monitor their language output (they "hear what they say" and make corrections), other types of aphasics can seem entirely unaware of their language deficits. |
395_16 | In the classical sense, expressive aphasia is the result of injury to Broca's area; it is often the case that lesions in specific brain areas cause specific, dissociable symptoms, although case studies show there is not always a one-to-one mapping between lesion location and aphasic symptoms. The correlation between damage to certain specific brain areas (usually in the left hemisphere) and the development of specific types of aphasia makes it possible to deduce (albeit very roughly) the location of a suspected brain lesion based only on the presence (and severity) of a certain type of aphasia, though this is complicated by the possibility that a patient may have damage to a number of brain areas and may exhibit symptoms of more than one type of aphasia. The examination of lesion data in order to deduce which brain areas are essential in the normal functioning of certain aspects of cognition is called the deficit-lesion method; this method is especially important in the branch of |
395_17 | neuroscience known as aphasiology. Cognitive science – to be specific, cognitive neuropsychology – are branches of neuroscience that also make extensive use of the deficit-lesion method. |
395_18 | Newer implications related to lesions in Broca's area
Since studies carried out in the late 1970s it has been understood that the relationship between Broca's area and Broca's aphasia is not as consistent as once thought. Lesions to Broca's area alone do not result in Broca's aphasia, nor do Broca's aphasic patients necessarily have lesions in Broca's area. Lesions to Broca's area alone are known to produce a transient mutism that resolves within 3–6 weeks. This discovery suggests that Broca's area may be included in some aspect of verbalization or articulation; however, this does not address its part in sentence comprehension. Still, Broca's area frequently emerges in functional imaging studies of sentence processing. However, it also becomes activated in word-level tasks. This suggests that Broca’s area is not dedicated to sentence processing alone, but supports a function common to both. In fact, Broca's area can show activation in such non-linguistic tasks as imagery of motion. |
395_19 | Considering the hypothesis that Broca's area may be most involved in articulation, its activation in all of these tasks may be due to subjects' covert articulation while formulating a response. Despite this caveat, a consensus seems to be forming that whatever role Broca's area may play, it may relate to known working memory functions of the frontal areas. (There is a wide distribution of Talairach coordinates reported in the functional imaging literature that are referred to as part of Broca's area.) The processing of a passive voice sentence, for example, may require working memory to assist in the temporary retention of information while other relevant parts of the sentence are being manipulated (i.e. to resolve the assignment of thematic roles to arguments). Miyake, Carpenter, and Just have proposed that sentence processing relies on such general verbal working memory mechanisms, while Caplan and Waters consider Broca’s area to be involved in working memory specifically for |
395_20 | syntactic processing. Friederici (2002) breaks Broca's area into its component regions and suggests that Brodmann's area 44 is involved in working memory for both phonological and syntactic structure. This area becomes active first for phonology and later for syntax as the time course for the comprehension process unfolds. Brodmann's area 45 and Brodmann's area 47 are viewed as being specifically involved in working memory for semantic features and thematic structure where processes of syntactic reanalysis and repair are required. These areas come online after Brodmann's area 44 has finished its processing role and are active when comprehension of complex sentences must rely on general memory resources. All of these theories indicate a move towards a view that syntactic comprehension problems arise from a computational rather than a conceptual deficit. Newer theories take a more dynamic view of how the brain integrates different linguistic and cognitive components and are examining |
395_21 | the time course of these operations. |
395_22 | Neurocognitive studies have already implicated frontal areas adjacent to Broca's area as important for working memory in non-linguistic as well as linguistic tasks. Cabeza and Nyberg's analysis of imaging studies of working memory supports the view that BA45/47 is recruited for selecting or comparing information, while BA9/46 might be more involved in the manipulation of information in working memory. Since large lesions are typically required to produce a Broca's aphasia, it is likely that these regions may also become compromised in some patients and may contribute to their comprehension deficits for complex morphosyntactic structures. |
395_23 | Broca's area as a key center in the linking of phonemic sequences |
395_24 | Broca's area has been previously associated with a variety of processes, including phonological segmentation, syntactic processing, and unification, all of which involve segmenting and linking different types of linguistic information. Although repeating and reading single words does not engage semantic and syntactic processing, it does require an operation linking phonemic sequences with motor gestures. Findings indicate that this linkage is coordinated by Broca's area through reciprocal interactions with temporal and frontal cortices responsible for phonemic and articulatory representations, respectively, including interactions with the motor cortex before the actual act of speech. Based on these unique findings, it has been proposed that Broca's area is not the seat of articulation, but rather is a key node in manipulating and forwarding neural information across large-scale cortical networks responsible for key components of speech production. |
395_25 | History
In a study published in 2007, the preserved brains of both Leborgne and Lelong (patients of Broca) were reinspected using high-resolution volumetric MRI. The purpose of this study was to scan the brains in three dimensions and to identify the extent of both cortical and subcortical lesions in more detail. The study also sought to locate the exact site of the lesion in the frontal lobe in relation to what is now called Broca's area with the extent of subcortical involvement.
Broca's patients
Louis Victor Leborgne (Tan)
Leborgne was a patient of Broca's. At 30 years old, he was almost completely unable to produce any words or phrases. He was able to repetitively produce only the word tan. After his death, a neurosyphilitic lesion was discovered on the surface of his left frontal lobe.
Lelong |
395_26 | Lelong was another patient of Broca's. He also exhibited reduced productive speech. He could only say five words, 'yes', 'no', 'three', 'always', and 'lelo' (a mispronunciation of his own name). A lesion within the lateral frontal lobe was discovered during Lelong's autopsy. Broca's previous patient, Leborgne, had this lesion in the same area of his frontal lobe. These two cases led Broca to believe that speech was localized to this particular area.
MRI findings |
395_27 | Examination of the brains of Broca's two historic patients with high-resolution MRI has produced several interesting findings. First, the MRI findings suggest that other areas besides Broca's area may also have contributed to the patients' reduced productive speech. This finding is significant because it has been found that, though lesions to Broca's area alone can possibly cause temporary speech disruption, they do not result in severe speech arrest. Therefore, there is a possibility that the aphasia denoted by Broca as an absence of productive speech also could have been influenced by the lesions in the other region. Another finding is that the region, which was once considered to be critical for speech by Broca, is not precisely the same region as what is now known as Broca's area. This study provides further evidence to support the claim that language and cognition are far more complicated than once thought and involve various networks of brain regions.
