Ms Office Slo Activation !!HOT!!
I just built my first Server 2016 XenApp server in App Layering, and the one issue I'm seeing is that the Office activation script apparently doesn't run at all. kmssetup.cmd does appear in the startup in AutoRuns, and Windows is being activated. I followed the same exact steps that I did in Windows 10 (which works perfectly), so I'm not sure if there's another step that needs to be done here. This is my process:
Ms Office Slo Activation
I just submitted my case with Citrix, but I think I'm onto something here. On a hunch, I replaced the kmssetup.cmd file on my layered image with the one from App Layering 1812 (and many versions before that), since it was modified in this new one. I sealed the image and rebooted, and now the Office Activation script is running and activating. The only change I see in that file is where the Office activation is actually running (it was moved to near the end of the script in 1901). If you compare the two files on your end you'll see what I mean. I'm going to replace that file in my Office layer and build another image to see if that resolves it. If so, I imagine I won't be the only one affected by this...
It looks like the kmssetup.cmd in 19.01 was edited to fix an order of operations problem between Windows and Office activation, and accidentally moved Office activation so that it only happens on the second boot. In MCS, that's OK, there are several boots in the preparation process. But with PVS, there is just one, so Office doesn't get activated. Support has a slightly modified copy of kmssetup.cmd which should work, but I haven't tested it myself.
After you download the Office Deployment Tool, double-click on the officedeploymenttool executable (.exe) file to extract the ODT files. When you're finished, you should have several files: setup.exe and some sample configuration.xml files. For an Office LTSC 2021-specific sample, see Sample configuration.xml file to use with the Office Deployment Tool.
Figure 3. Mechanism for the activation of the sAHP as proposed in this review. Global increases in cytosolic calcium lead to activation of diffusible neuronal calcium sensors (NCS: hippocalcin, neurocalcin δ). Binding of calcium to NCS exposes a previously sequestered myristoyl moiety allowing NCS to bind to the plasma membrane. Binding of NCS to plasma membrane leads to a transient increase in PtdIns(4,5)P2 levels and subsequent activation of the sAHP.
When you open an Office program for the first time, it will ask you to agree to the license agreement, so click Accept if you do. You might also see the Microsoft Office Activation Wizard; follow the instructions for this. It's always best to select I want to activate the software over the internet option for the speediest activation.
I am using Ubuntu and I need to do my project work. When I use libre office for the work purpose it stores in odt format and converting from odt to docx format changes the alignment of words and paragraphs in documentation.
Yes, there is a good alternative. Onlyoffice is free and open source (GitHub), and has excellent Microsoft Office compatibility (including viewing Annotated Powerpoint presentations).
Just from personal experience, I have found WPS office has the best compatibility with Desktop MS-Word and Excel; I've tried Libre Office, OnlyOffice, Office365 (Google Docs is better I think), an others I've forgotten about, but they all come up a bit short. Also since WPS's ribbon format seems to be an almost like-for-like rip-off of MS-Office, it has the shortest learning curve if you're a long-standing MS-Office user. I have tried to persevere with LibreOffice in the past, it's very comprehensive, but some features are still a bit clunky, and the rendering quite often is just a bit "off" (like Disney characters on the back of ice-cream vans), enough to make it a time-waster
Google docs is also a good alternative for microsoft office package. It's bit hard to truly dependent on microsoft office if you are on ubuntu. The best option is to stick permanently to one option. There is a burden to switch between softwares. I prefer google docs.
outside of running Microsoft Office 365 in a browser, depending on what functionality and version compatibility you need, you can use different alternative as already said before, but one important for me is the OLE automation.The only office alternative that has it to my knowledge is openoffice.note that it is not working when libre office is installed!
The following links point to the official download server officecdn.microsoft.com. Instead of ISO format, they come as IMG images. These files are pure backup media, and can't be installed without a retail product key.
