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This article is a case study, how to write a MVVM (Model View ViewModel) design pattern based X11/Windows (cross platform) 7 segment LCD display (utilizing WPF UserControls) with XAML using the Roma Widget Set (Xrw). The Roma Widget Set is a zero dependency GUI application framework for X11 (it requires only assemblies of the free Mono standard installation and libraries of the free X11 distribution; it doesn"t particularly require GNOME, KDE, cairo, pango or commercial libraries) and is implemented entirely in C#.

Micro-LED and micro-OLED are self-emissive display devices. They are usually more compact than LCoS and DMD because no illumination optics is required. The fundamentally different material systems of LED and OLED lead to different approaches to achieve full-color displays. Due to the “green gap” in LEDs, red LEDs are manufactured on a different semiconductor material from green and blue LEDs. Therefore, how to achieve full-color display in high-resolution density microdisplays is quite a challenge for micro-LEDs. Among several solutions under research are two main approaches. The first is to combine three separate red, green and blue (RGB) micro-LED microdisplay panels7a).

Form factor is another crucial aspect for the light engines of near-eye displays. For self-emissive displays, both micro-OLEDs and QD-based micro-LEDs can achieve full color with a single panel. Thus, they are quite compact. A micro-LED display with separate RGB panels naturally have a larger form factor. In applications requiring direct-view full-color panel, the extra combining optics may also increase the volume. It needs to be pointed out, however, that the combing optics may not be necessary for some applications like waveguide displays, because the EPE process results in system’s insensitivity to the spatial positions of input RGB images. Therefore, the form factor of using three RGB micro-LED panels is medium. For LCoS and DMD with RGB LEDs as light source, the form factor would be larger due to the illumination optics. Still, if a lower luminous efficacy can be accepted, then a smaller form factor can be achieved by using a simpler optics

Recently, another type of display in close relation with Maxwellian view called pin-light display11a. Each pin-light source is a Maxwellian view with a large DoF. When the eye pupil is no longer placed near the source point as in Maxwellian view, each image source can only form an elemental view with a small FoV on retina. However, if the image source array is arranged in a proper form, the elemental views can be integrated together to form a large FoV. According to the specific optical architectures, pin-light display can take different forms of implementation. In the initial feasibility demonstration, Maimone et al.11b). The light inside the waveguide plate is extracted by the etched divots, forming a pin-light source array. A transmissive SLM (LCD) is placed behind the waveguide plate to modulate the light intensity and form the image. The display has an impressive FoV of 110° thanks to the large scattering angle range. However, the direct placement of LCD before the eye brings issues of insufficient resolution density and diffraction of background light.

We used an miRNA array to compare the expression profiles of 180 mature mRNAs (miRNAs) in ESCs, NPCs, gliomas, and normal brains. Our initial panel contained 15 RNA samples derived from glial tumors of various grades, ESCs, NPCs, and normal adult brains from both humans and mice.

For human miRNA testing, fresh frozen tumors were acquired from the brain tumor bank of Hadassah Hebrew-University Medical Centre, in accordance with the regulations and approved procedures of the committee of human research. The initial human panel included a commercial mix of normal brain (Ambion, Austin, TX), an astrocytoma (A), an oligoastrocytoma, an oligodendroglioma (O), two glioblastoma multiforme (GBM), cell lines of an anaplastic astrocytoma (U87MG), and of a GBM (A172), a human ESC (hESC) line (HES-2)

The mouse panel included brains from adult C57BL/6 mice, a mouse glioma cell line (GL261), and one sample of each of the following: NPCs from a 14-day-old embryo (meNPCs), neonatal NPCs (mnNPCs), oligodendrocyte progenitor cells (mOPCs), and astrocytes (mAs), all isolated from brains of 1-day-old C57BL/6 mice. Each sample of precursor or progenitor cells contained pooled RNA extracted from different cell preparations. There were 3 to 7 biological replicates per cell line or tissue type and 3 technical replicates for each sample.

Later, we extended the panel by exploring and quantifying the expression of 5 additional miRNAs (a total of 13 miRNAs located in the Dlk1-Dio3 miRNAs cluster). For this evaluation, we used 12 human astrocytic tumors and 3 Os that do not contain a 1p/19q loss of heterozygosity (LOH).

