Gotowe bibliografie tematyczne / Motility

Gotowa bibliografia na temat „Motility”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 1 sierpnia 2024

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Artykuły w czasopismach na temat "Motility"

1

Boivin, M., M. Riberdy, M. C. Raymond, L. Trudel i P. Poitras. "Motilin and the postprandial motility of the antrum". Canadian Journal of Physiology and Pharmacology 70, nr 11 (1.11.1992): 1491–95. http://dx.doi.org/10.1139/y92-211.

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This study was designed to establish whether the rise in plasma motilin observed after a meal in humans can influence the postprandial motor activity of the antrum. Antroduodenal postprandial motility profiles and indices obtained from 5 controls and 5 subjects infused with exogenous synthetic motilin (0.1 μg∙kg−1) or with the motilin receptor agonist erythromycin lactobionate (200 mg) were compared. Motilin infusion increased plasma motilin concentrations about 5 times above the physiological range but failed to modify the normal postprandial contractile response. On the other hand, in 4 of the 5 subjects, erythromycin induced an intense motor response that mimicked phase III of the migrating motor complex. Our study demonstrates that, during the postprandial period, motilin antral receptors can be stimulated only with doses of motilin exceeding the physiological plasma concentrations, and that the motor effect obtained did not mimic the usual postprandial motility pattern. Our results, therefore, do not support the proposal that the postprandial motility of the antrum is regulated by the plasma levels of motilin.Key words: antral motility, gastrointestinal hormone, gastrointestinal motility, motilin, regulatory peptide, smooth muscle function.
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Layer, P., A. T. Chan, V. L. Go i E. P. DiMagno. "Human pancreatic secretion during phase II antral motility of the interdigestive cycle". American Journal of Physiology-Gastrointestinal and Liver Physiology 254, nr 2 (1.02.1988): G249—G253. http://dx.doi.org/10.1152/ajpgi.1988.254.2.g249.

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We determined if changes in the irregular motor activity of phase II, the dominant motility phase in awake fasting humans, are associated with fluctuations in pancreatic secretion by intubating the upper gastrointestinal tract of 15 healthy humans and recording antral and duodenal motility and obtaining duodenal samples for one or two interdigestive motility cycles. Antral phase II activity was graded as having low, intermediate, or high frequency of contractions and related to duodenal trypsin output and plasma concentrations of motilin and human pancreatic polypeptide (HPP), a marker of vagal cholinergic tone. Low, intermediate, and high phase II motor activities were significantly associated with trypsin outputs (U/10 min; mean +/- SE) of 576 +/- 137, 1,441 +/- 225, and 3,621 +/- 521, respectively (P less than 0.001). Plasma motilin levels did not vary with the grades of phase II motility (P greater than 0.1), but levels of plasma HPP and the grades of phase II motility were positively correlated (P less than 0.001). The close correlation among motility, pancreatic secretion, and plasma HPP during phase II suggests that vagal cholinergic pathways are involved in the common regulatory mechanism controlling phase II interdigestive motility and pancreatic secretion.
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Malfertheiner, P., M. G. Sarr, M. P. Spencer i E. P. DiMagno. "Effect of duodenectomy on interdigestive pancreatic secretion, gastrointestinal motility, and hormones in dogs". American Journal of Physiology-Gastrointestinal and Liver Physiology 257, nr 3 (1.09.1989): G415—G422. http://dx.doi.org/10.1152/ajpgi.1989.257.3.g415.

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We tested the hypothesis that the duodenum is necessary to coordinate interdigestive pancreatic trypsin secretion with gastrointestinal motility and determined whether duodenectomy altered interdigestive cycles of plasma motilin and pancreatic polypeptide and their relationship to trypsin secretion and motility. Consequently, in normal and duodenectomized dogs, we measured trypsin secretion, gastrointestinal motility, and plasma concentrations of motilin and pancreatic polypeptide during the interdigestive period. After duodenectomy, peaks of trypsin secretion continued to cycle at normal intervals (102 +/- 15 min), but the amounts of trypsin were reduced during peaks of secretion (P = 0.02) and throughout the entire cycle (P = 0.02). Trypsin secretory cycles after duodenectomy, however, were not coordinated with cycles of interdigestive motility, and the plasma concentrations of motilin (P = 0.02) and pancreatic polypeptide (P = 0.05) were reduced and had no cyclic pattern. In addition, we confirmed that duodenectomy alters canine interdigestive antral motility, interrupts coordination between antral and intestinal motility, and shortens the period of jejunal migrating motor complexes. We conclude that duodenectomy disrupts the relationship between the cycles of interdigestive gastrointestinal motility and trypsin secretion and reduces the amount of interdigestive trypsin secretion. These effects of duodenectomy may be due to interruption of the duodenopancreatic neural connections or the hormonal abnormalities we have described. The loss of the cyclic pattern of plasma pancreatic polypeptide after duodenectomy suggests that the duodenum controls the release of pancreatic polypeptide by either a neural or hormonal mechanism.
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Muller, E. L., P. A. Grace, R. L. Conter, J. J. Roslyn i H. A. Pitt. "Influence of motilin and cholecystokinin on sphincter of Oddi and duodenal mobility". American Journal of Physiology-Gastrointestinal and Liver Physiology 253, nr 5 (1.11.1987): G679—G683. http://dx.doi.org/10.1152/ajpgi.1987.253.5.g679.

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The sphincter of Oddi and the duodenum exhibit cyclical activity in phase with the migrating myoelectric complex. Both motilin and cholecystokinin have been shown to modulate gastrointestinal and sphincter of Oddi motility. However, previous studies have not monitored the effects of these hormones on simultaneously recorded sphincter of Oddi and duodenum pressures. The present investigation was undertaken, therefore, to determine the influence of both motilin and cholecystokinin on simultaneously recorded sphincter of Oddi and duodenal motility. In seven anesthetized prairie dogs, a triple-lumen, side-hole, pressure-monitored perfusion catheter was positioned with the proximal port in the sphincter of Oddi and the distal port in the duodenal lumen. Sphincter of Oddi and duodenal motility was recorded before and during 20-min infusions of motilin and cholecystokinin octapeptide (CCK-8) at 1, 10, and 100 ng.kg-1.min-1. Both hormones produced dose-related increases in sphincter of Oddi and duodenal motility. No response was observed with either hormone at 1 ng.kg-1.min-1. At 10 ng.kg-1.min-1, the duodenum was slightly more sensitive to motilin than to CCK-8, while the sphincter of Oddi was equally affected by both hormones. At 100 ng.kg-1.min-1, both hormones stimulated the sphincter of Oddi and the duodenum equally. These data indicate that in the prairie dog, both motilin and cholecystokinin stimulate sphincter of Oddi and duodenal motility.
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Sakahara, Satoshi, Zuoyun Xie, Kanako Koike, Satoya Hoshino, Ichiro Sakata, Sen-ichi Oda, Toku Takahashi i Takafumi Sakai. "Physiological characteristics of gastric contractions and circadian gastric motility in the free-moving conscious house musk shrew (Suncus murinus)". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, nr 4 (październik 2010): R1106—R1113. http://dx.doi.org/10.1152/ajpregu.00278.2010.

