msi lcd panel free sample

Make some noise for Intel Gamer Days 2022. An exclusive event featuring the best deals, promotions, and special giveaways on MSI"s Intel Core-powered PCs and hardware.

The most difference between the MSI desktop and the others is that the desktop series could bring best gaming experience to global gamer. Besides, the high performance is not only base on MSI extraordinary hardware design. Also, include with all MSI exclusive software (Like Command Center, Mystic Light, Realtek Audio Control and Super Charger). Those useful software applications could help on system performance and provide the whole new experience for all desktop users.

MSI Command Center is an user-friendly software and exclusively developed by MSI, helping users to adjust system settings and monitor status under OS. With the help of COMMAND CENTER, making it possible to achieve easier and efficient monitoring process and adjustments than that under BIOS. In addition, the COMMAND CENTER can be a server for mobile remote control application.

CPU Frequency control panel allows you to change CPU Ratio and Base clock. You can see the current frequency of each CPU core on the top of the panel.

CPU Fan control panel provides Smart mode and Manual Mode. You can switch the control mode by clicking the Smart Mode and Manual Mode buttons on the top of the CPU Fan control panel.

The control panel contains 4 dots allows you to drag and adjust the Smart Speed slopes. The fan speed will be changed along these lines with CPU temperature. The white dot will create strip chart in real time.

is only available for the motherboard with the built-in WiFi module. It allows you to enable/disable the COMMAND CENTER Remote Server. Please refer to the instruction on the Mobile Control control panel.

MYSTIC LIGHT is an application that allows you to control the LED light effects of MSI & partner products. For some earlier products, you can go to product download page to download the applicable LED control software.

Nahimic 3 is included in the audio driver. If you need to install it or update it, please use the Driver Disc with your motherboard or download the driver from MSI’s official website.

Super Charger provides i-Pad, i-Phone and iPod charging function. The iPad with very special charging requirements as it requires 1.6A power supply rather than the 0.5A current available with conventional USB interfaces. That is ordinary computer cannot charge your iPad even at power on status. The MSI Super Charger is a Windows resident program capable of revising power supply mode of your USB port. Once an iPad is connected to your USB port the Super Charger sends a signal to initiate its charging circuit.

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Duet turns your iPad or iPhone into the most advanced extra display for your MSI PC. Developed by a team of ex-Apple engineers, Duet offers unparalleled performance and display quality - all with zero lag.

TNM stage remains the key determinant of patient prognosis after surgical resection of colorectal cancer (CRC), and informs treatment decisions. However, there is considerable stage-independent variability in clinical outcome that is likely due to molecular heterogeneity. This variability underscores the need for robust prognostic and predictive biomarkers to guide therapeutic decision-making including the use of adjuvant chemotherapy. Although the majority of CRCs develop via a chromosomal instability pathway, approximately 12-15% have deficient DNA mismatch repair (dMMR) which is characterized in the tumor by microsatellite instability (MSI). Tumors with the dMMR/MSI develop from a germline mutation in an MMR gene (MLH1, MSH2, MSH6, PMS2), i.e., Lynch syndrome, or more commonly from epigenetic inactivation of MLH1 MMR gene. CRCs with dMMR/MSI status have a distinct phenotype that includes predilection for the proximal colon, poor differentiation, and abundant tumor infiltrating lymphocytes. Consistent data indicate that these tumors have a better stage-adjusted survival compared to proficient MMR or microsatellite stable (MSS) tumors, and may respond differently to 5-fluorouracil-based adjuvant chemotherapy. To increase the identification of dMMR/MSI patients in clinical practice that includes those with Lynch Syndrome, it is recommended that all resected CRCs to be analyzed for MMR status. Available data indicate that patients with stage II dMMR CRCs have an excellent prognosis and do not benefit from 5-FU-based adjuvant chemotherapy which supports their recommended management by surgery alone. In contrast, the benefit of standard adjuvant chemotherapy with the FOLFOX regiment in stage III dMMR CRC patients awaits further study and therefore, all patients should be treated with standard adjuvant FOLFOX.

TNM stage remains the gold standard for informing patient prognosis and guiding management after resection for non-metastatic colorectal cancer (CRC). Despite the same disease stage, however, CRC patients exhibit considerable variability in clinical outcome that is likely related to molecular tumor heterogeneity. Therefore, the molecular classification of CRC may identify patient subgroups at varying risk of recurrence and death and for who personalized approaches to therapy may beneficial. The majority of CRCs develop via the chromosomal instability pathway (CIN), whereas 12-15% arise from the microsatellite instability (MSI) pathway that is a consequence of deficient (d) DNA mismatch repair (MMR). Deficient MMR can develop from an inherited germline mutation in a MMR gene (MLH1, MSH2, MSH6, PMS2) i.e., Lynch Syndrome, or more commonly due to epigenetic inactivation of the MLH1 gene and the CpG island methylator phenotype (CIMP). These sporadic dMMR tumors carry somatic mutations in the BRAF oncogene in approximately half of cases. Studies have shown that dMMR tumors have phenotypic features including poor differentiation, proximal colon location, and abundant tumor-infiltrating lymphocytes. Furthermore, dMMR tumors have been consistently associated with a better stage-adjusted survival compared to proficient MMR (pMMR) tumors.