We also analyzed DNA samples from 40 human tumors (20 Os and 20 glioblastomas) previously extracted for routine genetic analysis. DNA was extracted from paraffin-embedded sections of the tumors used for histological diagnosis. The purpose of this analysis was to evaluate whether chromosomal deletion was associated with downregulation of the Dlk1-Dio3 miRNA cluster analyzed in the extended panel. All patients signed an informed consent form prior to DNA extraction and a neuropathologist (Y.F.) reviewed all tumor samples for verification of histological diagnosis and tumor grade.

A total of 180 miRNA genes were quantified in the miRNA array using the TaqMan® miRNA Assays Panel Early Access Kit (Applied Biosystems), according to the manufacturer"s instructions. Briefly, the assay included two steps: RT and PCR. Each RT reaction was incubated for 30 minutes at 16°C and then at 42°C. Real-time PCR was performed on an ABI 7000 sequence detection system in triplicate for each sample. The fold-change normalization was based on cycle threshold (CT) changes of the mean calculated values obtained by subtracting individual CTs for each tissue from a median CT (ΔCT). For the individual miRNA quantification, the fold change was normalized to the RNU6B transcript (ΔCT). Following normalization, the fold change of each miRNA was calculated between the analyzed tissue (tumor, cell line or SC) and normal brain reference (ΔΔCT).

As described above, miRNA expression was quantified by RT real-time PCR, using the expression profile of the normal adult brains as a reference for all other tissues, separately for each species. It is interesting to note that we observed 80% identity between the miRNA expression signature of human gliomas and the miRNA expression profile of methylcholanthrene-induced mouse glioma GL-261. In the human glioma panel, 71 of the 180 miRNAs showed a distinct expression pattern (defined as either less than 0.5-fold or more than 2-fold compared with adult brain). The expression pattern of these 71 miRNAs was remarkably reminiscent of the expression pattern observed in ESCs and NPCs (Fig. 1A, Table 1).

Heat maps displaying the expression of the miRNAs that showed distinct expression in gliomas, ESCs and NPCs, when compared with normal adult brains. (A) Hierarchical clustering of the 71 miRNAs showed distinct expression (less than 0.5-fold and more than 2-fold) in human gliomas, hESCs, and NPCs, when compared with normal brains. The clustergram was generated using MATLAB Version 7.5.0.342 (R2007b). The expression values ranged between + 20 log2 to −20 log2. (B) Heat map of the clustered miRNAs that showed significantly different expression when compared with normal adult brains. The chromosomal location of the miRNAs is specified in the right row of each species panel: human (right) and murine (left) panels. This figure also demonstrates the similarity in miRNA expression between human and murine gliomas. The expression values ranged between + 10 log2 to −10 log.

The large 7 + 46 bipartite Dlk1-Dio3 miRNA cluster on chromosome 14q32.31 was of special interest. This cluster was downregulated in the initial panel in all gliomas, ESCs, and NPCs. This suggests that this cluster might represent the largest tumor-suppressor miRNA cluster. For this reason, we further explored this region and quantified the expression of 13 miRNAs located along the Dlk1-Dio3 miRNA cluster. For this evaluation, we used 12 astrocytic tumors and 3 Os that did not contain 1p/19q LOH. All of the miRNAs that were tested appeared to be downregulated in hESCs, hNPCs, and in all of the gliomas (Fig. 3A). Because the miRNAs from this large miRNA cluster are expressed only from the maternally inherited allele,

Heat maps displaying the expression levels of miRNAs of 2 clusters in gliomas, hESCs and NPCs, relative to human brains. (A) Thirteen miRNAs within the miRNA cluster in the Dlk1-Dio3 genomic region 14q32.31 in 15 gliomas, hNPCs and hESCs (white cell represents untested). The expression values ranged between +10 log2 to −10 log2. (B) The ES-specific cluster, mir367-302, on chromosome 4q25 (fold change is specified in each cell) in human (left panel) and murine (right panel) tissues comprises gliomas and precursor cells.