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Although many studies have demonstrated the physiological action of motilin on the migrating motor complex, the precise mechanisms remain obscure. To obtain new insights into the mechanisms, we focused on the house musk shrew ( Suncus murinus, suncus used as a laboratory name) as a small model animal for in vivo motilin study, and we studied the physiological characteristics of suncus gastrointestinal motility. Strain gauge transducers were implanted on the serosa of the gastric body and duodenum, and we recorded gastrointestinal contractions in the free-moving conscious suncus and also examined the effects of intravenous infusion of various agents on gastrointestinal motility. During the fasted state, the suncus stomach and duodenum showed clear migrating phase III contractions (intervals of 80–150 min) as found in humans and dogs. Motilin (bolus injection, 100–300 ng/kg; continuous infusion, 10–100 ng·kg−1·min−1) and erythromycin (80 μg·kg−1·min−1) induced gastric phase III contractions, and motilin injection also increased the gastric motility index in a dose-dependent manner ( P < 0.05, vs. saline). Pretreatment with atropine completely abolished the motilin-induced gastric phase III contractions. On the other hand, in the free-feeding condition, the suncus showed a relatively long fasting period in the light phase followed by spontaneous gastric phase III contractions. The results suggest that the suncus has almost the same gastrointestinal motility and motilin response as those found in humans and dogs, and we propose the suncus as a new small model animal for studying gastrointestinal motility and motilin in vivo.
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Ayutama, Wanodia, Tuty Rizkianti i Cut Fauziah. "HUBUNGAN JUMLAH LEUKOSIT DENGAN MOTILITAS SPERMATOZOA PADA ANALISIS SEMEN PRIA DI SAMMARIE FAMILY HEALTHCARE 2019". Jurnal Muara Sains, Teknologi, Kedokteran dan Ilmu Kesehatan 4, nr 2 (29.10.2020): 335. http://dx.doi.org/10.24912/jmstkik.v4i2.7788.

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Infertility is one of the most common male reproductive health problems. Male infertility is the inability of a male to result pregnancy in a fertile female in one year of non-contracepting sexual intercourse. Male with poor sperm quality are more susceptible to infertility. One of the cause of infertility in men is disruption of spermatozoa motility. Imperfect motility will reduce the quality of spermatozoa and the probability of conception. One cause of decreased motility is inflammation of the male reproductive tract. Inflammation that occurs will increase the recruitment of leukocytes in the reproductive tract and increase the production of reactive oxygen species (ROS) so it can interfere the process of sperm formation and maturation. The purpose of this study was to determine the relationship between leukocyte counts and spermatozoa motility. The number of leukocytes and the percentage of spermatozoa motility were obtained from semen analysis as secondary data. The research design used was cross-sectional. The number of samples in this study were 66 respondents who met the inclusion criteria.The results of the study showed a significant inverse relationship (negative correlation) (p = 0.007, r = -0.328) between the number of leukocytes and spermatozoa motility, which means if the number of semen leukocytes increases, the percentage of spermatozoa motility will decrease. Keywords: inflammation; leukocyte counts; spermatozoa motility ABSTRAKInfertilitas merupakan salah satu masalah kesehatan reproduksi pria yang sering dijumpai. Infertilitas pada pria adalah ketidakmampuan seorang pria untuk menyebabkan kehamilan pada seorang wanita fertil setelah satu tahun hubungan seksual tanpa alat kontrasepsi. Pria dengan kualitas sperma yang kurang baik lebih rentan mengalami infertilitas. Salah satu penyebab infertilitas pada pria adalah gangguan pada motilitas spermatozoa. Motilitas yang kurang sempurna akan menyebabkan penurunan kualitas spermatozoa dan penurunan probabilitas terjadinya pembuahan. Salah satu penyebab penurunan motilitas adalah inflamasi pada saluran reproduksi pria. Inflamasi yang terjadi akan meningkatkan rekruitmen leukosit pada saluran reproduksi pria dan meningkatkan produksi reactive oxygen species (ROS) yang bersifat toksik bagi spermatozoa sehingga dapat mengganggu proses pembentukan dan pematangan spermatozoa. Tujuan penelitian ini adalah untuk mengetahui hubungan antara jumlah leukosit dengan motilitas spermatozoa. Jumlah leukosit dan persentase motilitas spermatozoa didapatkan dari data sekunder, yaitu data hasil analisis semen. Desain penelitian yang digunakan adalah potong lintang (cross-sectional). Jumlah sampel dalam penelitian ini sebanyak 81 pasien yang memenuhi kriteria inklusi. Hasil dari penelitian menunjukkan terdapat hubungan terbalik (korelasi negatif) yang bermakna dengan kekuatan korelasi sangat lemah (p = 0.007, r = -0.328) antara jumlah leukosit dengan motilitas spermatozoa, yang berarti jika jumlah leukosit semen semakin meningkat, maka persentase motilitas spermatozoa akan semakin rendah.
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Chung, S. A., G. R. Greenberg i N. E. Diamant. "Relationship of postprandial motilin, gastrin, and pancreatic polypeptide release to intestinal motility during vagal interruption". Canadian Journal of Physiology and Pharmacology 70, nr 8 (1.08.1992): 1148–53. http://dx.doi.org/10.1139/y92-159.