Evolution of language |
395_28 | The pursuit of a satisfying theory that addresses the origin of language in humans has led to the consideration of a number of evolutionary "models". These models attempt to show how modern language might have evolved, and a common feature of many of these theories is the idea that vocal communication was initially used to complement a far more dominant mode of communication through gesture. Human language might have evolved as the "evolutionary refinement of an implicit communication system already present in lower primates, based on a set of hand/mouth goal-directed action representations." |
395_29 | "Hand/mouth goal-directed action representations" is another way of saying "gestural communication", "gestural language", or "communication through body language". The recent finding that Broca's area is active when people are observing others engaged in meaningful action is evidence in support of this idea. It was hypothesized that a precursor to the modern Broca's area was involved in translating gestures into abstract ideas by interpreting the movements of others as meaningful action with an intelligent purpose. It is argued that over time the ability to predict the intended outcome and purpose of a set of movements eventually gave this area the capability to deal with truly abstract ideas, and therefore (eventually) became capable of associating sounds (words) with abstract meanings. The observation that frontal language areas are activated when people observe Hand Shadows is further evidence that human language may have evolved from existing neural substrates that evolved for the |
395_30 | purpose of gesture recognition. The study, therefore, claims that Broca's area is the "motor center for speech", which assembles and decodes speech sounds in the same way it interprets body language and gestures. Consistent with this idea is that the neural substrate that regulated motor control in the common ancestor of apes and humans was most likely modified to enhance cognitive and linguistic ability. Studies of speakers of American Sign Language and English suggest that the human brain recruited systems that had evolved to perform more basic functions much earlier; these various brain circuits, according to the authors, were tapped to work together in creating language. |
395_31 | Another recent finding has showed significant areas of activation in subcortical and neocortical areas during the production of communicative manual gestures and vocal signals in chimpanzees. Further, the data indicating that chimpanzees intentionally produce manual gestures as well as vocal signals to communicate with humans suggests that the precursors to human language are present at both the behavioral and neuronanatomical levels. More recently, the neocortical distribution of activity-dependent gene expression in marmosets provided direct evidence that the ventrolateral prefrontal cortex, which comprises Broca's area in humans and has been associated with auditory processing of species-specific vocalizations and orofacial control in macaques, is engaged during vocal output in a New World monkey. These findings putatively set the origin of vocalization-related neocortical circuits to at least 35 million years ago, when the Old and New World monkey lineages split. |
395_32 | Additional images
See also
Lobes of the brain
Progressive nonfluent aphasia
Wernicke's area
Jerome of Sandy Cove
References
External links
"Paul Broca's discovery of the area of the brain governing articulated language", analysis of Broca's 1861 article, on BibNum [click 'à télécharger' for English version].
Articles containing video clips
Cerebrum
Frontal lobe
Neurolinguistics |
396_0 | Remy de Gourmont (4 April 1858 – 27 September 1915) was a French symbolist poet, novelist, and influential critic. He was widely read in his era, and an important influence on Blaise Cendrars and Georges Bataille. The spelling Rémy de Gourmont is incorrect, albeit common.
Life
Gourmont was born at Bazoches-au-Houlme, Orne, into a publishing family from Cotentin. He was the son of Count Auguste-Marie de Gourmont and his countess, born Mathilde de Montfort. In 1866 he moved to a manor close to Villedieu near La Manche. He studied law at Caen, and was awarded a bachelor's degree in law in 1879; upon his graduation he moved to Paris. |
396_1 | In 1881, Gourmont was employed by the Bibliothèque nationale. He began to write for general circulation periodicals such as Le Monde and Le Contemporain. He took an interest in ancient literature, following the footsteps of Gustave Kahn. During this period, he also met Berthe Courrière, model for, and heir of, the sculptor Auguste Clésinger, with whom he formed a lifelong attachment, he and Berthe living together for the rest of their lives. |
396_2 | Gourmont also began a literary alliance with Joris-Karl Huysmans, to whom he dedicated his prose work Le Latin mystique (Mystical Latin). In 1889 Gourmont became one of the founders of the Mercure de France, which became a rallying point of the Symbolist movement. Between 1893 and 1894 he was the co-editor, along with Alfred Jarry, of L'Ymagier, a magazine dedicated to symbolist wood carvings. In 1891 he published a polemic called Le Joujou Patriotisme (Patriotism, a toy) in which he argued that France and Germany shared an aesthetic culture and urged a rapprochement between the two countries, contrary to the wishes of nationalists in the French government. This political essay led to his losing his job at the Bibliothèque Nationale, despite Octave Mirbeau's chronicles. |
396_3 | During this same period, Gourmont was stricken with lupus vulgaris. Disfigured by this illness, he largely retired from public view appearing only at the offices of the Mercure de France. In 1910, Gourmont met Natalie Clifford Barney, to whom he dedicated his Lettres à l'Amazone (Letters to the Amazon).
Gourmont's health continued to decline and he began to suffer from locomotor ataxia and be increasingly unable to walk. He was deeply depressed by the outbreak of World War I and died in Paris of cerebral congestion in 1915. Berthe Courrière was his sole heir, inheriting a substantial body of unpublished work which she sent to his brother Jean de Gourmont, and dying within the year. Gourmont and Courrière are buried Chopins tomb in Père-Lachaise Cemetery. |
396_4 | Works
Gourmont was a literary critic and essayist of great importance, most notably his Le Problème du Style. Created in response to Antoine Albalat's The Art of Writing in Twenty Lessons (1899), Le Problème du Style was a source book for many of the ideas that inspired the literary developments in both England and France and was also admired by T. S. Eliot and Ezra Pound in that capacity.
His novels, in particular Sixtine, explore the theme of Schopenhauerian Idealism with its emphasis on individual subjectivity, as well as the Decadent relationship between sexuality and artistic creativity. In 1922 Aldous Huxley translated Gourmont's novel A Virgin Heart. |
396_5 | Gourmont's poetic works include Litanies de la Rose (1892), Les Saintes du Paradis (1898), and Divertissements (1912). His anthology Hieroglyphes (1894), contains his experiments with the possibilities of sound and rhythm. It plunges from perhaps ironic piety to equally ironic blasphemy, reflecting, more than anything else, his interest in medieval Latin literature, and his works led to a fad for late Latin literature among authors like Joris-Karl Huysmans. Pound observed in 1915 that the English Imagist poetic movement derived from the French Symbolistes, Eliot describing Gourmont as the "critical conscience of his generation".
Bibliography
Poetry
Litanies de la Rose (1892).
Fleurs de Jadis (1893).
Hiéroglyphes (1894).
Les Saintes du Paradis (1899).
Oraisons Mauvaises (1900).
Simone (1901).
Divertissements (1912).
Poésies Inédites (1921).
Rimes Retrouvées (1979).
L'Odeur des Jacynthes (1991). |
396_6 | Fiction
Merlette (novel, 1886).
Sixtine (novel, 1890).
Le Fantôme (1893).
Le Château Singulier (1894).
Proses Moroses (short stories, 1894).
Histoire Tragique de la Princesse Phénissa (1894).
Histoires Magiques (1884).
Le Pèlerin du Silence (1896).
Phocas (1895).
Les Chevaux de Diomède (novel, 1897).
D'un Pays Lointain. Miracles. Visages de Femmes (1898).
Le Songe d'une Femme (novel, 1899).
Une Nuit au Luxembourg (1906).
Un Cœur Virginal (1907).
Couleurs, Contes Nouveaux Suivi de Choses Anciennes (1908).