The last 2 clusters identified, mir367-302 and hsa-mir-371/372/373/mmu-mir-290 (Table 2), both showed elevated expression in gliomas, hESCs, and hNPCs. The expression pattern of these miRNAs was similar in the mouse glioma GL261 line and in human gliomas. Importantly, in human tissues, these clusters demonstrated significantly higher expression in SCs when compared with gliomas (t-test P ≤ .05) (Fig. 3B, Table 1, bold and underlined). The differences in the expression levels between human gliomas and ESCs were very large, and less pronounced between human gliomas and hNPCs. In the murine samples, the expression level of these glioma miRNAs was within the same range as in meNPCs and mnNPCs (Fig. 3B). Recent work demonstrated that these clusters are strongly expressed in both hESCs3B, murine panel), with a presumably specific pattern of expression at each developmental stage. The similarities in the expression levels of these SC-specific clusters, mir302-367 and mir371-373, in both gliomas and NPCs, as well as the analog expression of these miRNAs in human and mouse gliomas (Fig. 3B) are unlikely to be coincidental. Based on these similarities, it is likely that the origin cells of gliomas are related to NPCs. Of course, there is not enough evidence to rule out the possibility that, following genetic and/or epigenetic alternations, further differentiated progeny are the true glioma-initiating cells that revert to a “stem-like” status. It is also interesting to note that several previous studies have linked the miR372/373 miRNAs to tumorigenesis. It has been shown that miR373 stimulates cancer cell migration and invasion in vitro and in vivo.LATS2.

We used an miRNA array to compare the expression profiles of 180 mature mRNAs (miRNAs) in ESCs, NPCs, gliomas, and normal brains. Our initial panel contained 15 RNA samples derived from glial tumors of various grades, ESCs, NPCs, and normal adult brains from both humans and mice.

For human miRNA testing, fresh frozen tumors were acquired from the brain tumor bank of Hadassah Hebrew-University Medical Centre, in accordance with the regulations and approved procedures of the committee of human research. The initial human panel included a commercial mix of normal brain (Ambion, Austin, TX), an astrocytoma (A), an oligoastrocytoma, an oligodendroglioma (O), two glioblastoma multiforme (GBM), cell lines of an anaplastic astrocytoma (U87MG), and of a GBM (A172), a human ESC (hESC) line (HES-2)

The mouse panel included brains from adult C57BL/6 mice, a mouse glioma cell line (GL261), and one sample of each of the following: NPCs from a 14-day-old embryo (meNPCs), neonatal NPCs (mnNPCs), oligodendrocyte progenitor cells (mOPCs), and astrocytes (mAs), all isolated from brains of 1-day-old C57BL/6 mice. Each sample of precursor or progenitor cells contained pooled RNA extracted from different cell preparations. There were 3 to 7 biological replicates per cell line or tissue type and 3 technical replicates for each sample.

Later, we extended the panel by exploring and quantifying the expression of 5 additional miRNAs (a total of 13 miRNAs located in the Dlk1-Dio3 miRNAs cluster). For this evaluation, we used 12 human astrocytic tumors and 3 Os that do not contain a 1p/19q loss of heterozygosity (LOH).

We also analyzed DNA samples from 40 human tumors (20 Os and 20 glioblastomas) previously extracted for routine genetic analysis. DNA was extracted from paraffin-embedded sections of the tumors used for histological diagnosis. The purpose of this analysis was to evaluate whether chromosomal deletion was associated with downregulation of the Dlk1-Dio3 miRNA cluster analyzed in the extended panel. All patients signed an informed consent form prior to DNA extraction and a neuropathologist (Y.F.) reviewed all tumor samples for verification of histological diagnosis and tumor grade.

A total of 180 miRNA genes were quantified in the miRNA array using the TaqMan® miRNA Assays Panel Early Access Kit (Applied Biosystems), according to the manufacturer"s instructions. Briefly, the assay included two steps: RT and PCR. Each RT reaction was incubated for 30 minutes at 16°C and then at 42°C. Real-time PCR was performed on an ABI 7000 sequence detection system in triplicate for each sample. The fold-change normalization was based on cycle threshold (CT) changes of the mean calculated values obtained by subtracting individual CTs for each tissue from a median CT (ΔCT). For the individual miRNA quantification, the fold change was normalized to the RNU6B transcript (ΔCT). Following normalization, the fold change of each miRNA was calculated between the analyzed tissue (tumor, cell line or SC) and normal brain reference (ΔΔCT).