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Experiments were performed to determine how postprandial motilin, gastrin, and pancreatic polypeptide plasma concentrations measured during vagal blockade relate to coincident small intestinal motility patterns. Feeding produced a postprandial pattern of intestinal motility coincident with a sustained increase in gastrin and pancreatic polypeptide and a decline in motilin plasma concentrations. Vagal blockade replaced the fed pattern with one similar to migrating motor complex (MMC) activity. Highest motilin plasma concentrations were observed during phase III of this MMC-like activity, as occurs in the fasted state. Vagal blockade reduced but did not abolish the postprandial increase in plasma gastrin and pancreatic polypeptide concentrations. Termination of vagal cooling produced a decline in motilin and an elevation in gastrin and pancreatic polypeptide concentrations, coincident with the return of the fed pattern. In conclusion, during vagal blockade in the fed state (i) motilin, but not gastrin or pancreatic polypeptide plasma concentrations, fluctuate with the MMC-like activity, and any measurement of motilin concentrations under these circumstances must be interpreted on the basis of gut motility patterns, and (ii) gastrin and pancreatic polypeptide concentrations are marginally elevated, but these changes are not enough to disrupt the MMC or have any motor effect. Lastly, the fed pattern and the postprandial changes in motilin, gastrin, and pancreatic polypeptide concentrations are in part dependent upon intact vagal pathways.Key words: gastrointestinal motility, vagus, motilin, gastrin, pancreatic polypeptide.
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Nahdiyah, Ayu Naila, Hari Santoso i Hasan Zayadi. "Pengaruh Fraksi Ejakulasi terhadap Motilitas Spermatozoa Kambing Peranakan Etawa (Capra aegagrus)". BIOSAINTROPIS (BIOSCIENCE-TROPIC) 5, nr 2 (10.01.2020): 72–76. http://dx.doi.org/10.33474/e-jbst.v5i2.288.

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The ejaculation fraction on Etawa crossbred goat (PE goat) has various standard spermatozoa qualitues, one of which ismotility of spermatozoa. The motility of spermatozoa is very important to note in the development of artificial insemination techniques, because the success in artificial insemination techniques is strongly influenced by the motility of spermatozoa. The motility of semen spermatozoa is known through the process of examining the movement of spermatozoa in microscopic testing. The aim of this research was find out the effect of ejaculation fraction on motility of PE goat spermatozoa. Using an experimental method with a group's random consisting of two treatment groups; K1 is fraction 1and K2 is a fraction 2. The Replication of each treatment was eight replications and a total of sample research was 16 unit. The semen was collected once a week using artificial vagina (VA) technique. The semen collecting until the second ejaculation and motility test of spermatozoa were immediately measured use sperm vision analyzers IVOS II. The test results of the ejaculation fraction observation using an independent sample t-test showed the value of t hit = 0.700 and t (0.025) than 2.14 t hit <t (0.025) meaning that H0 was received, there was no significant ejaculation fraction 1 with ejaculatory fraction 2; motility meaning of the spermatozoa from the PE goat of a fraction 1 and faction 2 not different significantly. Keywords: ejaculation fraction, motility of Spermatozoa, PE goat. ABSTRAK Fraksi Ejakulasi pada Kambing Peranakan Etawa (PE) mempunyai kualitas spermatozoa dengan berbagai standart, salah satunya motilitas spermatozoa. Motilitas Spermatozoa menjadi hal yang sangat penting untuk diperhatikan dalam pengembangan teknik Inseminasi Buatan, karena keberhasilan dalam teknik Inseminasi Buatan sangat dipengaruhi oleh motilitas yang dimiliki spermatozoa. Motilitas spermatozoa semen diketahui melalui proses pemeriksaan daya gerak spermatozoa dalam uji mikroskopis. Penelitian ini bertujuan untuk mengetahui pengaruh fraksi ejakulasi terhadap motilitas spermatozoa kambing PE. Menggunakan metode percobaan dengan rancangan acak kelompok (RAK) terdiri atas 2 kelompok perlakuan yakni Kelompok 1 (K1) adalah fraksi 1dan kelompok 2 (K2) adalah fraksi 2, ulangan masing-masing perlakuan 8 ulangan dan unit penelitian berjumlah 16. Penampungan semen dilakukan satu kali seminggu dengan teknik AV (Artificial Vagina). Penampungan dilakukan sampai ejakulat kedua. Segera setelah penampungan dilakukan pengukuran uji motilitas spermatozoa menggunakan sperm vision analyser IVOS II. Hasil uji pengamatan fraksi ejakulasi menggunakan t-test independent sample menunjukkan nilai t hit= 0,700 dan t (0,025)= 2,14 maka t hit < t (0,025) artinya H0 di terima, yang mempunyai arti motilitas spermatozoa kambing PE dari fraksi 1 dan fraksi 2 tidak berbeda nyata. Kata kunci: fraksi ejakulasi, motilitas spermatozoa, kambing PE
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Kellow, John E., i Yiu-Kay Chan. "Advanced motility and motility disorders". Current Opinion in Gastroenterology 11, nr 2 (marzec 1995): 106–11. http://dx.doi.org/10.1097/00001574-199503000-00003.

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Peeters, T. L., J. Janssens, C. Plets i G. Vantrappen. "Interdigestive Motility and Motilin in Hypophysectomized Patients". Scandinavian Journal of Gastroenterology 23, nr 1 (styczeń 1988): 71–74. http://dx.doi.org/10.3109/00365528809093850.

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Rozprawy doktorskie na temat "Motility"

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Cao, Luyan. "bases structurales de la motilité des kinésines". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS267/document.