Lettres d'un Satyre (1913).
Lettres à l'Amazone (1914).
Monsieur Croquant (1918).
La Patience de Grisélidis (1920).
Lettres à Sixtine (1921).
Le Vase Magique (1923).
Fin de Promenade et Trois Autres Contes (short stories, 1925).
Le Désarroi (novel, 2006).
Theatre
Lilith (1892).
Théodat (1893).
Le Vieux Roi (1897).
L'Ombre d'une Femme (1923). |
396_7 | Nonfiction
Un Volcan en Éruption (1882).
Une Ville Ressuscitée (1883).
Bertrand Du Guesclin (1883).
Tempêtes et Naufrages (1883).
Les Derniers Jours de Pompéi (1884).
En Ballon (1884).
Les Français au Canada et en Acadie (1888).
Chez les Lapons, Mœurs, Coutumes et Légendes de la Laponie Norvégienne (1890).
Le Joujou Patriotisme (1891).
Le Latin Mystique. Les Poètes de l'Antiphonaire et la Symbolique au Moyen Âge (with a preface by J. K. Huysmans, 1892).
L'Idéalisme (1893).
L'Ymagier (with Alfred Jarry, 1896).
La Poésie Populaire (1896).
Le Livre des Masques (1896).
Almanach de "L'Ymagier", Zodiacal, Astrologique, Littéraire, Artistique, Magique, Cabalistique et Prophétique (1897).
Le Deuxième Livre des Masques (1898).
Esthétique de la Langue Française (1899).
La Culture des Idées (1900).
Preface to Les Petites Revues (1900).
Le Chemin de Velours (1902).
Le Problème du Style (1902).
Épilogues: Réflexions sur la Vie, 1895-1898 (1903). |
396_8 | Physique de l'Amour. Essai sur l'Instinct Sexuel (1903).
Promenades Littéraires (1904).
Judith Gautier (1904).
Promenades Philosophiques (1905).
Dante, Béatrice et la Poésie Amoureuse. Essai sur l'Idéal Féminin en Italie à la Fin du XIIIe Siècle (1908).
Le Chat de Misère. Idées et Images (1912).
La Petite Ville (1913).
Des pas sur le Sable (1914).
La Belgique Littéraire (1915).
Pendant l'Orage, Bois d'André Rouveyre (1915).
Dans la Tourmente (Avril-juillet 1915) (with a preface by , 1916).
Pendant la Guerre. Lettres pour l'Argentine (with a preface by Jean de Gourmont, 1917).
Les Idées du Jour (1918).
Vol. I: (Octobre 1914-avril 1915).
Vol. II: (Mai 1915-septembre 1915).
Trois Légendes du Moyen Âge (1919).
Pensées Inédites (with a Preface by Guillaume Apollinaire, 1920).
Le Livret de "L'Ymagier" (1921).
Petits Crayons (1921).
Le Puits de la Vérité (1922).
Dernières Pensées Inédites (1924).
Dissociations (1925).
Nouvelles Dissociations (1925). |
396_9 | La Fin de l'Art (1925).
Les Femmes et le Langage (1925).
Deux Poètes de la Nature: Bryant et Emerson (1925).
Le Joujou et Trois Autres Essais (1926).
Lettres Intimes à l’Amazone (1926).
Promenades Littéraires (1929). |
396_10 | In English translation
A Night in the Luxembourg (with preface by Arthur Ransome, 1912).
"A French View of 'Kultur'," The New Republic (1915).
Theodat, a Play (1916).
Philosophic Nights in Paris (1920).
"Dust for Sparrows," Part II, Part III, Part IV, The Dial, Vol. LXIX, 1920; Part V, Part VI, Part VII, Part VIII, Part IX, The Dial, Vol. LXX, 1921.
The Book of Masks (1921).
A Virgin Heart (1921).
Decadence, and Other Essays on the Culture of Ideas (1922).
The Natural Philosophy of Love (1922).
Mr. Antiphilos, Satyr (1922).
Very Woman: A Cerebral Novel (1922).
The Horses of Diomedes (1923).
Epigrams of Remy de Gourmont (1923).
Stories in Yellow, Black, White, Blue, Violet, and Red (1924).
Stories in Green, Zinzolin, Rose, Purple, Mauve, Lilac, and Orange (1924).
Dream of a Woman (1927).
The Prostituted Woman: The Sexless One in the Singular Château (1929).
Letters to the Amazon (1931).
Lilith, a Play (1946).
The Angels of Perversity (1992). |
396_11 | French Decadent Tales, by Stephen Romer (2013). |
396_12 | Quotation
Que tes mains soient bénies, car elles sont impures!
Elles ont des péchés cachés à toutes les jointures;
Leur peau blanche s'est trempée dans l'odeur âpre des caresses
Secrètes, parmi l'ombre blanche où rampent les caresses,
Et l'opale prisonnière qui se meurt à ton doigt,
C'est le dernier soupir de Jésus sur la croix.
---Oraisons mauvaises
References
Further reading |
396_13 | Aldington, Richard (1915). "Remy de Gourmont," The Little Review, Vol. II, No. 3, pp. 10–13.
Aldington, Richard (1919). "Remy de Gourmont," The Living Age, Vol. CCCIII, pp. 665–668.
Aldington, Richard (1919). "Remy de Gourmont, After the Interim," The Little Review, Vol. V, No. 10/11, pp. 32–34.
Aldington, Richard (1928). Remy de Gourmont: A Modern Man of Letters. Seattle: University of Washington Book Store.
Amalric, Jean-Claude (1984). "Shaw, Hamon, and Rémy de Gourmont," Shaw, Vol. 4, pp. 129–137.
Burke, Kenneth (1921). "Approaches to Remy de Gourmont," The Dial, Vol. LXX, pp. 125–138.
Clayton, T. T. (1919). "Le Latin Mystique," The Little Review, Vol. V, No. 10/11, pp. 27–29.
Cornetz, Victor (1922). "Remy de Gourmont, J.H. Fabre and the Ants," The Living Age, Vol. CCCXV, pp. 105–110.
Ellis, Havelock (1915). "Remy de Gourmont," The New Republic, Vol. V, No. 59, pp. 166–167. |
396_14 | Ellis, Havelock (1936). "Remy de Gourmont." In: From Rousseau to Proust. London: Constable & Company, pp. 307–327.
Gosse, Edmund (1922). "Two French Critics: Émile Faguet—Remy de Gourmont." In: Aspects and Impressions. London: Cassell & Company, pp. 203–223.
Greene, Henry Copley (1894). "French Prose Symbolism," The Harvard Monthly, Vol. XVIII, pp. 106–121.
Huneker, James Gibbons (1917). "Remy de Gourmont," The North American Review, Vol. CCV, No. 739, pp. 935–942.
Jacob, Paul Emile (1931). "Remy de Gourmont," Illinois Studies in Language and Literature, Vol. XVI, No. 2, pp. 7–176.