Among early stage CRCs, the survival advantage of dMMR status appears to be greater among stage II compared to stage III patients. In patients with stage II colon cancers and dMMR, studies demonstrate a lack of benefit of adjuvant 5-FU-based chemotherapy. Among patients with stage III disease, the predictive impact of MMR status for adjuvant chemotherapy remains controversial. Multiple prior studies have demonstrating a lack of benefit for 5-fluorouracil (FU) as adjuvant chemotherapy, although only limited data exist for patients with stage III dMMR CRCs treated with standard the adjuvant FOLFOX regimen. In contrast to 5-FU, in vitro data indicate that dMMR/MSI CRC cell lines display sensitivity to oxaliplatin and accordingly, this agent may provide benefit in patients with dMMR CRCs.

The Cancer Genome Atlas (TCGA) Research Network has revealed a comprehensive characterization of the genomes of 224 cancerous colorectal tumors and normal pairs (1). Among CRCs studied, 16% of were found to be hypermutated, and 77% of these tumors displayed high frequency microsatellite instability (MSI-H) that was generally associated with hypermethylation and MLH1 gene. The remaining hypermutated tumors were primarily characterized by having mutations in somatic MMR pathways and in polymerase epsilon (POLE)[1].

The DNA MMR system repairs base-base mispairs introduced into microsatellites during DNA synthesis to maintain genomic stability (2). Microsatellites are short, tandemly-repeated sequences that occur throughout the genome and are used as markers of deficient (d) MMR. The DNA MMR system is composed of 4 MMR genes and their encoded proteins (MLH1, MSH2, MSH6, PMS2). Inactivation of MLH1 and MSH2 account for over 90% of dMMR cases. Deficiency of MMR results in production of a truncated, nonfunctional protein or loss of a protein that causes MSI. Therefore, dMMR is frequently analyzed by testing for loss of an MMR protein or for MSI using a PCR-based assay.

MSI testing can be performed on fresh, frozen or paraffin-embedded tumor tissue using a PCR-based assay for detection of instability (3, 4).The National Cancer Institute Workshop agreed on five microsatellite markers necessary to determine MSI (5) that include two mononucleotide – BAT25/26 and three dinucleotide markers – D2S123, D5S346, and D17S250. Interpretation of the profiles requires a comparison with normal DNA from each patient. An alternative molecular method based exclusively on quasi-monomorphic mononucleotide markers was developed to avoid the analysis of matching normal DNA. This method has been proven to be more specific and sensitive than the original NCI panel (5).

On the basis of the MSI status, CRCs can be classified into three groups: MSI-H, if two or more of the five microsatellite markers show instability; MSI-L (low-frequency MSI), if only one of five markers shows instability; and microsatellite stable (MSS) if none of the markers show instability (6).

MSI testing and IHC are complimentary, and loss of MMR protein expression by IHC has been shown to be highly concordant with DNA-based MSI testing with a good sensitivity (>90%) and a excellent specificity (100%) (4).

Tumors displaying loss of an MMR protein can be collectively referred to as dMMR and are considered to be MSI-H, whereas those with intact MMR proteins can be classified as pMMR are are expected to be microsatellite stable (MSS) or MSI-low (MSI-L).➢

LS accounts for approximately 3-4% of all CRCs and one third of all dMMR/MSI-associated CRCs. LS is inherited in an autosomal dominant manner and results from a germline loss-of-function mutation (9) that occurs more commonly in MLH1 or MSH2, and infrequently in MSH6 or PMS2 (10). A germline mutation in an MMR gene followed by a second hit (somatic event) to the wild-type copy is needed to produce LS, and can occur due to point mutation, loss of heterozygosity or methylation.

CRCs from LS patients are significantly less likely to carry KRAS mutations compared to pMMR/MSS cancers and importantly, BRAFV600E mutations are lacking in these patients. Among dMMR/MSI CRCs, BRAFV600E mutation testing can be performed to distinguish LS cases from sporadic dMMR tumors (13) (Figure 1).

Bethesda criteria were revised in 2004 to guide selection of patients for LS testing (14). The guideline indicated that tumors should be tested for MSI in the following clinical situations:

Families that meet the Amsterdam Criteria (15) but who lack a germline mutation in an MMR gene and an MSI-H tumor, have been termed familial CRC, type × (16).