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Les kinésines sont des protéines moteur liées au cytosquelette de microtubules. Elles convertissent l’énergie provenant de l’hydrolyse de l’ATP en un travail mécanique. Leur fonction typique est de se déplacer le long du microtubule pour véhiculer des charges. La plupart des kinésines sont des dimères. Elles comprennent un domaine moteur, qui porte à la fois les sites de liaison du nucléotide et du microtubule, un domaine intermédiaire de dimérisation et une partie dite « queue » qui confère la spécificité des charges à transporter. Mon objectif est d’établir le mécanisme moléculaire à la base de la motilité, avec un intérêt particulier pour la détermination des variations structurales du domaine moteur de la kinésine le long de son cycle mécano-chimique. Au cours de ma thèse, mon objet d’étude principal a été la kinésine-1 humaine, encore appelée kinésine conventionnelle.J’ai étudié plus particulièrement deux aspects du cycle mécano-chimique de la kinésine-1, en combinant des approches de biologie structurale et l’étude de mutants. Les deux aspects concernent l’étude de la fixation de la kinésine-ADP au microtubule, conduisant à l’éjection du nucléotide et à une liaison forte de la kinésine au microtubule. Dans un premier temps, j’ai déterminé la structure du domaine moteur de la kinésine-1, dépourvue de nucléotide, et sous forme d’un complexe avec la tubuline. La tubuline est la protéine constitutive des microtubules. Cette structure était la donnée principale qui nous manquait dans le cycle structural de la kinésine. En comparant cette structure avec celle de la kinésine dans un état ATP, on peut rendre compte des changements de conformation de la kinésine selon le mouvement de trois sous-domaines du domaine moteur. Cette analyse explique notamment le lien entre la fixation de l’ATP et l’ouverture d’une poche hydrophobe distante de 28 Å du site du nucléotide. Cette cavité va accommoder le premier résidu du neck linker, conduisant à la stabilisation de ce peptide situé en partie C-terminale du domaine moteur. En s’ordonnant, le neck linker va faire avancer la charge ainsi que l’autre domaine moteur de la kinésine dimérique. Il lie ainsi la fixation de l’ATP au mouvement. L’étude de l’effet de mutations du neck linker montre aussi comment, réciproquement, le neck linker bloque la kinésine dans la conformation active pour l’hydrolyse de l’ATP. Ceci diminue la probabilité que l’ATP soit hydrolysé avant que l’étape mécanique se soit produite; cet aspect est essentiel pour rendre compte de la processivité de la kinésine-1.Ces données structurales suggèrent également comment la fixation de la kinésine-ADP au microtubule accélère l’éjection de l’ADP. Pour étudier cet aspect plus en détail, j’ai étudié l’effet de mutations sur la vitesse de largage de l’ADP. L’idée était de mimer à l’aide de mutations la fixation au microtubule. J’ai identifié ainsi deux séries de mutants qui présentent une vitesse accélérée de largage spontané de l’ADP, ce qui suggère deux voies pour interférer avec la fixation du nucléotide. J’ai ensuite déterminé la structure de deux de ces mutants dépourvus de nucléotide, ainsi que celle de la kinésine de départ également dans une forme apo, obtenue par digestion de l’ADP. En absence de microtubule, la kinésine dépourvue de nucléotide adopte une conformation soit à l’image de celle de la kinésine-ADP, ou proche de celle de la kinésine-apo liée à la tubuline. Dans un contexte naturel, seule la deuxième conformation est compatible avec la fixation au microtubule. L’ensemble de ces résultats suggère que le microtubule accélère l’éjection du nucléotide par un double mécanisme : en interférant avec la liaison du magnésium et en déstabilisant le motif P-loop de liaison du nucléotide
Kinesins are a family of microtubule-interacting motor proteins that convert the chemical energy from ATP hydrolysis into mechanical work. Many kinesins are motile, walking along microtubules to fulfill different functions. Most kinesins are dimers, the monomer comprising a motor domain, a dimerizing stalk domain, and a tail domain. The motor domain contains both the nucleotide-binding site and the microtubule-binding site. I am interested in the molecular mechanism of kinesin's motility. In particular I want to establish the structural variations of the kinesin motor domain along with the mechanochemical cycle of this motor protein. During my thesis, I have focused my work on the human kinesin-1, also named conventional kinesin, which is the best characterized kinesin.I have studied two aspects of the kinesin mechanochemical cycle, by combining structural and mutational approaches. Both aspects rely on the binding of ADP-kinesin to a microtubule, which leads to the release of the nucleotide and to a tight kinesin-microtubule association. First I determined the crystal structure of nucleotide-free kinesin-1 motor domain in complex with a tubulin heterodimer, which is the building block of microtubule. This structure represented the main missing piece of the structural cycle of kinesin. Three subdomains in the kinesin motor domain can be identified through the comparison of my structure with ATP-analog kinesin-1-tubulin structure. The relative movements of these subdomains explain how ATP binding to apo-kinesin bound to microtubule triggers the opening of a hydrophobic cavity, 28 Å distant from the nucleotide-binding site. This cavity accommodates the first residue of the “neck linker”, a short peptide that is C-terminal to the motor domain, allowing the neck linker to dock on the motor domain. The docking of the neck linker is proposed to trigger the mechanical step, i.e. the displacement of the cargo and the stepping of the dimeric kinesin. By studying mutants of the neck linker, I have shown that, reciprocally, this peptide locks kinesin in the ATP state, which is also the conformation efficient for ATP hydrolysis. Doing so, it prevents the motor domain from switching back to the apo-state. It prevents also an untimely hydrolysis of ATP, before the mechanical step has occurred. These features are required for movement and processivity.Second, these structural data also suggest how the binding of ADP-kinesin to tubulin enhances nucleotide release from kinesin. To further study this step of the kinesin cycle, I studied the effect of kinesin-1 mutations. These mutations were designed in isolated kinesin to mimic the state when kinesin is bound to a microtubule. I identified two groups of mutations leading to a high spontaneous ADP dissociation rate, suggesting that there are two ways to interfere with ADP binding. Then I determined the crystal structures of the apo form of two mutants as well as that of the nucleotide-depleted wild type kinesin. It showed that apo-kinesin adopts either and ADP-like conformation or a tubulin-bound apo-like one. In the natural context, the second one is stabilized upon microtubule binding. Overall, the mutational and structural data suggest that microtubules accelerate ADP dissociation in kinesin by two main paths, by interfering with magnesium binding and by destabilizing the nucleotide-binding P-loop motif
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2

Gholami, Azam. "Actin-based motility". Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-72151.

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Patankar, RoySuneel V. "Studies in gallbladder motility". Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296188.

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Ullah, Sana. "Factors governing gastrointestinal motility". Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:7166.

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Introduction: The reasons for the rapid resolution of diabetes (DM) following bariatric surgery in a significant proportion of patients with morbid obesity remain unclear. This thesis investigates the putative role of changes in gastrointestinal (GI) motility and GI hormones as well as the possible significance of alterations in energy expenditure that occur as a consequence of weight loss. Methodology: My preliminary studies involved a systematic review of GI motility in obesity, and retrospective studies measuring GI motility with alternative methods including capsule endoscopy and hydrogen breath test. Subsequent to this I measured changes in GI motility in two very different patient cohorts; one following bariatric surgery for morbid obesity and the other a group of patients with proven gastroparesis treated with gastric neuromodulation (GNM). Parallel to the above I conducted studies of indirect calorimetry in these patients in an attempt to determine if changes in energy expenditure which occur as a consequence of weight loss were significant. Results: In our prospective study temporary GNM significantly improved gastric emptying and nutritional intake. There was conclusive evidence to causally relate alterations in GI motility and Glucagon like peptide -1 (GLP-1) with weight loss and resolution of DM following bariatric surgery. An interesting "spin off" result of my studies was validation of capsule endoscopy (CE) as a means of assessing GI motility. My results obtained from measure if indirect calorimetrty clearly show that standard equations tend to over estimate the energy requirements of this group. The implications of this are discussed. Conclusions: 1. Fast pouch emptying; an early and exaggerated GLP-1 response contributes in resolution of type 2 diabetes following RYGB. 2. GNM is an effective treatment for gastroparesis. 3. Capsule endoscopy may be used to assess GI motility. 4. Prediction equations over estimate energy requirements in morbidly obese patients.
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Stanley, Hugh Gerard. "Neural mechanisms in abomasal motility". Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/30009.