Krutch, Joseph Wood (1928). "The Nihilism of Remy de Gourmont," The Nation, pp. 357–359.
Lowell, Amy (1915). "Remy de Gourmont." In: Six French Poets. New York: The Macmillan Company, pp. 105–146.
Lewisohn, Ludwig (1916). The Poets of Modern France. New York: B.W. Huebsch.
Macy, John (1922). "Remy de Gourmont." In: The Critical Game. New York: Boni & Liveright, pp. 153–159. |
396_15 | Manning, Frederic (1919). "M. De Gourmont and the Problem of Beauty," The Little Review, Vol. V, No. 10/11, pp. 19–27.
Papini, Giovanni (1922). "Remy de Gourmont." In: Four and Twenty Minds. New York: Thomas Y. Crowell Company, pp. 198–207.
Parker, Robert Allerton (1915). "Remy de Gourmont's Criticism of Morality," The Forum, Vol. LV, pp. 593–600.
Pound, Ezra (1916). "Remy de Gourmont," Poetry, Vol. VII, No. 4, pp. 197–202.
Pound, Ezra (1919). "De Gourmont: A Distinction," The Little Review, Vol. V, No. 10/11, pp. 1–19.
Powys, John Cowper (1916). "Remy de Gourmont." In: Suspended Judgements. New York: G. Arnold Shaw, pp. 225–254.
Ransome, Arthur (1913). "Remy de Gourmont." In: Portraits and Speculations. London: Macmillan & Co., pp. 161–186.
Rodker, John (1919). "De Gourmont―Yank," The Little Review, Vol. V, No. 10/11, pp. 29–32.
Symons, Arthur (1919). The Symbolist Movement in Literature. New York: E.P. Dutton & Company. |
396_16 | External links
Works by Remy de Gourmont, at JSTOR
Works by Remy de Gourmont, at Hathi Trust
Selected Poems by Remy de Gourmont (in French)
Les Amateurs de Remy de Gourmont (In French)
Selections (in English) from Le Probléme du Style
Ezra Pound on Remy de Gourmont
Richard Aldington on Remy de Gourmont
1858 births
1915 deaths
People from Orne
19th-century French novelists
20th-century French novelists
French poets
Symbolist novelists
Symbolist poets
Burials at Père Lachaise Cemetery
French male poets
French male novelists
19th-century French male writers
20th-century French male writers |
397_0 | Parkin is a 465-amino acid residue E3 ubiquitin ligase, a protein that in humans and mice is encoded by the PARK2 gene. Parkin plays a critical role in ubiquitination – the process whereby molecules are covalently labelled with ubiquitin (Ub) and directed towards degradation in proteasomes or lysosomes. Ubiquitination involves the sequential action of three enzymes. First, an E1 ubiquitin-activating enzyme binds to inactive Ub in eukaryotic cells via a thioester bond and mobilises it in an ATP-dependent process. Ub is then transferred to an E2 ubiquitin-conjugating enzyme before being conjugated to the target protein via an E3 ubiquitin ligase. There exists a multitude of E3 ligases, which differ in structure and substrate specificity to allow selective targeting of proteins to intracellular degradation. |
397_1 | In particular, parkin recognises proteins on the outer membrane of mitochondria upon cellular insult and mediates the clearance of damaged mitochondria via autophagy and proteasomal mechanisms. Parkin also enhances cell survival by suppressing both mitochondria-dependent and -independent apoptosis. Mutations are associated with mitochondrial dysfunction, leading to neuronal death in Parkinson’s disease and aberrant metabolism in tumourigenesis.
Structure
The precise function of parkin is unknown; however, the protein is a component of a multiprotein E3 ubiquitin ligase complex which in turn is part of the ubiquitin-proteasome system that mediates the targeting of proteins for degradation. Mutations in this gene are known to cause a familial form of Parkinson's disease known as autosomal recessive juvenile Parkinson's disease (AR-JP). Moreover, parkin is described to be necessary for mitophagy (autophagy of mitochondria). |
397_2 | However, how loss of function of the parkin protein leads to dopaminergic cell death in this disease is unclear. The prevailing hypothesis is that parkin helps degrade one or more proteins toxic to dopaminergic neurons. Putative substrates of parkin include synphilin-1, CDC-rel1, cyclin E, p38 tRNA synthase, Pael-R, synaptotagmin XI, sp22 and parkin itself (see also ubiquitin ligase). Additionally, parkin contains a C-terminal motif that binds PDZ domains. Parkin has been shown to associate in a PDZ dependent manner with the PDZ domain containing proteins CASK and PICK1. |
397_3 | Like other members of the RING-between-RING (RBR) family of E3 ligases, parkin possesses two RING finger domains and an in-between-RING (IBR) region. RING1 forms the binding site for E2 Ub-conjugating enzyme while RING2 contains the catalytic cysteine residue (Cys431) that cleaves Ub off E2 and transiently binds it to E3 via a thioester bond. Ub transfer is aided by neighbouring residues histidine His433, which accepts a proton from Cys431 to activate it, and glutamate Glu444, which is involved in autoubiquitination. Together these form the catalytic triad, whose assembly is required for parkin activation. Parkin also contains an N-terminal Ub-like domain (Ubl) for specific substrate recognition, a unique RING0 domain and a repressor (REP) region that tonically suppresses ligase activity. |
397_4 | Under resting conditions, the tightly coiled conformation of parkin renders it inactive, as access to the catalytic RING2 residue is sterically blocked by RING0, while the E2 binding domain on RING1 is occluded by Ubl and REP. Activating stimuli disrupt these interdomain interactions and induce parkin to collapse along the RING1-RING0 interface. The active site of RING2 is drawn towards E2-Ub bound to RING1, facilitating formation of the Ub-thioester intermediate. Parkin activation requires phosphorylation of serine Ser65 in Ubl by serine/threonine kinase, PINK1. Addition of a charged phosphate destabilises hydrophobic interactions between Ubl and neighbouring subregions, reducing autoinhibitory effects of this N-terminus domain. Ser65Ala missense mutations were found to ablate Ub-parkin binding whilst inhibiting parkin recruitment to damaged mitochondria. PINK1 also phosphorylates Ub at Ser65, accelerating its discharge from E2 and enhancing its affinity for parkin. |
397_5 | Although structural changes following phosphorylation are uncertain, crystallisation of parkin revealed a cationic pocket in RING0 formed by lysine and arginine residues Lys161, Arg163 and Lys211 that forms a putative phosphate binding site. Considering that RING0 is unique to parkin and that its hydrophobic interface with RING1 buries Cys431 in inactive parkin, targeting of phosphorylated Ub and/or Ubl towards this binding niche might be critical in dismantling autoinhibitory complexes during parkin activation.
