Recto and verso are the text written or printed on the "right" or "front" side and on the "back" side of a leaf of paper in a bound item such as a codex, broadsheet, or pamphlet. The terms are shortened from Latin rectō foliō and versō foliō, translating to "on the right side of the leaf" and "on the back side of the leaf"; the two opposite pages themselves are called folium rectum and folium versum in Latin, the ablative recto, verso imply that the text on the page are referred to. In codicology, each physical sheet of a manuscript is numbered and the sides are referred to as rectum and folium versum, abbreviated as r and v respectively. Editions of manuscripts will thus mark the position of text in the original manuscript in the form fol. 1r, sometimes with the r and v in superscript, as in 1r, or with a superscript o indicating the ablative recto, verso, as in 1ro. This terminology has been standard since the beginnings of modern codicology in the 17th century. Lyons argues that the term rectum "right, proper" for the front side of the leaf derives from the use of papyrus in Late Antiquity, as a different grain ran across each side, only one side was suitable to be written on, so that papyrus would carry writing only on the "correct", smooth side.
The terms "recto" and "verso" are used in the codiology of manuscripts written in right-to-left scripts, like Syriac and Hebrew. However, as these scripts are written in the other direction to the scripts witnessed in European codices, the recto page is to the left while the verso is to the right; the reading order of each folio remains first verso recto regardless of writing direction. The terms are carried over into printing; the distinction between recto and verso can be convenient in the annotation of scholarly books in bilingual edition translations. The "recto" and "verso" terms can be employed for the front and back of a one-sheet artwork in drawing. A recto-verso drawing is a sheet with drawings on both sides, for example in a sketchbook—although in these cases there is no obvious primary side; some works are planned to exploit being on two sides of the same piece of paper, but the works are not intended to be considered together. Paper was expensive in the past. By book publishing convention, the first page of a book, sometimes of each section and chapter of a book, is a recto page, hence all recto pages will have odd numbers and all verso pages will have numbers.
In many early printed books or incunables and still in some 16th-century books, it is the folia rather than the pages, that are numbered. Thus each folium carries a consecutive number on its recto side, while on the verso side there is no number; this was very common in e.g. internal company reports in the 20th century, before double-sided printers became commonplace in offices. Book design Obverse and reverse in coins Page spread
The 2013–14 Nemzeti Bajnokság I is the 62nd season of the Nemzeti Bajnokság I, Hungary's premier Handball league. The following 13 clubs compete in the NB I during the 2013–14 season: Following is the list of clubs competing in 2013–14 Nemzeti Bajnokság I, with their manager, kit manufacturer and shirt sponsor. *: Hungary national junior handball team played only in regular season. Pld - Played. In the table below the home teams are listed on the away teams along the top. Source: Teams in bold won the playoff series. Numbers to the left of each team indicate the team's original playoff seeding. Numbers to the right indicate the score of each playoff game. Balatonfüredi KSE advanced to Semifinals. Csurgói KK advanced to Semifinals. MKB-MVM Veszprém advanced to Final. Pick Szeged advanced to Final. MKB-MVM Veszprém won Championship final series 2–0. Team Roster 1 Nándor Fazekas, 2 Uros Vilovski, 3 Péter Gulyás, 4 Gergő Iváncsik, 5 Timuzsin Schuch, 9 Tamás Iváncsik, 11 Carlos Ruesga, 13 Momir Ilić, 18 Tamás Mocsai, 19 László Nagy, 21 Iman Jamali, 23 Cristian Ugalde, 25 Chema Rodriguez, 30 Mirsad Terzić, 32 Mirko Alilović, 33 Renato Sulić and 35 Živan Pešić Head Coach: Antonio Carlos Ortega Balatonfüredi KSE won series 2–1 and won the Third Place.