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Ross, Oliver N. "Algal motility in variable turbulence". Thesis, University of Southampton, 2004. https://eprints.soton.ac.uk/45995/.

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Biondini, Marco. "RALlying through cell motility and invasion". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T042.

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La formation des métastases est un processus en plusieurs étapes à travers lequel les cellules néoplasiques se détachent de la tumeur primaire pour constituer des tumeurs secondaires à distance. Les capacités à migrer et à envahir, des cellules tumorales sont cruciales dans la cascade métastatique. Selon le type cellulaire et les stimuli présents dans le microenvironnement tumoral, les cellules peuvent se déplacer collectivement ou individuellement selon un programme de migration mésenchymateuse ou amiboïde. Différentes voies de signalisation sont liées à la régulation de la motilité cellulaire. Les GTPases Rho (Rac1, Cdc42 et RhoA) contrôlent la migration en régulant la dynamique du cytosquelette d’actine, la contraction acto-myosine et les microtubules. Rac1 régule la motilité mésenchymateuse en favorisant la formation des lamellipodes via un complexe multiprotéique, le « Wave Regulatory Complex (WRC) » et RhoA contrôle la motilité amiboïde en favorisant la contraction du cytosquelette d'acto-myosine. Les protéines Ral (RalA et RalB) appartenant à une autre famille de petites G, ont été récemment impliquées dans la régulation de la migration cellulaire. RalB, à travers le complexe « Exocyst » joue un rôle essentiel dans la motilité. Dans ce travail de thèse, nous avons étudié les mécanismes moléculaires par lesquels la voie RalB/Exocyste contrôle la motilité et l'invasion cellulaire. La première partie de ce travail démontre que l’Exocyste interagit avec SH3BP1, une protéine GAP (GTPase Activating Protein) (projet 1). Nous montrons que l’interaction entre SH3BP1 et Rac1 est nécessaire à l’activité de Rac1 au front de migration. Dans le projet 2, nous montrons que l’Exocyste interagit directement avec WRC, ce qui est un élément clé de la polymérisation de l'actine. Cette interaction est nécessaire à la localisation du complexe WRC au front de migration où il contrôle la formation de protrusions membranaires. Dans de nombreux carcinomes, la transition épithélio-mésenchymateuse (EMT) joue un rôle important dans la promotion de la migration, l’invasion et la formation des métastases. Le projet 3 a permis de mieux caractériser la plasticité de migration et l’invasion des cellules cancéreuses post-EMT et d’étudier la contribution de Ral dans l'invasion des cellules post-EMT. Nous montrons qu’après l’EMT les cellules envahissent la matrice individuellement ? en utilisant la contraction du cytosquelette d'acto-myosine. Nous montrons que RalB est nécessaire à l’invasion des cellules post-EMT, et à la contractilité cellulaire. Nous proposons que le rôle de RalB dans l'invasion passe par GEF-H1 qui est une protéine GEF (Guanine Nucleotide Exchange Factor) de Rho associée à l’Exocyste. Dans la dernière partie de ce manuscrit, nous présentons le logiciel « AVeMap » que nous avons développé afin d’automatiser la quantification des paramètres de la migration cellulaire.En résumé, dans ce travail de thèse nous montrons que la voie Ral/Exocyste est un organisateur moléculaire nécessaire à l’exécution à la fois de la motilité cellulaire contrôlée par Rac1 et à la motilité contrôlée par Rho
Metastasis is a multistep process by which cancer cells migrate away from the primary neoplastic mass to give rise to secondary tumors at distant sites. Thus, the acquisition of motility and invasive traits by tumor cells is a crucial step for metastasis to occur. Depending on the cell type and the environment, cells can move collectively keeping stable cell-cell contacts or as individual cells, which translocate by exploiting either mesenchymal or amoeboid motility programs.Different molecules and pathways have been linked to the regulation of cell motility. Rho small GTPases (Rac1, Cdc42 and RhoA) control cell migration through their actions on actin assembly, actomyosin contractility and microtubules. Rac1 drives mesenchymal-type motility by promoting lamellipodia formation via the Wave Regulator Complex (WRC). On the contrary, amoeboid motility is governed by RhoA which promotes cell movement via the generation of actomyosin contractile force. Another family of small GTPases, the Ral proteins, was recently involved in the regulation of cell migration. RalB, through the mobilization of its main effector the Exocyst complex, was shown to play an essential role in cell motility. In this work of thesis we investigated the molecular mechanisms through which RalB/Exocyst pathway controls cell motility and invasion.In the first part of this manuscript we show that Exocyst interacts with the RacGAP SH3BP1 (project 1). In mesenchymal moving cells Exocyst/SH3BP1 interaction is required to organize membrane protrusion formation by spatially regulating the activity of Rac1 at the cellular front. In addition, in project 2, we show that the Exocyst binds to the wave regulator complex (WRC), a key promoter of actin polymerization. We provide evidences for Exocyst to be involved in driving the WRC to the leading edge of motile cells, where it can stimulate actin polymerization and membrane protrusions. Reactivation of a developmental program termed epithelial-mesenchymal transition (EMT) was recently shown to promote motility, invasion and metastasis of neoplastic cells. Tumor cells undergoing EMT loose cell-cell contacts acquire a fibroblastoid phenotype and invade the surrounding tissues as individual cells. In project 3 we characterized the invasion plasticity of cancer cells after EMT and we investigated the molecular contribution of Ral to post-EMT invasion. We showed that upon EMT cells disseminate individually in a Rho-driven fashion exploiting the generation of actomyosin force to deform the extracellular matrix. We document that RalB silencing severely impairs actomyosin contractility and dissemination of post-EMT cells. We hypothesize that RalB regulates invasion by controlling the dynamics of the Rho pathway via the Exocyst-associated RhoGEF GEF-H1 in post-EMT cells. Finally, in the last part of this thesis manuscript, we present the PIV-based “AVeMap” software which has been developed to quantify in a fully automated way cell migration and its parameters (Project 4).Taken together the results presented in this thesis manuscript point out the Ral/Exocyst pathway as a key molecular organizer of the execution of both Rac1- and Rho-driven motility programs
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Chemeris, Angelina. "Régulation du suppresseur d'invasion Arpin par les Tankyrases". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLX073.

