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At the start of play, the entire tube is rotated so that a hole in the base of the tube is aligned with the active player's tray. Players take turns removing a single straw from the tube while trying to minimize the number of marbles that fall through the web and into their trays. Once a player has committed themselves to a particular straw by touching it, they must remove it. The player who accumulates the fewest dropped marbles wins.

The video plays directly from the website, and it has the site's controls for playing, pausing, volume, and so on. The PowerPoint playback features (Fade, Bookmark, Trim, and so on) don't apply to online videos.

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By default, videos from YouTube and Vimeo play in "click sequence." You can play the video without having to click the Play button. Just tap the spacebar to advance to the next step in your click sequence.

For the purpose of playing videos in PowerPoint, Internet Explorer 11 is required to be on your computer. You don't have to use it to browse the web; you simply have to have it installed, because under the covers, PowerPoint needs its technology to play videos on Windows.

A video rectangle is placed on your slide, which you can move and resize as you like. To preview your video on your slide, right-click the video rectangle, select Preview, and then click the play button on the video.

YouTube videos on PowerPoint 2010 have stopped working. YouTube recently has discontinued support for the Adobe Flash Player, which PowerPoint 2010 uses behind the scenes to play a YouTube video embedded on a slide.

The standard model THR, the THR10 sounds great in a wide range of genres, whether played delicatedly with a clean sound, or with a more edgy, distorted tone.Now the THR10 has been upgraded to version 2, delivering even better quality sound.

THR5A is optimized for use with electric-acoustic and Silent Guitars. Utilising advanced modeling technologies developed by Yamaha, THR5A offers simulations of classic tube condenser and dynamic mics combined with studio-grade effects to create recording-studio tone direct from your guitar and wherever you are.

Do you want to watch YouTube videos offline? Watching Youtube videos can be a fun way to pass the time. But what do you do if you don't have an internet connection? Luckily, there are some ways you can download YouTube videos to watch offline. If you are in the U.S, you need a subscription to YouTube Premium to download videos to watch offline on YouTube. In some areas, certain videos may be available to download for all users. If you don't have Premium, you can use an app like 4K Video Downloader, or an online converter to download videos. This wikiHow teaches you how to download a YouTube video to watch offline on a computer, phone, or tablet.

I am developing an app for Wp7.x and Wp8 which runs YouTube Video with lock screen disabled.I have seen that new version of MyTube App and Microsoft version of your tube app which has been pulled back had a feature which allows user to keep listening to Video(Audio part) when phone is locked via lock screen. I want to Develop a YouTube Radio type of app which keeps pulling new Specific type of Viedo Url from youTube site and play the audio part even if running in background or In a Locked screen.

In Windows Phone 8, you can actually give video URLs to the BackgroundAudioPlayer class and it will play them in the background. I use this technique in Podcaster to switch between audio and video, though it's a user interaction that triggers the switch.

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As a major component of the extracellular matrix, hyaluronan is particularly abundant in the extracellular matrix of embryonic tissues, where its expression is dynamically regulated during tissue morphogenetic processes. Tissue levels of hyaluronan are regulated not only by its synthesis but also by its degradation. Curiously, mice lacking known hyaluronidase molecules, including HYAL1 and HYAL2, exhibit minimal embryonic phenotypes. As a result, our understanding of the role of the catabolic aspect of hyaluronan metabolism in embryonic development is quite limited. Here, we show that TMEM2, a recently identified hyaluronidase that degrades hyaluronan on the cell surface, plays a critical role in the development of neural crest cells and their derivatives. Our analyses of Tmem2 conditional knockout mice, Tmem2 knock-in reporter mice, and in vitro cell cultures demonstrate that TMEM2 is essential for generating a tissue environment needed for efficient migration of neural crest cells from the neural tube. Our paper reveals for the first time that the degradation of hyaluronan plays a specific regulatory role in embryonic morphogenesis, and that dysregulation of hyaluronan degradation leads to severe developmental defects.

Craniofacial anomalies, including midface hypoplasia and cleft lip and/or palate, account for one-third of all congenital birth defects [1]. Normal craniofacial development is an intricate biological process that requires the action of a number of distinct cell autonomous and cell non-autonomous factors and pathways. Among these, the extracellular matrix (ECM) plays a particularly important role. Neural crest cells (NCCs) are a migratory population of cells that arise at the edge of the neural tube during neurulation, and contribute to the formation of a variety of tissues, including the cardiovascular system, peripheral nervous system, skeleton, and craniofacial tissues [2]. After induction and specification at the edge of the neural tube, NCCs undergo a process called delamination, in which they emigrate from their site of origin and subsequently migrate toward target sites. Mutations in genes involved in NCC development can lead to a wide range of human congenital malformations, including craniofacial anomalies.