As described above, miRNA expression was quantified by RT real-time PCR, using the expression profile of the normal adult brains as a reference for all other tissues, separately for each species. It is interesting to note that we observed 80% identity between the miRNA expression signature of human gliomas and the miRNA expression profile of methylcholanthrene-induced mouse glioma GL-261. In the human glioma panel, 71 of the 180 miRNAs showed a distinct expression pattern (defined as either less than 0.5-fold or more than 2-fold compared with adult brain). The expression pattern of these 71 miRNAs was remarkably reminiscent of the expression pattern observed in ESCs and NPCs (Fig. 1A, Table 1).

Heat maps displaying the expression of the miRNAs that showed distinct expression in gliomas, ESCs and NPCs, when compared with normal adult brains. (A) Hierarchical clustering of the 71 miRNAs showed distinct expression (less than 0.5-fold and more than 2-fold) in human gliomas, hESCs, and NPCs, when compared with normal brains. The clustergram was generated using MATLAB Version 7.5.0.342 (R2007b). The expression values ranged between + 20 log2 to −20 log2. (B) Heat map of the clustered miRNAs that showed significantly different expression when compared with normal adult brains. The chromosomal location of the miRNAs is specified in the right row of each species panel: human (right) and murine (left) panels. This figure also demonstrates the similarity in miRNA expression between human and murine gliomas. The expression values ranged between + 10 log2 to −10 log.

The large 7 + 46 bipartite Dlk1-Dio3 miRNA cluster on chromosome 14q32.31 was of special interest. This cluster was downregulated in the initial panel in all gliomas, ESCs, and NPCs. This suggests that this cluster might represent the largest tumor-suppressor miRNA cluster. For this reason, we further explored this region and quantified the expression of 13 miRNAs located along the Dlk1-Dio3 miRNA cluster. For this evaluation, we used 12 astrocytic tumors and 3 Os that did not contain 1p/19q LOH. All of the miRNAs that were tested appeared to be downregulated in hESCs, hNPCs, and in all of the gliomas (Fig. 3A). Because the miRNAs from this large miRNA cluster are expressed only from the maternally inherited allele,

Heat maps displaying the expression levels of miRNAs of 2 clusters in gliomas, hESCs and NPCs, relative to human brains. (A) Thirteen miRNAs within the miRNA cluster in the Dlk1-Dio3 genomic region 14q32.31 in 15 gliomas, hNPCs and hESCs (white cell represents untested). The expression values ranged between +10 log2 to −10 log2. (B) The ES-specific cluster, mir367-302, on chromosome 4q25 (fold change is specified in each cell) in human (left panel) and murine (right panel) tissues comprises gliomas and precursor cells.

The last 2 clusters identified, mir367-302 and hsa-mir-371/372/373/mmu-mir-290 (Table 2), both showed elevated expression in gliomas, hESCs, and hNPCs. The expression pattern of these miRNAs was similar in the mouse glioma GL261 line and in human gliomas. Importantly, in human tissues, these clusters demonstrated significantly higher expression in SCs when compared with gliomas (t-test P ≤ .05) (Fig. 3B, Table 1, bold and underlined). The differences in the expression levels between human gliomas and ESCs were very large, and less pronounced between human gliomas and hNPCs. In the murine samples, the expression level of these glioma miRNAs was within the same range as in meNPCs and mnNPCs (Fig. 3B). Recent work demonstrated that these clusters are strongly expressed in both hESCs3B, murine panel), with a presumably specific pattern of expression at each developmental stage. The similarities in the expression levels of these SC-specific clusters, mir302-367 and mir371-373, in both gliomas and NPCs, as well as the analog expression of these miRNAs in human and mouse gliomas (Fig. 3B) are unlikely to be coincidental. Based on these similarities, it is likely that the origin cells of gliomas are related to NPCs. Of course, there is not enough evidence to rule out the possibility that, following genetic and/or epigenetic alternations, further differentiated progeny are the true glioma-initiating cells that revert to a “stem-like” status. It is also interesting to note that several previous studies have linked the miR372/373 miRNAs to tumorigenesis. It has been shown that miR373 stimulates cancer cell migration and invasion in vitro and in vivo.LATS2.