Pectoral Fin Anomalies in tbx5a Knockdown Zebrafish Embryos Related to the Cascade Effect of N-Cadherin and Extracellular Matrix Formation

Functional knockdown of zebrafish tbx5a causes hypoplasia or aplasia of pectoral fins. This study aimed to assess developmental pectoral fin anomalies in tbx5a morpholino knockdown zebrafish embryos. The expression of cartilage-related genes in the tbx5a morphant was analyzed by DNA microarray, immunostaining, and thin-section histology to examine the detailed distribution of the extracellular matrix (ECM) during different pectoral fin developmental stages. Chondrogenic condensation (CC) in the tbx5a morpholino knockdown group was barely recognizable at 37 h postfertilization (hpf); the process from CC to endoskeleton formation was disrupted at 48 hpf, and the endoskeleton was only loosely formed at 72 hpf. Microarrays identified 18 downregulated genes in tbx5a-deficient embryos, including 2 fin morphogenesis-related (cx43, bbs7), 4 fin development-related (hoxc8a, hhip, axin1, msxb), and 12 cartilage development-related (mmp14a, sec23b, tfap2a, slc35b2, dlx5a, dlx1a, tfap2b, fmr1, runx3, cdh2, lect1, acvr2a, mmp14b) genes, at 24 and 30 hpf. The increase in apoptosis-related proteins (BAD and BCL2) in the tbx5a morphant influenced the cellular component of pectoral fins and resulted in chondrocyte reduction throughout the different CC phases. Furthermore, tbx5a knockdown interfered with ECM formation in pectoral fins, affecting glycosaminoglycans, fibronectin, hyaluronic acid (HA), and N-cadherin. Our results provide evidence that the pectoral fin phenotypic anomaly induced by tbx5a knockdown is related to disruption of the mesoderm and ECM, consequently interfering with mesoderm migration, CC, and subsequent endoskeleton formation

Complete Genome Sequence of Streptococcus iniae 89353, a Virulent Strain Isolated from Diseased Tilapia in Taiwan