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Le complexe Arp2/3, conservé sur le plan évolutif, joue un rôle central dans la nucléation d’actine branchée, qui entraîne la migration cellulaire, l’endocytose et d’autres processus cellulaire. Récemment, une petite protéine, Arpin, qui inhibe le complexe Arp2/3 au front du lamellipode a été découverte et caractérisée. Sur sa partie C-terminale, Arpin possède un motif acide (A), qui est homologue au motif A des différents NPF (Nucleation Promoting Factor). Il a été prédit qu’Arpin peut se lier à deux sites de liaison au complexe Arp2/3, similaire aux domaines VCA des NPF. Ici, nous utilisons la microscopie électronique de particules uniques pour obtenir une reconstruction 3D du complexe Arp2/3 lié à Arpin, à une résolution de 25 Å. Nous avons montré que la liaison d’Arpin induit la conformation ouverte, standard, du complexe Arp2/3. Nous avons confirmé qu’il y a deux sites de liaison sur le complexe Arp2/3 pour Arpin : un à l’arrière de la sous-unité Arp3, et le second localisé entre les sous-unités Arp2 et ARPC1. La distance entre le complexe Arp2/3 et Arpin (5nm) confirme qu’Arpin interagit avec son partenaire via sa queue acide C-terminale non structurée.Nous avons, ensuite, identifié Tankyrases1/2, comme un nouveau partenaire qui se lie à Arpin, par « pull-down ». De façon intéressante, les sites de liaisons d’Arpin aux Tankyrases et à Arp2/3 se chevauchent. Nous avons, par conséquent, démontré qu’il y a une compétition dose-dépendante entre le domaine ARC4 de Tankyrase1 et le complexe Arp2/3.Pour comprendre les principes de l’interaction entre Arpin et Tankyrases, nous avons créé un mutant d’Arpin (ArpinG218D) qui, in vitro, se lie toujours au complexe Arp2/3, mais plus aux Tankyrases. In vivo, ArpinG218D n’est pas capable d’inhiber le complexe Arp2/3, ce qui suggère que Tankyrase pourrait être nécessaire pour l’interaction entre Arpin et le complexe Arp2/3. Arpin est le facteur responsable du changement de direction des cellules migrantes. Nous avons donc analysé, la migration de cellules MCF10A exprimant soit la forme sauvage d’Arpin (ArpinWT) soit son mutant ArpinG218D en parallèle de la déplétion d’Arpin endogène. Les cellules exprimant ArpinG218D ont une persistance de migration supérieure, similaire à celles déplétées d’Arpin endogène. Nous avons, ainsi, fait l’hypothèse que le mutant ArpinG218D ne peut pas inactiver le complexe Arp2/3 car il n’est pas présent au niveau du lamellipode. Nous avons donc comparé la quantité de protéine d’ArpinWT et d’ArpinG218D dans la fraction membranaire de cellules migrantes. Une différence significative (44%) dans la quantité d’ArpinWT et d’ArpinG218D a confirmé notre hypothèse.Les Tankyrases sont des cibles thérapeutiques dans de nombreux cancers, mais il n’existe pas de modèle structural pour ces protéines grandes et flexibles. Dans ce travail, nous avons, pour la première fois, obtenu deux reconstructions 3D de Tankyrase1 et Tankyrase2 complètes liées à Arpin en utilisant la microscopie électronique de particules uniques. La résolution obtenue (27 Å) a été suffisante pour détecter un changement de conformation dramatique des domaines SAM et PARP de Tankyrase après fixation d’Arpin. Dans notre reconstruction, trois molécules d’Arpin se lient aux domaines ARC1, ARC4 et ARC5 de Tankyrase1. ARC5 a été montré pour être la partie le plus flexible de l’ensemble des domaines ARC.Grâce aux données que nous avons obtenues, nous avons suggéré un modèle de régulation de l’activité d’Arpin par les Tankyrases. Selon notre modèle, les Tankyrases se lient à Arpin dans le cytoplasme, changent sa conformation et amènent Arpin au niveau de la membrane dans le lamellipode. Traduisant les signaux extracellulaires, la GTPase Rac active Arpin, qui séquentiellement inactive le complexe Arp2/3, tandis que les Tankyrases sont libérées
The evolutionarily conserved Arp2/3 complex plays a central role in nucleating the branched actin filament arrays that drive cell migration, endocytosis, and other processes. Recently, an inactivator of the Arp2/3 complex at the lamellipodium tip, a small protein, Arpin, was discovered and characterized. On its C-terminus, Arpin possesses an acidic (A) motif, which is homologous to the A-motif of various Nucleation Promoting Factors (NPFs). It was predicted that Arpin can bind at two binding sites to the Arp2/3 complex, similar to VCA domains of NPFs. Here, we used single particle electron microscopy to obtain a 3D reconstruction of the Arp2/3 complex bound to Arpin at a 25Å resolution. We showed that the binding of Arpin causes the standard open conformational of the Arp2/3 complex. We confirmed that there are two binding sites on the Arp2/3 complex for Arpin: one on the back of the Arp3 subunit, and the second is located between Arp2 and ARPC1 subunits. The distance between the Arp2/3 complex and Arpin (5 nm) supports the view that Arpin interacts with its partner via its unstructured C-terminal acidic tail.Next, using the pull-down assay, we identified the new Arpin binding partners, Tankyrases1/2. Interestingly, Tankyrases and the Arp2/3 complex possess overlapping amino acid sequences at Arpin binding sites. Hence, we demonstrated a competition between the ARC4 domain of Tankyrase1 and the Arp2/3 complex in a dose-dependent manner.To understand the principles of Tankyrases-Arpin interaction, we created a mutant Arpin (ArpinG218D) that lacks its ability to interact with Tankyrases, but not with the Arp2/3 complex in vitro. Interestingly, ArpinG218D was not able to inhibit the Arp2/3 complex in vivo, suggesting that Tankyrase may be necessary for Arpin-Arp2/3 complex interaction. Arpin is the turning factor of migrating cells, so we performed a migration analysis of MCF10-A cells expressing either wild type Arpin (ArpinWT) or mutant ArpinG218D in parallel with the depletion of endogenous Arpin. Cells expressing ArpinG218D had higher directional persistence, similar to the cells where the endogenous Arpin was knocked down. Thus, we suggested that mutant ArpinG218D cannot inactivate the Arp2/3 complex since it is not present at the lamellipodial tip. We compared the amount of protein for both ArpinWT and ArpinG218D in the membrane fraction of the migrating cells. A significant difference (44%) in the amount of ArpinWT and Arpin G218D was consistent with our hypothesis.Tankyrases are therapeutic targets in a variety of cancers, but currently there is no structural model available for these large and flexible proteins. In this work, we obtained for the first time two 3D reconstructions of full-length Tankyrase1 and Tankyrase1 bound to Arpin using single particle electron microscopy. The achieved resolution (27Å) was enough to detect a dramatic conformational change in Tankyrase SAM and PARP domains upon binding of Arpin molecules. In our reconstruction, three Arpins were bound to the ARC1, ARC4 and ARC5 domains of Tankyrase1. ARC5 was shown to be the most flexible part of the ARC cluster.Based on the obtained data, we suggested a model of regulation of the activity of Arpin by Tankyrases. According to our model, Tankyrases bind Arpin in the cytoplasm, change their conformational state and bring Arpin closer to the membrane in the lamellipodia. Deciphering the extracellular signals, Rac GTPase activates Arpin, which sequentially inactivates the Arp2/3 complex, while Tankyrases are released
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Macdonald, Julie. "Studies on motility in Rhodomicrobium vannielii". Thesis, University of Warwick, 1987. http://wrap.warwick.ac.uk/98453/.