Function
Mitophagy |
397_6 | Parkin plays a crucial role in mitophagy and clearance of reactive oxygen species. Mitophagy is the elimination of damaged mitochondria in autophagosomes, and is dependent on a positive feedback cycle involving synergistic action of parkin and PINK1. Following severe cellular insult, rundown of mitochondrial membrane potential prevents import of PINK1 into the mitochondrial matrix and causes it to aggregate on the outer mitochondrial membrane (OMM). Parkin is recruited to mitochondria following depolarisation and phosphorylated by PINK1, which simultaneously phosphorylates Ub pre-conjugated to mitochondrial membrane proteins. PINK1 and Ub phosphorylation facilitate parkin activation and further assembly of mono- and poly-Ub chains. Considering the proximity of these chains to PINK1, further phosphorylation of Ub at Ser65 is likely, potentiating parkin mobilisation and substrate ubiquitination in a self-reinforcing cycle. |
397_7 | Parkin substrates include mitofusins Mfn1 and Mfn2, which are large GTPases that promote mitochondria fusion into dynamic, tubular complexes that maximise efficiency of oxidative phosphorylation. However, upon mitochondrial damage, degradation of fusion proteins is necessary to separate them from the network via mitochondrial fission and prevent the corruption of healthy mitochondria. Parkin is therefore required before mitophagy as it ubiquinates Mfn1/2, labelling it for proteasomal degradation. Proteomic studies identified additional OMM proteins as parkin substrates, including fission protein FIS, its adaptor TBC1D15 and translocase TOMM20 and TOMM70 that facilitate movement of proteins such as PINK1 across OMM. Miro (or RHOT1/RHOT2) is an OMM protein critical for axonal transport, and may be ubiquitinated and targeted towards proteasomal degradation by parkin. Miro breakdown produced a marked decrease in migration of compromised mitochondria along axons of mouse hippocampal |
397_8 | neurons, reinforcing the importance of parkin in segregating defective mitochondria from their functioning counterparts and limiting the spatial spread of mitochondrial dysfunction, prior to autophagy. |
397_9 | During mitophagy, parkin targets VDAC1, a voltage-gated anion channel that undergoes a conformational change upon mitochondrial membrane depolarisation, exposing a cytosolic domain for ubiquitination. Silencing of VDAC1 expression in HeLa cells significantly reduced parkin recruitment to depolarised mitochondria and their subsequent clearance, highlighting the critical role of VDAC1 as a selective marker of mitochondrial damage and instigator of mitophagy. Following Ub conjugation, parkin recruits autophagy receptors such as p62, TAX1BP1 and CALCOCO2, facilitating assembly of autophagosomes that digest defective mitochondria.
Cell survival |
397_10 | Through activation of NF-κB signalling, parkin enhances survival and protects cells from stress-induced apoptosis. Upon cellular insult, parkin activates the catalytic HOIP subunit of another E3 ligase LUBAC. HOIP triggers assembly of linear Ub polymers on NF-κB essential modulator (NEMO), potentiating transcription of mitochondrial GTPase OPA1. Increased OPA1 translation maintains cristae structure and reduces cytochrome C release from mitochondria, inhibiting caspase-mediated apoptosis. Importantly, parkin activates HOIP with greater potency than other LUBAC-associated factors HOIL-1 and sharpin, meaning that parkin mobilisation significantly enhances tolerance to moderate stressors. |
397_11 | Parkin possesses DNA binding affinity and produces a dose-dependent reduction in transcription and activity of pro-apoptotic factor p53. Transfection of p53 promoter with truncated versions of parkin into SH-SY5Y neurons revealed that parkin directly binds to the p53 promoter via its RING1 domain. Conversely, parkin may be a transcriptional target of p53 in H460 lung cells, where it mediates the tumour suppressor action of p53. Considering its role in mitochondrial homeostasis, parkin aids p53 in maintaining mitochondrial respiration while limiting glucose uptake and lactate production, thus preventing onset of the Warburg effect during tumourigenesis. Parkin further elevates cytosolic glutathione levels and protects against oxidative stress, characterising it as a critical tumour suppressor with anti-glycolytic and antioxidant capabilities.
Clinical significance |
397_12 | Parkinson’s disease
PARK2 (OMIM *602544) is the parkin gene that may cause a form of autosomal recessive juvenile Parkinson disease (OMIM 600116) due to a mutation in the parkin protein. This form of genetic mutation may be one of the most common known genetic causes of early-onset Parkinson disease. In one study of patients with onset of Parkinson disease prior to age 40 (10% of all PD patients), 18% had parkin mutations, with 5% homozygous mutations. Patients with an autosomal recessive family history of parkinsonism are much more likely to carry parkin mutations if age at onset is less than 20 (80% vs. 28% with onset over age 40). |
397_13 | Patients with parkin mutations (PARK2) do not have Lewy bodies. Such patients develop a syndrome that closely resembles the sporadic form of PD; however, they tend to develop symptoms at a much younger age.
In humans, loss-of-function mutations in parkin PARK2 gene have been implicated in 50% of inherited and 15% of juvenile-onset sporadic forms of Parkinson’s disease (PD). While PD is traditionally regarded a late-onset neurodegenerative condition characterised by alpha-synuclein-enriched Lewy bodies, autosomal recessive PD due to parkin mutations is often early onset and lack the ubiquitinated protein deposits pathognomonic for sporadic PD. Parkin-mutant PD could also involve loss of noradrenergic neurons in the locus coeruleus alongside the hallmark degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). However, its symptoms resembles those of idiopathic PD, with patients presenting with resting tremors, postural instability and bradykinesia. |
397_14 | While mitochondria are essential for ATP generation in any eukaryotic cell, catecholaminergic neurons are particularly reliant on their proper function for clearance of reactive oxygen species produced by dopamine metabolism, and to supply high energy requirements of catecholamine synthesis. Their susceptibility to oxidative damage and metabolic stress render catecholaminergic neurons vulnerable to neurotoxicity associated with aberrant regulation of mitochondrial activity, as is postulated to occur in both inherited and idiopathic PD. For example, enhanced oxidative stress in neurons, skeletal muscle and platelets, corresponding with reduced activity of complex I in the electron transport chain were reported in PD patients, while deletions in the mitochondrial genome were found in the SNpc. |
397_15 | In accordance with its critical role in mitochondrial quality control, more than 120 pathogenic, PD-inducing mutations have been characterised on parkin. Such mutations may be hereditary or stochastic and are associated with structural instability, reduced catalytic efficiency and aberrant substrate binding and ubiquitination. Mutations can generally be categorised into three groups, depending on their location. Firstly, those clustered around Zn-coordinating residues on RING and IBR might compromise structural integrity and impair catalysis. A second class of mutations, including Thr240Arg, affect residues in and around the E2 binding site and alter autoinhibition of RING1 by REP. Finally, Cys431Phe and Gly430Asp mutations impair ligase activity at the catalytic site and significantly reduce parkin function. |
397_16 | The discovery of numerous non-mitochondrial parkin substrates reinforces the importance parkin in neuronal homeostasis, beyond its role in mitochondrial regulation. Potent neuroprotective abilities of parkin in attenuating dopaminergic neurotoxicity, mitochondrial swelling and excitotoxicity were demonstrated in cell cultures over-expressing parkin, although the existence of such mechanisms at physiological parkin levels in vivo is yet unconfirmed. Another parkin substrate, synphilin-1 (encoded by SNCAIP), is an alpha-synuclein interacting protein that is enriched in the core of Lewy bodies and ubiquitinated by parkin in a manner abolished by familial PD-associated mutations. Parkin might promote aggregation of alpha-synuclein and synphilin-1 into Lewy bodies, which are conjugated to Lys63-linked poly-Ub chains and directed towards autophagic degradation. Parkin mutations therefore inhibit this mechanism, leading to toxic accumulation of soluble proteins that overloads the |
397_17 | proteasome. Protein aggregation triggers neuronal toxicity, whilst accounting for lack of ubiquitinated Lewy bodies in parkin-mutant PD. Similarly, native parkin reduces death of SH-SY5Y neurons by ubiquitinating other Lewy body constituents, such as the p38 subunit of aminoacyl-tRNA synthetase complex and far upstream element-binding protein 1 through addition of Lys48-linked poly-Ub chains and directing them towards proteasomal degradation. Parkin also influences axonal transport and vesicle fusion through ubiquitination of tubulin and synaptotagmin XI (SYT11) respectively, giving it a modulatory role in synapse function. |
397_18 | Finally, parkin protects dopaminergic neurons from cytotoxicity induced by PD-mimetic 6-OHDA, mediated by suppression of neuronal p53 expression and its downstream activation of the apoptotic cascade. Several PD-associated parkin mutations are localised to RING1 and might impair its ability to bind and downregulate the p53 promoter, leading to enhanced p53 expression. Parkin-mutant PD patients also exhibit a four-fold elevation in p53 immunoreactivity, insinuating that failure of parkin-mediated anti-apoptosis might be involved in etiology of PD.