Sporadic MSI-H CRCs show loss of MLH1 that generally occurs in a background of the CpG island methylator phenotype (CIMP) (17, 18). CIMP represents dense promoter hypermethylation of cancer-specific genes. CIMP-related silencing of the MLH1 gene is responsible for about 80% of cases in which MLH1/PMS2 protein expression are lost (7).

Patients with MSI-H sporadic CRCs share most of the clinicopathological features with LS cases, yet have distinct epidemiological features including older age at diagnosis, predominance of female gender and increased rate of cigarette smoking (21).

CRC with dMMR is more frequent in stage II (almost 20%) compared to stage III (12%), and are relatively uncommon among metastatic tumors (4%) (22). This highlights the importance of MSI testing in early stage disease where patients can be potentially cured by surgery alone or combined with adjuvant chemotherapy.

A meta-analysis from 32 studies with 1,277 MSI/dMMR cases included 7,642 patients with stage I-IV CRC. A better prognosis was found for patients with MSI/dMMR than those with MSS, MSI-L/pMMR tumors (28) among patients that were untreated or treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy. The hazard ratio (HR) for overall survival (OS) was 0.65 [95 % confidence interval (CI), 0.59-0.71] in favor of dMMR CRC patients. Results were confirmed when the analyses was restricted to patients with stage II or III CRC participating in clinical trials (28).

In a retrospective analysis of the CALGB 89803 trial where patients with stage III colon cancer were randomly assigned to weekly bolus 5-FU/leucovorin (LV) or weekly bolus irinotecan, 5-FU, and LV (IFL), IFL-treated patients with dMMR/MSI-H tumors showed improved 5-year DFS as compared to pMMR tumors (HR=0.76; 95% CI, 0.64 to 0.88 vs. 0.59; 95% CI, 0.53 to 0.64; P = .03), which was not observed among patients treated with 5-FU/LV (63). However, data from the PETACC-3 study (64) failed to show a benefit for irinotecan in patients with dMMR colon cancers.

This study showed that BRAF mutation was not prognostic for recurrence-free survival but was for overall survival, particularly in patients with MSI-L and MSI-S tumors.

Adjuvant study found that MSI-H was significantly associated with RFS in stage II and III colon cancer patients treated with 5-FU/LV alone or combined with irinotecan. However, the relationship with OS was only significant for stage II patients.

We recommend that you uninstall any previous versions of Office before installing Microsoft 365 Apps. To help you uninstall versions of Office that use Windows Installer (MSI) as the installation technology, you can use the Office Deployment Tool and specify the RemoveMSI element in your configuration.xml file.

RemoveMSI doesn’t uninstall prior versions of Office, including Visio and Project, that use Click-to-Run as the installation technology. You can uninstall those versions of Office through Control Panel or by running the Office Deployment Tool and using the Remove element in your configuration.xml file.

To uninstall all versions of Office, including Visio and Project, that are already installed on the computer, add to your configuration.xml file. Language resources – for example, language packs, language interface packs, or proofing tools – will also be removed.

Here’s an example of a configuration.xml file that installs the 64-bit Current Channel version of Microsoft 365 Apps for enterprise in English from the Office Content Delivery Network (CDN) on the internet and uninstalls any Windows Installer (MSI) versions of Office on the computer.

If there are language resources – for example, language packs, language interface packs, or proofing tools – already installed on the computer, you can get Click-to-Run versions of the same language resources installed when you install Microsoft 365 Apps. To install the same language resources, add to your configuration.xml file.

Here’s an example of a configuration.xml file that installs the 64-bit Monthly Enterprise Channel version of Microsoft 365 Apps for enterprise in English, along with any existing languages on the computer, from the Office Content Delivery Network (CDN) on the internet and uninstalls any Windows Installer (MSI) versions of Office on the computer.

Here’s an example of a configuration.xml file that installs the 64-bit Monthly Enterprise Channel version of Microsoft 365 Apps for enterprise in English from the Office Content Delivery Network (CDN) on the internet and uninstalls any Windows Installer (MSI) versions of Office, except for Visio Professional, on the computer.

You can use the RemoveMSI element in conjunction with the MSICondition attribute. That attribute allows you to control the installation of an Office product based on whether a particular MSI-based product is already installed on the device. For example, only install Project Online Desktop Client if Project Professional is already installed on the device. For more information, see MSICondition attribute.

A reboot is required to finish uninstalling the Windows Installer (MSI) versions of Office, but the reboot isn’t enforced. You can reboot after the Microsoft 365 Apps installation is finished.

If you"re using RemoveMSI on a Windows 7 SP1 computer, pinned shortcuts that the user created might sometimes remain even though the previous version of Office and all of its other shortcuts have been removed. To remove the pinned shortcut, simply click on it and you"ll be prompted to remove it. Or, sign in as the user who created the pinned shortcut, and then run the Office Deployment Tool to upgrade to Microsoft 365 Apps.