Grundfos-Tatabány KC won series 2 -- won 5th Place. Pld - Played. In the table below the home teams are listed on the away teams along the top. = Champion. Hungarian Handball Federaration
Huang Jing is a Chinese-American political scientist and alleged spy. He was the director of the Centre on Asia and Globalisation and the Lee Foundation Professor on US-China Relations at the National University of Singapore's Lee Kuan Yew School of Public Policy until his permanent residence was revoked after the Ministry of Home Affairs called him "an agent of influence of a foreign country" on August 4, 2017. Huang Jing was born in China in 1956, his parents were military doctors. While a teenager, he was sent to Yunnan as part of the Down to the Countryside Movement. Huang graduated from Sichuan University, where he earned a bachelor of arts degree in English, he went on to earn a master's degree in history from Fudan University and a PhD from Harvard University in 1995. Huang taught at Harvard University from 1993 to 1994, he was an associate professor of political science at Utah State University from 1994 to 2004, where he was the director of the Asia Studies Program, he was granted tenure in 1998.
He taught at Shandong University. He was a Shorenstein Fellow at Stanford University from 2002 to 2003, a Senior Fellow at the Brookings Institution's John Thornton China Center from 2004 to 2008. In 2008, Huang joined the Lee Kuan Yew School of Public Policy at the National University of Singapore, where he was the director of the Centre on Asia and Globalisation and the Lee Foundation Professor on US-China Relations, he became an analyst for Xinhua News Agency. He is the author of several books, including Factionalism in Chinese Communist Politics, which won the 2002 Masayoshi Ohira Memorial Prize. On August 4, 2017, his permanent residence in Singapore was cancelled, he and his wife were denied re-entry, on the assumption that he was "an agent of influence of a foreign country", he was accused by the Singaporean Ministry of Home Affairs of "subversion and foreign interference in Singapore’s domestic politics."According to The New York Times, "ome view his academic writings as pro-Chinese."
Huang is married to Shirley Yang Xiuping. They are both U. S. citizens, resided in Singapore. Huang, Jing. Factionalism in Chinese Communist Politics. Cambridge, U. K.: Cambridge University Press. ISBN 9780521622844. OCLC 779692468. Huang, Jing. Inseparable Separation: The Making of China's Taiwan Policy. Singapore: World Scientific. ISBN 9789814287364. OCLC 401147121
The Institut für Dokumentologie und Editorik is a German association of researchers working on the application of digital methods to historical documents. Fields of interest include digitization, text encoding, textual criticism, critical scholarly editing, digital palaeography, digital codicology, it was established in 2006 and has contributed in several ways to the field of digital humanities and has organized Summer Schools on a regular basis at various universities in Germany and Austria. Most notably, the IDE publishes the series Schriften des Instituts für Dokumentologie und Editorik distributed in print and online; the IDE supports open access. The series is reviewed in German and international journals. Since July 2014 the IDE publishes the open access journal RIDE: A Review Journal for Digital Editions and Resources. Documentation science Official website
Maria Theresia is a 2017 Austrian-Czech historical film. The film was a coproduction of the Czech Republic, Austria and Hungary. Marie-Luise Stockinger as Maria Theresa Vojtěch Kotek as Francis of Lorraine Zuzana Stivínová as Elisabeth Christine of Brunswick-Wolfenbüttel Anna Posch as Maria Anna of Austria Karl Markovics as Prince Eugene of Savoy Fritz Karl as Charles VI, Holy Roman Emperor Jiří Dvořák as Friedrich August von Harrach-Rohrau Alexander Bárta as Philip Kinsky of Wchinitz and Tettau Tatiana Pauhofová as Elisa Fritz Maria Theresia on IMDb
WNK known as WNK1, is an enzyme, encoded by the WNK1 gene. WNK1 is serine-threonine kinase and part of the "with no lysine/K" kinase WNK family; the predominant role of WNK1 is the regulation of cation-Cl− cotransporters such as the sodium chloride cotransporter, basolateral Na-K-Cl symporter, potassium chloride cotransporter located within the kidney. CCCs mediate ion homeostasis and modulate blood pressure by transporting ions in and out of the cell. WNK1 mutations as a result have been implicated in blood pressure disorders/diseases; the WNK1 protein is composed of 2382 amino acids. The protein contains a kinase domain located within its short N-terminaldomain and a long C-terminal tail; the kinase domain has some similarity to the MEKK protein kinase family. As a member of the WNK family, the kinase's catalytic lysine residue is uniquely located in beta strand 2 of the glycine loop. In order to have kinase activity, WNK1 must autophosphorylate the serine 382 residue found in its activation loop.
