The taskbar has seen the biggest visual changes, where the old Quick Launch toolbar has been replaced with the ability to pin applications to the taskbar. Buttons for pinned applications are integrated with the task buttons. These buttons also enable Jump Lists to allow easy access to common tasks, and files frequently used with specific applications.[66] The revamped taskbar also allows the reordering of taskbar buttons. To the far right of the system clock is a small rectangular button that serves as the Show desktop icon. By default, hovering over this button makes all visible windows transparent for a quick look at the desktop.[67] In touch-enabled displays such as touch screens, tablet PCs, etc., this button is slightly (8 pixels) wider in order to accommodate being pressed by a finger.[68] Clicking this button minimizes all windows, and clicking it a second time restores them.
Se7en Activator V3 - Windows 7 B
Window management in Windows 7 has several new features: Aero Snap maximizes a window when it is dragged to the top, left, or right of the screen.[69] Dragging windows to the left or right edges of the screen allows users to snap software windows to either side of the screen, such that the windows take up half the screen. When a user moves windows that were snapped or maximized using Snap, the system restores their previous state. Snap functions can also be triggered with keyboard shortcuts. Aero Shake hides all inactive windows when the active window's title bar is dragged back and forth rapidly.
Hi, I upgraded from win 7 pro to 10. My laptop worked fine for weeks, then refused to start windows one morning. I tried the repairs available (advanced options, etc). I then downloaded the ISO file for win 10, that contains all the win 10 versions, I retrieved the win 10 pro product key from my drive, but during the win 10 installation it says the the key is invalid. Can anyone advise me, please. Thank you.
A product riddled with problems.When an update of windows TEN is done,some of my progremmes simply disappear.On windows 8 I never had any problems whatsoever.The latest problem .I cannot link to my printer. Got an expert in at great cost,he managed the link but as soon as the computer is switched off,that`s it,no more link.My ONLY alternative now is to go back to windows 8 until your team sort out all the crap on the system.
question then say that i have 2 desktops and 3 hard drives all of them have windows and i take harddrive 3 and make it windows 10 from windows 7 on computer b and then go to computer a and launch the hardrive on it useing its windows 10 why does it now say windows 10 is not activated because that happened to my 1tb that is windows 10 home please help
I previously had a windows 7 home premium original copy which I did bought spending my money. It worked well. After win 10 launch I could successfully upgrade to windows 10 and the copy got activated automatically. There were talks around saying Microsoft is giving away free windows activation this time. So i made a USB copy of windows 10 PRO in to my flash drive and I DID A CLEAN INSTALL FROM THAT VERY COPY. Now I have Windows 10 PRO not activated. I cannot activate this using my windows 7 home premium product key. PLEASE HELP!
If the above methods fail to activate Windows 7, you can try third-party software like Windows 7 activator or other Windows KMS tools. Download these tools and run them. They will activate Windows 7 for you automatically. If necessary, you should disable the firewall or antivirus software before running these tools.
Windows displays the live previews of all running instances of IE. When the mouse hovers over one of the live previews, the selected window appears, and the rest of the windows turn transparent. To select the window, simply click the live preview.
Another very useful UI feature in Windows 7 is Aero Snap. How many times have you tried to arrange multiple windows on your desktop so that you see the windows side-by-side? In Windows 7, when you drag a window to the left side of the screen, the window is automatically docked onto the left of the screen (see Figure 1-15), occupying half the screen. Likewise, when dragged to the right, the window will be docked to the right. When dragged to the top, the window will be maximized. Besides dragging, Windows 7 provides several shortcuts (see Table 1-1) for window management.
During spliceosome assembly, protein-protein interactions (PPI) are sequentially formed and disrupted to accommodate the spatial requirements of pre-mRNA substrate recognition and catalysis. Splicing activators and repressors, such as SR proteins and hnRNPs, modulate spliceosome assembly and regulate alternative splicing. However, it remains unclear how they differentially interact with the core spliceosome to perform their functions.
SR proteins [7] and hnRNPs [8] are two important families of splicing factors. The SR proteins SRSF1-7 typically activate exon inclusion through sequence-specific binding to exonic enhancers [7]. SRSF9-11 share sequence and structure similarity with the rest of the SR family, but they uncharacteristically act as repressors [7]. The hnRNPs are also diverse: a recent study [9] addressing the sequence specificity and splicing activity of five hnRNPs using high-throughput techniques, concluded that hnRNPF, H1, M, and U are primarily activators, whereas hnRNPA1 and A2B1 are primarily repressors.
