N4 is built for flexible control of virtually any music source. You can use its built-in mixer to bring external sources into your mix including turntables, CD players and MP3 players: choose in an instant to switch from controlling four decks of software to controlling two decks of software plus two channels of external source.
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Microsoft omitted multi-user support from MS-DOS because Microsoft's Unix-based operating system, Xenix, was fully multi-user.[12] The company planned, over time, to improve MS-DOS so it would be almost indistinguishable from single-user Xenix, or XEDOS, which would also run on the Motorola 68000, Zilog Z8000, and the LSI-11; they would be upwardly compatible with Xenix, which Byte in 1983 described as "the multi-user MS-DOS of the future".[13][14] Microsoft advertised MS-DOS and Xenix together, listing the shared features of its "single-user OS" and "the multi-user, multi-tasking, UNIX-derived operating system", and promising easy porting between them.[15] After the breakup of the Bell System, however, AT&T Computer Systems started selling UNIX System V. Believing that it could not compete with AT&T in the Unix market, Microsoft abandoned Xenix, and in 1987 transferred ownership of Xenix to the Santa Cruz Operation (SCO).
On March 25, 2014, Microsoft made the code to SCP MS-DOS 1.25 and a mixture of Altos MS-DOS 2.11 and TeleVideo PC DOS 2.11 available to the public under the Microsoft Research License Agreement, which makes the code source-available, but not open source as defined by Open Source Initiative or Free Software Foundation standards.[16][17][18][19] Microsoft would later re-license the code under the MIT License on September 28, 2018, making these versions free software.[2]
Microsoft and IBM together began what was intended as the follow-on to MS-DOS/PC DOS, called OS/2. When OS/2 was released in 1987, Microsoft began an advertising campaign announcing that "DOS is Dead" and stating that version 4 was the last full release. OS/2 was designed for efficient multi-tasking and offered a number of advanced features that had been designed together with similar look and feel; it was seen as the legitimate heir to the "kludgy" DOS platform.
Microsoft had been accused of carefully orchestrating leaks about future versions of MS-DOS in an attempt to create what in the industry is called FUD (fear, uncertainty, and doubt) regarding DR DOS. For example, in October 1990, shortly after the release of DR DOS 5.0, and long before the eventual June 1991 release of MS-DOS 5.0, stories on feature enhancements in MS-DOS started to appear in InfoWorld and PC Week. Brad Silverberg, then Vice President of Systems Software at Microsoft and general manager of its Windows and MS-DOS Business Unit, wrote a forceful letter to PC Week (November 5, 1990), denying that Microsoft was engaged in FUD tactics ("to serve our customers better, we decided to be more forthcoming about version 5.0") and denying that Microsoft copied features from DR DOS:
MS-DOS 6.0 and 6.20 were released in 1993, both including the Microsoft DoubleSpace disk compression utility program. Stac successfully sued Microsoft for patent infringement regarding the compression algorithm used in DoubleSpace. This resulted in the 1994 release of MS-DOS 6.21, which had disk compression removed. Shortly afterwards came version 6.22, with a new version of the disk compression system, DriveSpace, which had a different compression algorithm to avoid the infringing code.
The 16-bit versions of Windows (up to 3.11) ran as a Graphical User Interface (GUI) on top of MS-DOS. With Windows 95, 98, and Me, the role of MS-DOS was reduced to a boot loader according to Microsoft, with MS-DOS programs running in a virtual DOS machine within 32-bit Windows, with ability to boot directly into MS-DOS retained as a backward compatibility option for applications that required real mode access to the hardware, which was generally not possible within Windows.[77] The command line accessed the DOS command line (usually COMMAND.COM) through a Windows module (WINOLDAP.MOD).[clarification needed]
All versions of Windows for Itanium (no longer sold by Microsoft) and x86-64 architectures no longer include the NTVDM and can therefore no longer natively run DOS or 16-bit Windows applications. There are alternatives such as virtual machine emulators such as Microsoft's own Virtual PC, as well as VMware, DOSBox etc., unofficial compatibility layers such as NTVDMx64, OTVDM (WineVDM), Win3mu and others.