Diethylcarbamazine is a drug that is used for the treatment of filariasis in humans and animals; it also has effects on intestinal nematodes, but its mechanism of action remains unclear. Emodepside is a resistance-busting anthelmintic approved for treating intestinal parasitic nematodes in animals. The novel mode of action and resistance-breaking properties of emodepside has led to its use against intestinal nematodes of animals, and as a candidate drug for treating filarial parasites. We have previously demonstrated effects of emodepside on SLO-1 K+-like currents in Ascaris suum. Here, we demonstrate that diethylcarbamazine, which has been proposed to work through host mediated effects, has direct effects on a nematode parasite, Ascaris suum. It increases activation of SLO-1 K+ currents and potentiates effects of emodepside. Our results suggest consideration of the combination of emodepside and diethylcarbamazine for therapy, which is predicted to be synergistic. The mode of action of diethylcarbamazine may involve effects on parasite signaling pathways (including nitric oxide) as well as effects mediated by host inflammatory mediators.
Filarial parasites and soil-transmitted nematodes (STNs) are Neglected Tropical Diseases (NTDs) that affect millions of people in the developing world. There is an urgent need for novel drugs and improved use of existing drugs, because of concerns about the development of resistance. The mode of action of one of these drugs, diethylcarbamazine, remains unclear, despite the fact that it has been used for a long time for treatment and prevention of filariae and STNs. The resistance-busting anthelmintic emodepside also has effects against filariae and STNs, with a mode of action that involves activation of nematode SLO-1 K+ channels. The effects of both diethylcarbamazine and emodepside may be increased by inflammatory mediators, which suggests that the effects of diethylcarbamazine and emodepside will be additive. We used our Ascaris suum preparation to test the activation of SLO-1 K+ channels by diethylcarbamazine and its potentiating effect on emodepside. Our results suggest potential for diethylcarbamazine and emodepside in combination therapy for parasitic nematodes.
Funding: The research project culminating in this paper was funded by the National Institute of Allergy and Infectious Diseases (NIH) grant R 01 A1 047194 to RJM and the Iowa Center for Advanced Neurotoxicity (ICAN) seed grant to APR. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIAID awarding office or NIH.
Emodepside, a semisynthetic derivative of PF1022A, has a novel mechanism of action, different from other anthelmintics; it is effective against a broad spectrum of parasitic nematodes, including soil-transmitted nematodes [7], [8]. Emodepside has a complex mode of action involving activation of a voltage-activated calcium-dependent K+ channel (SLO-1) at the neuromuscular junction [9], [10] and potentiation of its effects by drugs that increase levels of nitric oxide [11]. Emodepside has potential as a drug for the treatment of filarial parasites: it is larvicidal and adulticidal in vitro and in vivo but the efficacy of emodepside against filariae depends on species, being quite low against Brugia pahangi and Brugia malayi in comparison to other filariae [12], [13], [14].
We were interested to determine: how diethylcarbamazine would affect calcium-dependent SLO-1 K+ currents in isolated Ascaris suum muscle flap preparations and; how diethylcarbamazine interacts with emodepside. The interest was prompted by observations in vertebrates [17] which show that nitric oxide activates SLO-1 K+ channels and observations on Ascaris indicating the presence nitric oxide synthase [18] and of SLO-1 K+ channels which show positive modulation by a nitric oxide pathway [11], [19]. We hypothesized that diethylcarbamazine, with effects on arachidonic acid and nitric oxide pathways, may increase activation of SLO-1 K+ currents in Ascaris suum muscle and potentiate effects of emodepside on membrane potential. We conducted experiments in the presence of sufficient calcium to allow activation of the SLO-1 K+ currents. Here we show that diethylcarbamazine, by itself, can increase activation of SLO-1 K+ currents and potentiate effects of emodepside.
We have shown that emodepside increases SLO-1 K+ currents by shifting V50 of the voltage-activation curve in the hyperpolarizing direction [11]. Consequently, we investigated the effects of diethylcarbamazine on the voltage-activation of SLO-1 K+ currents by itself and in combination with emodepside. Fig. 1 A shows a representative recording of the control SLO-1 K+ current produced by holding the cell at -50 mV and stepping to 0 mV; the arrow, Fig. 1 A indicates the time-point in the depolarizing pulse at which the current measurements were taken for plotting results. The application of diethylcarbamazine by itself significantly increased the peak K+ currents by 213% (p 350c69d7ab
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