To understand the contextual differences shaping the behavior of activators and repressors, we assembled and studied the PPI networks of all SR proteins and hnRNPs. We conducted a top-down study in three stages: first, we predicted PPIs in the human spliceosome through a probabilistic model that integrates annotated PPIs with gene-expression microarray profiles; second, we implemented the resulting interactome network to investigate the connectivity of SR proteins and hnRNPs to the rest of the spliceosome; and third, we validated the structure of the network by performing immunoprecipitation and mass spectrometry (IP-MS) of two prototypical splicing factors: the activator SRSF1 and the repressor hnRNPA1.
The proteins in the PS-network are not randomly distributed, but instead are clustered in topological modules or FCs (Fig. 2d, Additional file 2: Table S1C). A compacted version of the PS-network (Fig. 2d) shows that early (3 and 8) and late (4, 7, and 10) spliceosomal FCs, as well as pre- (1) and post-splicing FCs (2, 6), are physically separated and resemble functional modules. Of particular interest for this study, FC5 comprises a mixture of nine splicing activators (SRSF1-7, hnRNPU, and RBMX) and five splicing repressors (hnRNAPA1, A2B1, C, H, and SRSF10). In addition FC9 contains a number of activators (hnRNPs F, K, and SRSF9) and repressors (hnRNPL and PTBP1). The activator/repressor activities were assigned based on comprehensive aggregation of literature references derived from the RegRNA database [26] (Additional file 5: Table S3). Although both SR proteins and hnRNPs have been documented to function as activators or repressors depending upon the context, in each individual case one of these two functions occurs much more frequently, allowing for a clear cutoff to distinguish between both groups (Additional file 6: Figure S2).
To validate the predictability of our model, we performed IP-MS of the prototypical splicing activator SRSF1 and splicing repressor hnRNPA1 (Additional file 11: Figure S4A, B), using T7-tagged constructs that accurately replicate the activities of endogenous SRSF1 and hnRNPA1 (Additional file 11: Figure S4C-M). IP-MS is a useful technique to identify large multimeric protein assemblies. Unlike Y2H, which is designed to capture direct PPIs, IP-MS identifies mixed populations of proteins held in physical proximity through direct or indirect interactions [29].
SR proteins and hnRNPs regulate splicing cooperatively or antagonistically, as in the case of the splicing activator SRSF1 and the repressor hnRNPA1 [10, 14]. Here we found that the connectivities of these two proteins to the spliceosome are substantially different. Whereas SRSF1 shows high connectivity to multiple spliceosomal subgroups, the hnRNPA1 interactome is largely restricted (that is, it is mostly composed of additional members of the hnRNP superfamily). In addition, we found that the SRSF1 interactome is rich in direct and RNA-independent PPIs (Fig. 6a, c). In contrast, the hnRNPA1 interactome is smaller and more RNA-dependent (Fig. 6b, d).
Analysis of the PS-network revealed a trend whereby splicing activators engage in a relatively large number of PPIs with other proteins in the spliceosome, perhaps playing an active role in recruiting spliceosomal proteins. In contrast, repressors display fewer PPIs (as was the case for hnRNPA1), suggesting that they predominantly affect splicing by steric interference through RNA binding. IP-MS experiments confirmed these rules for the prototypical splicing factors SRSF1 and hnRNPA1. In both cases, IP-MS fractions were enriched in high-probability interactions, as predicted by our model. This was especially noticeable for the samples treated with nuclease.
References for splicing activator or repressor activities of SR proteins and hnRNPs . Following annotations in RegRNA [26] and additional literature sources ESE (exonic splicing enhancer), ESS (exonic splicing silencer), ISE (intronic splicing enhancer), ISS (intronic splicing silencer).
Intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) within 3 h of symptom onset is currently approved for treatment of acute ischemic stroke. Those who present within 3 h and have a vascular occlusion and a good CT scan are the ideal candidates for thrombolysis. Clinical trials and phase IV data has shed substantial light on the factors associated with more favorable outcomes with tPA. In the 3-6 h time window, cerebral perfusion information can be used for selection of patients for thrombolytic therapy. In many special circumstances, such as seizure at stroke onset, stroke on awakening, age more than 80 years, and patients with rapidly improving symptoms, the decision to treat depends on expert judgment. Due to the narrow time window, the fear of bleeding complications, and doubts regarding its effectiveness, tPA is still underused. Constant efforts are required to educate the public on the fact that stroke is a treatable emergency. 2ff7e9595c
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