Tumourigenesis |
397_19 | Consistent with parkin’s potent anti-tumourigenic abilities, negative mutations and deletions have been reported in various tumours. For example, PARK2 copy number was reduced in 85% of glioblastoma samples while lung cancers were associated with heterozygous deletion of PARK2 at 6q25-q27 locus. Parkin deficiency further diminished disease-free survival in infrared-irradiated mice without increasing tumour incidence rate, suggesting that parkin deficiencies increase susceptibility to tumour-promoting events, rather than initiating tumour formation. Similarly, chromosomal breaks in PARK2 suppressed expression of afadin scaffold protein in breast cancer, thereby comprising epithelial integrity, enhancing metastatic potential and worsening overall prognosis. Haploinsufficient PARK2 expression, either due to reduced copy number or DNA hypermethylation, was further detected in spontaneous colorectal cancer where it accelerated all stages of intestinal adenoma development in mouse models. |
397_20 | Parkin is therefore a potent modulator of tumour progression, without directly instigating tumourigenesis. |
397_21 | Interactions
Parkin (ligase) has been shown to interact with:
Alpha-synuclein,
CASK,
CUL1,
FBXW7 and
GPR37,
HSPA1A,
HSPA8,
Multisynthetase complex auxiliary component p38,
PDCD2,
SEPT5,
SNCAIP,
STUB1,
SYT11, and
Ubiquitin C.
References
Further reading
Vanjski linkovi
GeneReviews/NCBI/NIH/UW entry on Parkin Type of Juvenile Parkinson Disease
EC 6.3 |
398_0 | "I Wanna Have Your Babies" is a song by British recording artist Natasha Bedingfield. It was written by Steve Kipner, Andrew Frampton, Wayne Wilkins and Bedingfield for her second album, N.B. (2007). The song's musical-style and production was inspired by hip hop music, and its lyrics discuss a woman's battle to stop herself from rushing into relationships in an effort to find the right man to be the father of her children.
The song was released as the album's first single in the second quarter of 2007. The track received mixed reviews from pop music critics, who generally found it to be less impressive than past singles. It entered the top forty in Germany, Ireland and The Netherlands, and became Bedingfield's fourth United Kingdom top ten single release. Calvin Harris covered it in 2009. |
398_1 | Background and writing
In 2006, Bedingfield began writing and recording material with previous collaborators Steve Kipner, Andrew Frampton and Wayne Wilkins in Los Angeles, California. During one of their sessions, they penned "I Wanna Have Your Babies", which was inspired by a year-and-a-half of touring across the United States. Bedingfield had never been away from her family and friends for an extended period of time and "realised how important relationships are". She wanted to write songs that matched who she was, commenting that her "first album was about independence and opportunism. I’m in a different place now. I've been dating, searching for a partner, looking for Mr Right." |
398_2 | In the song, Bedingfield discusses a woman's fight to stop herself from rushing into relationships in an effort to find the right man to father her children. Bedingfield stated that she does not want to have children at this point in time, but that she is thinking about it. According to her, "the song is about pacing yourself and taking everything slowly." |
398_3 | Critical reception
"I Wanna Have Your Babies" had a polarizing effect on music critics. Channel 4 described it as a "well thought out pop record", and Paul Taylor of the Manchester Evening News said it had a "sing-song melody" and "ragged hip-hop beats". Tony Cummings called the song's "R&B pop confection hugely catchy". Online magazine Drowned in Sound ridiculed the track, writing that it is "polluting the airwaves with its beyond-banal lyrics." The song's music video was also described in the review as "unforgivable". The BBC was equally unimpressed with the song, claiming it stole the melody of The Jackson 5 song "I Want You Back". |
398_4 | Chart performance
"I Wanna Have Your Babies" was officially solicited to radio in the United Kingdom on 12 March 2007. The song was released as a download on 2 April 2007, two weeks before its physical release. It debuted on the UK Singles Chart at number 25 on 8 April 2007, on download sales only. A week after its physical release the song reached the top 10, rising from number 15 to number seven. In Ireland the song debuted at number 36 on the singles chart and peaked at number eight. "I Wanna Have Your Babies" proved popular on Irish radio, charting at number 14. The single had moderate success in Europe. After three weeks on the European Hot 100 Singles chart, the track peaked at number 23. The single reached the top 50 in Italy, the Netherlands and Sweden. In Australia, the song debuted on the singles chart at number 50 on 21 May 2007. The track was more successful on the Physical Singles chart, debuting at number 37.