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The change from swarmer cell to non-motile reproductive cell was examined as a landmark event in differentiation of the purple non-sulphur bacterium, Rhodomicrobium vannielii, using synchronised swarmer cell populations. It was found that shed flagella from Rm. vannielii consisted of 3 proteins: flagellin, Mr 34k, hook protein, Mr 36k and a polypeptide of Mr 37k, possibly rod protein. No methyl-accepting chemotaxis proteins were detected in Rm. vannielii. Radioimmunoprecipitation was used to determine the period of flagellin synthesis during differentiation. Synthesis of flagellin was switched off in Rm. vannielii swarmer cells after 1-2 hours anaerobic incubation in the light. If swarmer cells were held anaerobically in the dark, flagellin synthesis continued for at least 6 hours. Thus, swarmer cells, which have a dispersal role in nature, detect whether environmental conditions are conducive to completion of the cell cycle, and regulate their gene expression accordingly. This contrasts with conclusions drawn from work with the non-photosynthetic aquatic bacterium, Caulobacter crescentus, whose cell cycle also includes a swarmer cell to non-motile reproductive cell transition. In order to study control of flagellin expression further, cloning of the gene(s) was attempted. Heterologous Southern hybridisations between restricted Rm. vannielii chromosomal DNA and the cloned 29k flagellin gene from C. crescentus showed that 55-60% homology existed between the two. This was judged to be too weak a signal to allow cloning of Rm. vannielii flagellin genes by hybridisation. Antibodies raised against Rm. vannielii flagellin and hook protein did cross react with C. crescentrus flagellins and hook protein. Screening a library of EcoRl digested Rm. vannielii chromosomal DNA in the vector λgt11 with anti-flagella antiserum indicated that Rm. vannielii flagellin and hook protein were not expressed in E. coli from DNA cut in such a way. Eleven Tn5-induced motility mutants of Rm. vannielii were isolated (3 of which were chemotaxis deficient), and these should enable the cloning of genes for motility from this organism in the future.
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Wang, Qingqi. "Regulation of motility in Listeria monocytogenes". Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490996.

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Listeria monocytogenes is a saprophytic food borne microorganism which is pathogenic to humans and animals. The pathogenicity and physiological features of L. monocytogenes have been studied for many years. Some characteristics of this microorganism have been described, such as its low temperature growth and adaptation, the expression of its flagellin gene, and the regulation of its virulence genes. Previous studies imply a possible reversed relationship that may exist between the regulation of the listerial flagellin gene, flaA and its virulence regulator gene, prfA.
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Książki na temat "Motility"

1

Bray, Dennis. Cell movements: From molecules to motility. Wyd. 2. New York: Garland Pub., 2001.

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Ridley, Anne, Michelle Peckham i Peter Clark, red. Cell Motility. Chichester, UK: John Wiley & Sons, Ltd, 2004. http://dx.doi.org/10.1002/0470011742.

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Grundy, David. Gastrointestinal Motility. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-010-9355-2.

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Rao, Satish S. C., Jeffrey L. Conklin, Frederick C. Johlin, Joseph A. Murray, Konrad S. Schulze-Delrieu i Robert W. Summers, red. Gastrointestinal Motility. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4803-4.

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W, Read N., red. Gastrointestinal motility : which test? Peterfield: Wrightson Biomedical, 1989.

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Melkonian, Michael, red. Algal Cell Motility. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-9683-7.

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Goldberg, I. D., red. Cell Motility Factors. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7494-6.

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Carlier, Marie-France, red. Actin-based Motility. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9301-1.

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Verma, Navin Kumar, red. T-Cell Motility. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9036-8.

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Bardan, Eytan, i Reza Shaker, red. Gastrointestinal Motility Disorders. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59352-4.

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Części książek na temat "Motility"

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Turnbull, Lynne, i Cynthia B. Whitchurch. "Motility Assay: Twitching Motility". W Methods in Molecular Biology, 73–86. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0473-0_9.

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Amils, Ricardo. "Motility". W Encyclopedia of Astrobiology, 1097–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_1028.

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Huang, Cheng-Long. "Motility". W Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_3842-3.

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Amils, Ricardo. "Motility". W Encyclopedia of Astrobiology, 1644–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_1028.

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Huang, Cheng-Long. "Motility". W Encyclopedia of Cancer, 2924–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_3842.

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Huang, Cheng-Long. "Motility". W Encyclopedia of Cancer, 2374–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3842.

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Anderson, O. Roger. "Motility". W Comparative Protozoology, 350–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-662-11340-0_18.

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Amils, Ricardo. "Motility". W Encyclopedia of Astrobiology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27833-4_1028-2.

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Amils, Ricardo. "Motility". W Encyclopedia of Astrobiology, 2029–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-65093-6_1028.

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Guraya, Sardul S. "Sperm Motility". W Biology of Spermatogenesis and Spermatozoa in Mammals, 338–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71638-6_13.

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Streszczenia konferencji na temat "Motility"

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"1st World Congress on Pediatric Neurogastroenterology and Motility". W 1st World Congress on Pediatric Neurogastroenterology and Motility. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-544-0.