exterior, steps leading up to terrace with mosque portal and minaret, 1981minaret is unusually tapered, almost conical Two kilometers east of the Silk Road town of Turfan stands the Amin Mosque with its monumental minaret, the tallest in China. The mosque was built in 1779 during the Qing Dynasty in memory of the Uygur King Amin Khoja (also known as Imin Khoja, Emin Hejo, or Emin Hedro) by his son King Suleiman. The mosque was alternately known as the Su Gong Ta Mosque, or the Mosque of the Su Minaret with reference to Prince Su. His father, King Amin, who died in 1777, had collaborated with Emperors Yongzheng (1723-1736) and Qianlong (1736-1796) to unify Xinjiang and annexed it to the Chinese between 1756-1759 putting an end to local rebellions. The large fortified mosque, raised on a platform, stands alone outside the city, devoid of any auxiliary buildings. It combines the local Xinjiang hypostyle prayer hall (built of mud brick, with brick patterning and arched niches) with influences from Persia and Central Asia, seen mainly in the domineering pishtaq, or tall projecting portal, and the minaret. The imposing pishtaq stands at the center of the mosque's eastern elevation and has a large, arched portal niche, similar to portals of mosques, madrasas and tombs stretching from Persia across Central Asia. It is preceded by a protected terrace that is accessed by a single set of stairs from the street. The pishtaq is decorated on its main façade, and on its sides with rectangular panels containing arched niches similar to the portal of the Aitika Mosque in Kashi. The top tier of the panels are pierced with arched windows on all sides creating a narrow, partially enclosed, gallery atop the pishtaq. A domed octagonal vestibule leads from the portal to the prayer hall. To the right of this vestibule is a rectangular hall with a stairway giving access to the roof. To its left, is a narrow corridor flanked by two rooms that give access to the minaret steps. The prayer hall mostly borrows from the building traditions of the immediate Turfan region. Poplar beams and stone-based poplar columns support the low, flat roof of the large, covered court, which is enveloped by stone galleries on three sides. Two small apertures in the woven vegetal roof of the court allow light into the dimly lit main prayer hall, creating a somber atmosphere. The mihrab is set in a domed room at the center of the qibla wall, with doors to the side galleries and to the main court. The two-bay deep stone galleries surrounding the court recall the structure of Abbasid mosques. Their domes are carried on pointed arches falling on heavy piers. Some bays along the outer ring of the galleries are enclosed into rooms. Unlike the mosques and mausoleums of Kashi, there is minimal sculptural and chromatic decoration inside the King Amin Mosque, which is simply adorned with arched niches carved into the plain mud brick walls. The floor is paved with square cut stone and partially covered with woven mats. The mihrab chamber is covered with a large conical dome, the drum of which is encircled with windows. The drum sits upon an octagonal base bearing blind arches gracefully aligned with the doorways, corners and the mihrab niche. This western qibla dome is balanced at the eastern end of the prayer hall by the rounded dome of the entry vestibule. A mausoleum in the cemetery adjoining the qibla wall is said to be that of a foreign saint, and is a popular pilgrimage site. Located at the southeast corner of the mosque, the minaret is the tallest in China at forty-four meters. Its circular shaft measures fourteen meters across and tapers down to 2.8 meters in diameter at the top. The spiraling internal support also serves as a stairway with seventy-two steps for the imam to perform the call to prayer from a room with latticed windows at the top. The ornamental brickwork of the tower consists of fifteen bands of various widths and patterns. The fine precision of the bricklaying creates a rich texture that is reminiscent of the fine brickwork of the world renowned Kalyan, or Poi Minaret in Bukhara. A Uygur architect named Ibrahim is said to have designed the minaret of the Great Mosque of King Amin. The Great Mosque of King Amin, like other Uygur mosques of the Xinjiang Province, is closer in style and decoration to Uzbek and other Central Asian building traditions than to those of the Hui. The mosque has been closed to prayer since 1992, when it was placed under protection by the Chinese government.Sources: Chang, Jing Qi. 1982. Islamic Architecture in China. In The Changing Rural Habitat; Volume 2 : Background Papers. Brian Brace Taylor (ed). Singapore: Concept Media/The Aga Khan Award for Architecture, 74. http://archnet.org/library/documents/one-document.tcl?document_id=4279 [Accessed October 22, 2004] Dazhang, Sun. 2003. Ancient Chinese Architecture: Islamic Buildings. New York: Springer-Verlag/Wien, 146, 166. Fiala, Robert D. 2004. "Emin Minaret". Asian Historical Architecture Website. http://www.orientalarchitecture.com/turpan/eminminaretindex.htm [Accessed October 22, 2004] Loubes, Jean-Paul. 1998. Architecture et Urbanisme de Turfan: Une Oasis du Turkestan Chinois. Paris: L'Harmattan, 169. Martin Frishman and Hasan-Uddin Khan, eds. 1994. The Mosque: History, Architectural Development and Regional Diversity. London: Thames and Hudson, 128. Petersen, Andrew. 1996. "China". In Dictionary of Islamic Architecture. London: Routledge, 52-54. http://archnet.org/library/dictionary/entry.tcl?entry_id=DIA0074 [Accessed October 22, 2004] Zhang, Jing-qui. 1982. "Mosques of Northern China". In MIMAR 3: Architecture in Development. Singapore: Concept Media Ltd, 58, 67. http://archnet.org/library/documents/one-document.tcl?document_id=4433 [Accessed October 22, 2004

Inhibition of the P2X7 Receptor Reduces Cystogenesis in PKD

[[abstract]]The P2X7 receptor participates in purinergic signaling, which may promote the progression of ADPKD. We examined the effects of a P2X7 receptor antagonist and a P2X7 receptor agonist on cyst development in a zebrafish model of polycystic kidney disease in which we knocked down pkd2 by morpholinos. We used live wt-1b pronephric-specific GFP-expressing zebrafish embryos to directly observe changes in the pronephros. Exposure of pkd2-morphant zebrafish to a P2X7 receptor antagonist (oxidized ATP [OxATP]) significantly reduced the frequency of the cystic phenotype compared with either exposure to a P2X7 receptor agonist (BzATP) or with no treatment (P ＜ 0.01). Histology confirmed improvement of glomerular cysts in OxATP-treated pkd2 morphants. OxATP also reduced p-ERK activity and cell proliferation in pronephric kidneys in pkd2 morphants. Inhibition of P2X7 with an additional specific antagonist (A-438079), and through morpholino-mediated knockdown of p2rx7, confirmed these effects. In conclusion, blockade of the P2X7 receptor reduces cyst formation via ERK-dependent pathways in a zebrafish model of polycystic kidney disease, suggesting that P2X7 antagonists may have therapeutic potential in ADPKD.[[journaltype]]國外[[incitationindex]]SCI[[booktype]]紙本[[countrycodes]]US