Music video |
398_5 | The music video was directed by Dave Meyers and filmed in Los Angeles, California in January 2007. The video opens with a scene of Bedingfield working out in a gym with a male instructor. Bedingfield and the instructor are then shown running through a park, when a baby stroller suddenly appears. Frightened, the instructor runs away from Bedingfield and the baby. She is next shown playing tennis and flirting with another man. The two are then shown riding on a boat with a toddler, in a race with another couple. The third scene features Bedingfield at a nightclub flirting with yet another man, before they are shown together at his home. In the final scene, she meets a man working at a coffee shop. They are shown in a play room with multiple babies. The video ends with Bedingfield hugging the coffee shop worker, who appears to be undeterred by her thoughts about having babies. |
398_6 | Nadine Coyle, member of the pop group Girls Aloud, makes a cameo appearance in the nightclub scene. The complete version of "I Wanna Have Your Babies" featured in the music video has been released commercially through CD singles and digital downloads, and some include remixes by Snowflakers. The video debuted on Bedingfield's official Bebo website on 6 March 2007. On 21 May 2007, the video debuted in North America on Bedingfield's official U.S. website under the title "Babies". The music video for "I Wanna Have Your Babies" was mocked in an article written by Anna Pickard and published in The Guardian. Pickard made fun of Bedingfield's "clean-cut, straight-toothed, good Christian girl" image, writing that the video was an effort by Bedingfield and her management to be provocative to sell more records.
Formats and track listings
UK CD single
"I Wanna Have Your Babies"
"Unwritten" (live at the Nokia Theater, New York) |
398_7 | Australian CD single
"I Wanna Have Your Babies"
"What If's"
"Unwritten" (Live at The Nokia Theatre, New York)
"I Wanna Have Your Babies" (Snowflakers remix)
"I Wanna Have Your Babies" (video)
German CD single
"I Wanna Have Your Babies"
"Unwritten" (live at the Nokia Theater, New York)
Digital single
"I Wanna Have Your Babies" (radio promo mix) – 3:38
Official remixes
"I Wanna Have Your Babies" (Kardinal Beats Mix)
"I Wanna Have Your Babies" (Soul Avengerz Mix)
Charts
References
External links
NatashaBedingfield.com – Official website
IWannaHaveYourBabies.com – Official single microsite
2007 singles
2007 songs
Music videos directed by Dave Meyers (director)
Natasha Bedingfield songs
Phonogenic Records singles
Songs about parenthood
Songs about pregnancy
Songs written by Andrew Frampton (songwriter)
Songs written by Natasha Bedingfield
Songs written by Steve Kipner
Songs written by Wayne Wilkins |
399_0 | 1: Nenokkadine () is a 2014 Indian Telugu-language psychological action thriller film directed by Sukumar. T The film was written by Jakka Hariprasad and produced by Ram Achanta, Gopichand Achanta, and Anil Sunkara as 14 Reels Entertainment and distributed by Eros International, the film stars Mahesh Babu and Kriti Sanon who makes her debut. Nassar, Pradeep Rawat and Kelly Dorji appear in supporting roles. Babu's son, Gautham Krishna, made his debut in the film as a younger version of the protagonist.
1: Nenokkadine revolves around the search by Gautham, a schizophrenic Indian rock musician missing 25 per cent of his brain's grey matter, for his parents, whom he believes were murdered by three men. Sameera, a journalist, convinces him that he is an orphan and is hallucinating. When Gautham kills one of the "imaginary" men for his psychological satisfaction, he realises that the dead man is real and leaves for London to find his roots and the other two men behind his parents' death. |
399_1 | Sukumar began working on 1: Nenokkadine script after completing 100% Love (2011), making a bus driver's tale about a boy who claimed that his parents were murdered on his bus the film's base. R. Rathnavelu was the film's director of photography, and Karthika Srinivas, its editor. Devi Sri Prasad composed the soundtrack and background score. 1: Nenokkadine was introduced on 12 February 2012, and principal photography, which began on 23 April 2012, was completed in late October 2013. It was filmed in London, Belfast, Bangkok and Indian cities including Hyderabad, Mumbai, Goa, Chennai and Bangalore. |
399_2 | Produced on a budget of 70 crores, 1: Nenokkadine was released on 10 January 2014 on about 1,500 screens during the Sankranti festival season while the Tamil version titled as Number 1 was released in 2015.
Grossing over $1.327 million, 1: Nenokkadine became the fourth-highest-grossing Telugu film at the United States box office then. The film won three awards from eight nominations at the 4th South Indian International Movie Awards, and two awards at the 11th CineMAA Awards. The film is considered one of the "25 Greatest Telugu Films Of The Decade" by Film Companion.
Plot
Gautham is a schizophrenic Indian rock musician who is missing 25 per cent of his grey matter. He hallucinates a mysterious person he believes is one of the three murderers of his parents. As a child, Gautham was convinced that he was an orphan and assumes that his parents are dead; he does not remember their names or what they looked like. |
399_3 | At one of his concerts, Gautham sees one of the three men and chases him. Sameera, a journalist at the concert, films Gautham fighting his imaginary opponent. Gautham surrenders to the police after "killing" the man, confessing that he killed three men: one in Belfast, one in Pune and one just now in Hyderabad. He is released from custody after Sameera broadcasts the video on television. According to his doctor, if Gautham can hallucinate a person other than the three men, he can be treated. Gautham goes to Goa on vacation. Sameera stalks him, convincing him that two people are stalking him: a journalist who wants to interview him (imaginary), and a person claiming to be his fan (real). Gautham begins to fall in love with Sameera. He saves her from a group of people trying to murder her; on an isolated island together, Gautham learns the truth behind the fourth imaginary person and writes Sameera off as a disturbed journalist. By the time he learns about Sameera's intentions, she has |
399_4 | left for Hyderabad; Gautham pursues her. |
399_5 | In Hyderabad, Gautham accidentally spoils Sameera's birthday plans, infuriating her. Although he is convinced that he has made up an enemy to cope with being an orphan, a mysterious person tries to kill Sameera. Gautham saves her and proposes marriage, which she accepts. Sameera learns that the mysterious person is Antonio Rosarios, a Goa-based crime boss who wants to kill her because she tried to expose the presence of hydrogen cyanide in seeds sold by Rosarios' company, AG1. Gautham meets Rosarios in the lobby of Sameera's office building. Assuming that he is an illusion, he shoots Rosarios in his head. By the time Gautham realises Rosarios is real, he is dead, and Gautham learns that his parents were murdered. He catches an aged taxi driver who was stalking him (one of the three men he imagined), and learns that two London-based Indians (one of whom was Rosarios) killed his parents; his father gave the taxi driver a bag to give to Gautham. In the bag is an old Rubik's Cube, a key |
399_6 | and a British coin. |
399_7 | Gautham and Sameera go to London, where they and their driver Gulaab Singh escape from a murder attempt; Gautham's manager, Michael, is killed. The Rubik's Cube, when solved a certain way, reveals a safe-deposit-box number in which Gautham finds a preserved rice sample. After escaping another murder attempt in a parking lot, he eludes the police and the two men with Sameera and Singh's help. One of the men—a fan—seeks revenge for his father (one of the other murderers, according to the aged taxi driver), who was killed by Gautham in Belfast when he performed there. Gautham learns that the aged taxi driver he met previously is a businessman and the murderer; the person hit by the businessman's car in Gautham's presence was the actual, innocent taxi driver. |