Further, phosphorylation at another site increases WNK1 activity. An autoinhibitory domain is located within the C-terminal domain along with a HQ domain, needed for WNK1 interactions with other WNKs; the interactions between WNKs play an important role in function. The WNK1 gene encodes a cytoplasmic serine-threonine kinase expressed in the distal nephron. Studies have shown. WNK1 however, does not directly phosphorylate the CCCs themselves rather it phosphorylates other serine-threonine kinases: Sterile20 related proline-alanine-rich kinase and oxidative stress response kinase 1. Phosphorylation of SPAK's T loop located in its catalytic domain will activate SPAK, which will go on to phosphorylation the CCC's N-terminaldomain. Hence, WNK1 activates CCCs indirectly as an upstream regulator of SPAK/OSR1. In the distal convoluted tubule, WNK1 is a potent activator of the NCC that results in an increase in sodium re absorption that drives an increase in blood pressure; the WNK1 mutant found in FHHt harbors a large deletion within intron 1 that causes an increase in the expression of full length WNK1.
The boost in WNK1 leads to increases in NCC activation that promotes the high blood pressure/hypertension associated with FHHt. WNK1 activates the serum-and glucocorticoid-inducible protein kinase SGK1, leading to increased expression of the epithelial sodium channel, which promotes sodium re absorption. WNK1 regulates potassium channels found in the cortical connecting tubule. Renal outer medullar potassium 1 and large conductance calcium-activated potassium channel are the two primary channels for potassium secretion. WNK1 indirectly stimulates clathrin-dependent endocytosis of ROMK1 by a potential interaction with intersectin. Another possible mechanism of ROMK1 regulation is via autosomal recessive hypercholeserolemia, a clathrin adaptor molecule. ACH phosphorylation by WNK1 promotes the translocation of ROMK1 to clathrin coated pits triggering endocytosis. WNK1 may indirectly activate BKCa by inhibiting the actions of extracellular signal–regulated kinases that lead to lysomal degradation.
The NKCC1/2 cotransporters are regulated by intracellular Cl− concentration. Studies point to WNK1 as key effector. In hypertonic conditions that trigger cell shrinkage, an unknown mechanism upregulates WNK1 expression to counteract the volume loss; the increased WNK1 leads to activation of SPAK/OSR1 that activate NKCC1/2 via subsequent phosphorylation. NKCC1/2 will promote the influx of Na+, K+, Cl− ions into the cell thereby causing the flow of water into the cell. In the reverse circumstances, where hypotonic conditions induce cell swelling, WNK1 is inhibited. Another cotransporter, KCC is inactive; the cotransporter will promote the efflux of K+ and Cl− ions and cause the flow of water out of the cell to combat swelling. In the mature brain, the GABA neurotransmitter represents the major inhibitory signal used in neuronal signaling. GABA activates the GABAA receptor, a Cl− ion channel. Cl − ions will enter the neuron causing inhibition of signaling. During brain development however, GABAA activation will allow Cl− ions to leave the neuron causing the neuron to depolarize.
Thus, GABA is an excitatory neurotransmitter during development. WNK1 has been implicated in the developmental switch from excitatory to inhibitory GABA signaling via interaction with NKCC1 and KCCs. WNK1 phosphorylates SPAK/OSR1 which phosphorylates KCC2 inhibiting the flow of Cl− ions out of the cell during development; the concentrations of Cl− ions and K+ ion play a major role in regulating WNK1 activity. In the DCT, the plasma concentration of K+ ion is thought to impact the concentration Cl− ions within the nephron. High plasma K+ concentration down regulates WNK1 activity and prevents Cl− ion from entering the nephron via the NCC; the opposite occurs. When there is an abundance of Cl− ions within the nephron, WNK1 activity is inhibited by the binding of a Cl− ion to WNK1's catalytic domain. Furthermore, WNK1 and WNK4 may interact to form heterodimers. WNK4 release from the heterodimer allows WNK1 monomer to bind anoth