The introduction of Windows 3.0 in 1990, with an easy-to-use graphical user interface, marked the beginning of the end for the command-line driven MS-DOS. With the release of Windows 95 (and continuing in the Windows 9x product line through to Windows Me), an integrated version of MS-DOS was used for bootstrapping, troubleshooting, and backwards-compatibility with old DOS software, particularly games, and no longer released as a standalone product.[78] In Windows 95, the DOS, called MS-DOS 7, can be booted separately, without the Windows GUI; this capability was retained through Windows 98 Second Edition. Windows Me removed the capability to boot its underlying MS-DOS 8.0 alone from a hard disk, but retained the ability to make a DOS boot floppy disk (called an "Emergency Boot Disk") and can be hacked to restore full access to the underlying DOS. On December 31, 2001, Microsoft declared all versions of MS-DOS 6.22 and older obsolete and stopped providing support and updates for the system.[79] As MS-DOS 7.0 was a part of Windows 95, support for it also ended when Windows 95 extended support ended on December 31, 2001.[80] As MS-DOS 7.10 and MS-DOS 8.0 were part of Windows 98 and Windows ME respectively, support ended when Windows 98 and ME extended support ended on July 11, 2006, thus ending support and updates of MS-DOS from Microsoft.[81]
Due to the historical nature of the software, Microsoft will not accept any pull requests to the code; only pull requests for modified and translated documentation will be accepted. Users, however, are allowed and fully encouraged to fork the repository containing the MS-DOS source code and make their own modifications, and do whatever they like with it.
A substantial body of evidence supports that the gut microbiota plays a pivotal role in the regulation of metabolic, endocrine and immune functions. In recent years, there has been growing recognition of the involvement of the gut microbiota in the modulation of multiple neurochemical pathways through the highly interconnected gut-brain axis. Although amazing scientific breakthroughs over the last few years have expanded our knowledge on the communication between microbes and their hosts, the underpinnings of microbiota-gut-brain crosstalk remain to be determined. Short-chain fatty acids (SCFAs), the main metabolites produced in the colon by bacterial fermentation of dietary fibers and resistant starch, are speculated to play a key role in neuro-immunoendocrine regulation. However, the underlying mechanisms through which SCFAs might influence brain physiology and behavior have not been fully elucidated. In this review, we outline the current knowledge about the involvement of SCFAs in microbiota-gut-brain interactions. We also highlight how the development of future treatments for central nervous system (CNS) disorders can take advantage of the intimate and mutual interactions of the gut microbiota with the brain by exploring the role of SCFAs in the regulation of neuro-immunoendocrine function.
Figure 1. Potential pathways through which SCFAs influence gut-brain communication. Short-chain fatty acids (SCFAs) are the main metabolites produced by the microbiota in the large intestine through the anaerobic fermentation of indigestible polysaccharides such as dietary fiber and resistant starch. SCFAs might influence gut-brain communication and brain function directly or indirectly. Following their production, SCFAs are absorbed by colonocytes, mainly via H+-dependent monocarboxylate transporters (MCTs) or sodium-dependent monocarboxylate transporters (SMCTs). Through binding to G protein-coupled receptors (GPCRs) such as free fatty acid receptor 2 and 3 (FFAR2 and FFAR3), as well as GPR109a/HCAR2 (hydrocarboxylic acid receptor) and GPR164 or by inhibiting histone deacetylases, SCFAs influence intestinal mucosal immunity, and barrier integrity and function. SCFA interaction with their receptors on enteroendocrine cells promotes indirect signaling to the brain via the systemic circulation or vagal pathways by inducing the secretion of gut hormones such as glucagon-like peptide 1 (GLP1) and peptide YY (PYY), as well as γ-aminobutyric acid (GABA), and serotonin (5-HT). Colon-derived SCFAs reaches the systemic circulation and other tissues, leading to brown adipose tissue activation, regulation of liver mitochondrial function, increased insulin secretion by β-pancreatic cells, and whole-body energy homeostasis. Peripherally, SCFAs influence systemic inflammation mainly by inducing T regulatory cells (Treg) differentiation and by regulating the secretion of interleukins. SCFAs can cross the blood-brain barrier (BBB) via monocarboxylate transporters located on endothelial cells and influence BBB integrity by upregulating the expression of tight junction proteins. Finally, in the central nervous system (CNS) SCFAs also influence neuroinflammation by affecting glial cell morphology and function as well as by modulating the levels of neurotrophic factors, increasing neurogenesis, contributing to the biosynthesis of serotonin, and improving neuronal homeostasis and function. Together, the interaction of SCFAs with these gut-brain pathways can directly or indirectly affect emotion, cognition, and pathophysiology of brain disorders. Figure of this review was created with BioRender ( ).
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