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Hidayatullah, Priyanto, Iwan Awaludin, Reyhan Damar Kusumo i Muhammad Nuriyadi. "Automatic sperm motility measurement". W 2015 International Conference on Information Technology Systems and Innovation (ICITSI). IEEE, 2015. http://dx.doi.org/10.1109/icitsi.2015.7437674.

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Vourc’h, Thomas, Julien Léopoldès, Annick Méjean i Hassan Peerhossaini. "Motion of Active Fluids: Diffusion Dynamics of Cyanobacteria". W ASME 2016 Fluids Engineering Division Summer Meeting collocated with the ASME 2016 Heat Transfer Summer Conference and the ASME 2016 14th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/fedsm2016-7526.

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Cyanobacteria are photosynthetic micro-organisms colonizing all aquatic and terrestrial environments. The motility of such living micro-organisms should make their diffusion distinct from typical Brownian motion. This diffusion can be investigated in terms of global behavior (Fickian or not) and in terms of displacement probabilities, which provide more detail about the motility process. Using cyanobacterium Synechocystis sp. PCC 6803 as the model micro-organism, we carry out time-lapse video microscopy to track and analyze the bacteria’s trajectories, from which we compute the mean-squared displacement (MSD) and the distribution function of displacement probabilities. We find that the motility of Synechocystis sp. PCC 6803 is intermittent: high-motility “run” phases are separated by low-motility “tumble” phases corresponding to trapped states. However, this intermittent motility leads to a Fickian diffusive behavior, as shown by the evolution of the MSD with time.
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Yunardi, Riky Tri, Agung Budianto Achmad i Qurrotul A'yun. "Imaging Motility Pattern Analyzer Based on Optical Flow on Mice Sperm Cells Motility". W 2020 10th Electrical Power, Electronics, Communications, Controls and Informatics Seminar (EECCIS). IEEE, 2020. http://dx.doi.org/10.1109/eeccis49483.2020.9263448.

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Fadlallah, Hadi, Hassan Peerhossaini, Christopher De Groot i Mojtaba Jarrahi. "Motility Response to Hydrodynamic Stress During the Growth Cycle in Active Fluid Suspensions". W ASME 2020 Fluids Engineering Division Summer Meeting collocated with the ASME 2020 Heat Transfer Summer Conference and the ASME 2020 18th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/fedsm2020-20125.

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Abstract In this work, we focus on the motility behavior of two model microorganisms widely used in the study of active fluids: Chlamydomonas reinhardtii microalga and Synechocystis sp. Cyanobacterium. Understanding the physiological responses of microorganisms under variable environmental conditions is essential for bioreactor engineering. Yet, most of the previous studies focused on the observation of cellular motility regardless of the growth process. Here, we measure the motility of Chlamydomonas reinhardtii and Synechocystis sp. during their growth when subjected to different intensities of hydrodynamic shear stress. The results demonstrate a significant difference in the motility response of the two species against the applied hydrodynamic shear stress. Mechanical agitation appears to affect the motility of Chlamydomonas reinhardtii microalgae by stimulating the growth process and increasing the magnitude of the cellular swimming velocity. The motility varies following 3 different phases: the rising phase starting almost at the middle of the exponential growth phase, and the decay and damped phases during the stationary phase. This behavior is described using a linear model for the rising phase and a damped oscillatory model for the decay and damped phases. The motility of Synechocystis does not follow a well-defined pattern in time. However, it seems that the peak of the swimming velocity occurs always in the middle of exponential phase of growth. Synechocystis cells show a high endurance to the applied shear such that the global effect of agitation intensity on their motility is insignificant.
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Biener, Gabriel, Emmanuel Vrotsos, Kiminogu Sugaya i Aristide Dogariu. "Optical Torques Guide Cell Motility". W Conference on Lasers and Electro-Optics. Washington, D.C.: OSA, 2009. http://dx.doi.org/10.1364/cleo.2009.cmmm2.

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Smallwood, Nour, Mangnall, Smythe i Brown. "Impedance Imaging and Gastric Motility". W Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.590125.

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Smallwood, R. H., S. Nour, Y. Mangnall, A. Smythe i B. H. Brown. "Impedance imaging and gastric motility". W 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5762022.

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Iglesias, Pablo A. "Excitable systems in cell motility". W 2013 IEEE 52nd Annual Conference on Decision and Control (CDC). IEEE, 2013. http://dx.doi.org/10.1109/cdc.2013.6759973.

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Xiong, Yuan, i Pablo A. Iglesias. "Automated characterization of amoeboid motility". W 2009 43rd Annual Conference on Information Sciences and Systems (CISS). IEEE, 2009. http://dx.doi.org/10.1109/ciss.2009.5054747.

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Raporty organizacyjne na temat "Motility"

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Wells, Alan, Douglas A. Lauffenburger i Timothy Turner. Cell Motility in Tumor Invasion. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2004. http://dx.doi.org/10.21236/ada428576.

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Wells, Alan, Douglas A. Lauffenburger i Timothy Turner. Cell Motility in Tumor Invasion. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2002. http://dx.doi.org/10.21236/ada410314.

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Wells, Alan, Douglas A. Lauffenburger i Timothy Turner. Cell Motility in Tumor Invasion. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2003. http://dx.doi.org/10.21236/ada417877.

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Bodt, B. A., i R. J. Young. Hyperactivated Rabbit Sperm Cell Motility Parameters. Fort Belvoir, VA: Defense Technical Information Center, marzec 1995. http://dx.doi.org/10.21236/ada294502.

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Chirgwin, John. Role of Autocrine Motility in Osteolytic Metastasis. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2000. http://dx.doi.org/10.21236/ada391901.

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Brackanbury, Robert W. Control of Carcinoma Cell Motility by E-Cadherin. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2001. http://dx.doi.org/10.21236/ada403381.

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Chirgwin, John M. Role of Autocrine Motility Factor in Osteolytic Metastasis. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2002. http://dx.doi.org/10.21236/ada408718.

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Brackenbury, Robert W. Control of Carcinoma Cell Motility by E-Cadherin. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2002. http://dx.doi.org/10.21236/ada409404.

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Brackenbury, Robert. Control of Carcinoma Cell Motility by E-Cadherin. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1999. http://dx.doi.org/10.21236/ada390725.

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Brackenbury, Robert. Control of Carcinoma Cell Motility by E-cadherin. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2000. http://dx.doi.org/10.21236/ada393429.

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