Transmembrane protein 2 (TMEM2; gene symbol CEMIP2) was originally identified as a large type II transmembrane protein with an unknown function. Even in the absence of a defined function, zebrafish tmem2 mutants (frozen ventricles and wickham) were nevertheless found to exhibit a developmental heart phenotype related to endocardial cushion defect, accompanied by excessive accumulation of HA [28,29]. Subsequently, we demonstrated that TMEM2 is a hyaluronidase that degrades extracellular high-molecular weight HA into intermediate-sized HA fragments at near neutral pH [30]. In mouse embryos, Tmem2 is expressed in a developmentally regulated manner, with the peak of expression prior to E11 and with prominent sites of expression in the neural tube, the first branchial arch, and the frontonasal processes [31]. More recently, we have demonstrated that TMEM2 plays a critical role in promoting integrin-mediated cell adhesion and migration via its removal of anti-adhesive HA from focal adhesion sites [32]. These observations suggest to us that TMEM2 may be the key hyaluronidase that regulates dynamic remodeling of the HA-rich ECM during embryonic development.

To gain initial insight into the role of TMEM2 during NCC development, we used in situ hybridization to examine the spatiotemporal expression pattern of Tmem2 during the mid-gestation period. In whole mount preparations at E8.5 and 9.0, robust Tmem2 expression is detected in the neural tube, frontonasal region, branchial arches, and heart (S1A Fig). Transverse sections of the E9.0 neural tube further demonstrate that Tmem2 expression in the neural tube is concentrated mainly in its dorsal region (S1A Fig, Transverse), from which NCCs arise. At E9.5 and E10.5, robust Tmem2 expression is also seen in tissues with contributions from NCCs, including the forebrain, midbrain, hindbrain, trigeminal ganglion, branchial arches, heart, and dorsal root ganglia (S1B Fig).

The Wnt1-Cre driver has been used to determine the function of genes in NCC development, migration, and subsequent differentiation [33,34]. To determine the role of Tmem2 in the development of NCCs and their derivatives, we crossed a conditional Tmem2 allele (Tmem2flox) into Wnt1-Cre mice (see Materials and Method). While heterozygous Wnt1-Cre;Tmem2flox/wt mice were born alive without detectable developmental defects and were fertile, no homozygous conditional mutants (i.e., Wnt1-Cre;Tmem2flox/flox; hereafter referred to as Tmem2CKO, hereafter) were recovered at birth. Therefore, we performed timed matings to obtain homozygous embryos at several time points between E10.5 and E12.5. At E10.5, Tmem2CKO embryos exhibit hypoplasia of the frontonasal, maxillary, and mandibular processes (Fig 1A, open arrowheads). Hemorrhage and edema were frequently observed in the craniofacial regions of Tmem2CKO embryos at times later than E10.5 (Fig 1A, arrow). In addition, growth retardation is often observed in Tmem2CKO embryos at this stage. At gestational stages later than E12.5, 100% (42 of 42 embryos) of Tmem2CKO embryos exhibit severe craniofacial abnormalities, characterized by reduced outgrowth of the frontonasal and maxillary processes, lack of fusion of the medial nasal and mandible processes at the midline, lack of fusion between frontonasal process and maxillary process, and wide nasal cavity (Fig 1B and 1C). Histomorphological analysis of E12.5 Tmem2CKO embryos further demonstrates the hypoplastic, laterally expanded maxillary components in these mice and the absence of fusion of the facial processes (Fig 1D-ii and 1D-iv). Epithelial blistering was frequently observed in the lateral portion of the frontonasal process and in the midline region of the mandibular arches (34 of 42 embryos, 81.0%) (arrows in Fig 1D-ii and 1D-iv). Defects in branchial arch derivatives, such as the tongue, are also observed in Tmem2CKO embryos. NCC-derived peripheral nervous tissues, such as trigeminal, facial, and vestibular ganglia, are consistently smaller in Tmem2CKO embryos than in control embryos (Fig 1D-vi). In addition, neural tube defects, including exencephaly, were detected in a fraction of Tmem2CKO embryos (4 of 42 embryos, 9.5%) (Figs 1B and S2). No live Tmem2CKO embryos were recovered past E13.5. All Tmem2CKO embryos recovered at E13.5 exhibited severe craniofacial and cardiovascular abnormalities. Cardiac NCCs, a subpopulation of cranial NCCs, migrate into the third, fourth and sixth branchial arches and give rise to the aortic and pulmonary trunk, the cap of the intraventricular septum, the developing outflow tract cushions, and the parasympathetic system of the heart [35]. This is consistent with the fact that Wnt1-Cre is also active in cardiac NCCs [36]. Consistent with the functional role for TMEM2 in cardiac NCCs, Tmem2CKO embryos exhibit expanded endocardial cushions and lack of the aorticopulmonary septum in the outflow tract region (S3 Fig). 17dc91bb1f