399_8 | Gautham and the businessman confront each other, and the businessman says that he and Gautham's father was an intelligent and shrewd scientist and entrepreneur. The businessman and Gautham's father were childhood best friends and worked in the same company. They worked on cultivating Golden rice, a variety which could grow in any weather. When Gautham's father refused to sell it in favour of distributing it globally for free, the businessman and Rosarios killed his parents. When he refuses to tell Gautham about his parents, Gautham kills him. On his way to the airport, Gautham passes the school he had attended and hears children singing a rhyme. It reminds him of a similar rhyme he learned from his mother, and he remembers his way back to his house. At his house (a dilapidated villa), Gautham finds a photo of his parents, Chandrasekhar and Kalyani. He later introduces the rice variety at a global convention as "the second green revolution", and the film ends with Gautham standing in |
399_9 | his field of Golden rice. |
399_10 | Cast
Mahesh Babu as Gautham
Gautham as young Gautham (cameo appearance)
Kriti Sanon as Sameera
Nassar as an unnamed businessman, Chandrashekar's friend
Kelly Dorji as Antonio Rosarius
Pradeep Rawat Taxi Driver
Anand as entrepreneur Chandrashekhar, Gautham's father
Anu Hasan as Kalyani, Gautham's mother
Sayaji Shinde as Inspector John Baadshah
Posani Krishna Murali as Gulaab Singh
Srinivasa Reddy as Baadshah's subordinate
Naveen Polishetty as Naveen, the taxi driver's son
Ravi Varma as Michael
Surya as Gautham's doctor
Amit Tiwari as actual businessman's henchman
Banerjee as Sameera's boss
Sophie Choudry in the item number "London Babu"
Production |
399_11 | Development
After completing 100% Love (2011), Sukumar began working on a psychological thriller with Mahesh Babu in mind as the protagonist because he felt that Babu had universal appeal. An incident in which a bus driver talked about a young boy who said that his parents were murdered on his bus became the story's base. Babu met Sukumar on the set of Businessman (2012) in Goa, and listened to the script for 25 minutes. Although Sukumar could not describe the story well in the noisy restaurant, Babu agreed to appear in the film within half an hour. Sukumar worked on 1: Nenokkadine script for two months, and considered it his dream project. |
399_12 | Ram Achanta, Gopichand Achanta and Anil Sunkara of 14 Reels Entertainment, who produced Babu's Dookudu (2011) and Aagadu (2014), agreed to produce 1: Nenokkadine after hearing the script. Asked about his frequent collaboration with them, Babu said that Sukumar clearly indicated the risk of budget escalation and longer production and said that he and Sukumar could be viewed as criminals if it was produced by someone else. Sunil Lulla and Andrew Hefferman were credited as co-producers, and Koti Paruchuri was its executive producer. The film, introduced on 12 February 2012 in Hyderabad, received its title in May 2013.
Casting |
399_13 | Babu agreed to be fit and healthy, since the film emphasised action scenes. He followed a 12-week Dynamic Transformation Plan (DTP) supervised by Kris Gethin, developing his abdominal muscles and losing weight. Babu then followed a Yoda Three Training regime (Y3T), supervised by Neil Hill, further developing his muscles. His stylist, Ashwin Malwe, said that his appearance and style would be "sophisticated and classy" in the film. Sukumar had Babu wear eyeglasses, since the director felt that audiences tended to consider a bespectacled character to be perfectionistic and positive, and the actor's hairstyle was changed. |
399_14 | Tamannaah was considered for the female lead, since the producers were impressed with her performance in 100% Love. She declined the offer, citing scheduling conflicts, and the Producer's Council told her not to sign for any new films until she completed her current assignments. After auditioning two actresses, Sukumar chose Kajal Aggarwal in March 2012 as the female lead. She was replaced by Kriti Sanon in October 2012, due to scheduling conflicts. Sanon was signed for Heropanti (2014) after completing one shooting schedule for 1: Nenokkadine, and divided her time between the films. Sanon, who was involved in several action scenes filmed on the sea, was apprehensive about a scene in which Babu took her from a yacht since she did not know how to swim. |
399_15 | Babu's seven-year-old son, Gautham Krishna, was chosen to play the younger version of the protagonist in his Telugu cinema debut. According to Sukumar, Gautham looked like the actor did as a child. When the director approached Babu and his wife, Namrata Shirodkar, Gautham Krishna was only six and they were apprehensive. His introduction scene was filmed silently by Peter Hein, since the boy was afraid of gunfire. Naveen Polishetty played a supporting role as Babu's friend in the film, and Vikram Singh was signed as an antagonist. Nassar, Pradeep Rawat, Kelly Dorji, Sayaji Shinde and Anu Hasan were cast in other supporting roles. |
399_16 | Jacqueline Fernandez was approached to perform an item number in the film, but the producers failed to make a deal and instead signed Sophie Choudry after seeing her performance in "Aala Re Aala" from Shootout at Wadala (2013). For her first Telugu song, Choudry joined the film's set in September 2013. Sukumar said about the item number, "It's a superstar's film and it should reach all. Item numbers are common these days, and people expect to see them. The situation was that Babu had to go to a pub to get information about the person he was looking for. So there was an occasion to put in an item number".
Crew |
399_17 | R. Rathnavelu, who collaborated with Sukumar on Arya (2004) and Jagadam (2007), was the film's director of photography in his return to Telugu cinema after seven years. Rathnavelu called the film "more challenging aesthetically" and compared it to Enthiran (2010), which he considered his technically-toughest film. He created the film's visual style in a week with a variety of cameras, such as Red Epic, Body Rigs, Doggies and an underwater scuba camera. For the climaxes, Rathnavelu shifted from chrome to black-and-white to full colour in synchronisation with the story's mood.
Rathnavelu had to address the protagonist's mood swings and hallucinations, replicating scenes with minor differences. The film was shot in locations with a variety of climates, and new technical crews were hired in those places. Sukumar said, "We looked at world technicians and saw their work and can use whatever we learnt" and called it a "new yet learning experience" . |
399_18 | Sukumar's usual composer, Devi Sri Prasad, was chosen for the film's soundtrack and score in Prasad's first Babu film. He went through the script and discussed it with Sukumar, who felt that Prasad translated his vision in the background score. Prasad finished re-recording the film's second half in four days. Eleven-year-old journalist Smrithika Thuhina's father was an associate director of the film, and Prasad emailed him the rhyme's tune with several stills from the scene; his daughter wrote the lyrics for the rhyme. P. Madhusudhan Reddy was the film's audiographer. |
399_19 | Peter Hein choreographed 1: Nenokkadine action sequences, and Prem Rakshith choreographed its songs. Jakka Hari Prasad and Palnati Surya Pratap worked on the film's story, and Y. K. Arjun, Thota Srinivas and Potluri Venkateswara Rao developed the script. Jeremy Zimmerman was credited with the screenplay, assisted by Sunil Madhav. V. Srinivas Mohan was 1: Nenokkadine visual-effects producer and R. C. Kamalakannan and Adel Adili's visual-effects company, Makuta, worked on the film. Karthika Srinivas was its chief editor, assisted by Siva Saravanan.
Filming |
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