Analogue Media Technologies continues its growth with the expansion of their 200 Middlefield Rd. factory and warehouse in Scarborough, Ontario! Our facilities include a professional CD/DVD pressing plant, a high-quality printshop specializing in digital and offset print, and an audio cassette duplication center. We offer top quality and fast service to artists, labels, brokers, resellers, printshops, government, and corporate accounts.
We ship to the USA by UPS and our shipping rates are very competitive. Transport time can be as quick as 2 days depending on the area. We offer FREE SHIPPING TO THE USA AND CANADA on tape duplication packages.
Duplication.ca (Analogue Media Technologies Inc., Amtech) is your most reliable duplication source in Canada for more than 30 years. We offer quick turnaround on CD and DVD duplication, DVD replication and audio cassette manufacturing, even same-day service. We offer CD and CD-ROM replication of any quantity starting from 100 pieces. We once again offer 12 inch and 7 inch vinyl pressing. We also offer an extensive variety of printed inserts, mailers, boxes, and posters - and we have the graphic arts and prepress skills to make sure your CDs or cassettes look great. And to round out our product line to make us truly a one-stop shop, we have very competitive prices on blank CD-Rs and DVD-Rs, cassettes and accessories.
MECP2 duplication syndrome is a condition that occurs almost exclusively in males and is characterized by moderate to severe intellectual disability. Most people with this condition also have weak muscle tone in infancy, feeding difficulties, poor or absent speech, or muscle stiffness (rigidity). Individuals with MECP2 duplication syndrome have delayed development of motor skills such as sitting and walking. About half of individuals have seizures, often of the tonic-clonic type. This type of seizure involves a loss of consciousness, muscle rigidity, and convulsions and may not respond to medication. Some affected individuals experience the loss of previously acquired skills (developmental regression). Approximately half of individuals learn to walk, and about one-third of people with this condition require assistance when walking. Many individuals with MECP2 duplication syndrome have recurrent respiratory tract infections. These respiratory infections are a major cause of death in affected individuals, with only half surviving past age 25.
The prevalence of MECP2 duplication syndrome is unknown; more than 200 affected individuals have been described in the scientific literature. It is estimated that this condition is responsible for 1 to 2 percent of all cases of intellectual disability caused by changes in the X chromosome.
MECP2 duplication syndrome is caused by a genetic change in which there is an extra copy of the MECP2 gene in each cell. This extra copy of the MECP2 gene is caused by a duplication of genetic material on the long (q) arm of the X chromosome. The size of the duplication varies from 100,000 to a few million DNA building blocks (base pairs). The MECP2 gene is always included in this duplication, and other genes may also be involved, depending on the size of the duplicated segment. It is unclear whether extra copies of these other genes affect the severity of the condition.
The MECP2 gene provides instructions for making a protein called MeCP2 that is critical for normal brain function. Researchers believe that this protein has several functions, including regulating other genes in the brain by controlling when they are able to participate in protein production. An extra copy of the MECP2 gene leads to the production of excess MeCP2 protein and an increase in protein function. The resulting changes in gene regulation and protein production in the brain lead to abnormal nerve cell (neuronal) function. These neuronal changes disrupt normal brain activity, causing the signs and symptoms of MECP2 duplication syndrome.
MECP2 duplication syndrome is inherited in an X-linked pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes in each cell. In males (who have only one X chromosome), a duplication of the only copy of the MECP2 gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a duplication of one of the two copies of the gene typically does not cause the disorder, but can be associated with behavioral and psychiatric symptoms such as depression, anxiety, and features of autism spectrum disorder that affect communication and social interaction.
Females with a MECP2 gene duplication tend to be unaffected or less severely affected than males because the X chromosome that contains the duplication may be turned off (inactive) in many of their cells due to a process called X-inactivation. Early in embryonic development in females, one of the two X chromosomes is permanently inactivated in somatic cells (cells other than egg and sperm cells). X-inactivation ensures that females, like males, have only one active copy of the X chromosome in each body cell. Usually X-inactivation occurs randomly, such that each X chromosome is active in about half of the body's cells. Sometimes X-inactivation is not random, and one X chromosome is active in more than half of cells. When X-inactivation does not occur randomly, it is called skewed X-inactivation.
Females with a MECP2 gene duplication often have skewed X-inactivation, which results in the inactivation of the X chromosome containing the duplication in most cells of the body. Although this skewed X-inactivation ensures that the chromosome with the normal MECP2 gene is active most often, some of these females develop behavioral and psychiatric symptoms thought to be related to the additional genetic material. It is unclear why these features develop in a small number of females with skewed X-inactivation. Researchers speculate that in these females some cells in the brain may have a different pattern of X-inactivation than the cells in the rest of the body so that the X chromosome with the duplicated MECP2 gene is active, resulting in behavioral and psychiatric symptoms.
Windows 8 disables standard Windows 2000 Display Driver Model (XDDM) mirror drivers and offers the desktop duplication API instead. The desktop duplication API provides remote access to a desktop image for collaboration scenarios. Apps can use the desktop duplication API to access frame-by-frame updates to the desktop. Because apps receive updates to the desktop image in a DXGI surface, the apps can use the full power of the GPU to process the image updates.
You must add explicit code to your desktop duplication client app to support rotated modes. In a rotated mode, the surface that you receive from IDXGIOutputDuplication::AcquireNextFrame is always in the un-rotated orientation, and the desktop image is rotated within the surface. For example, if the desktop is set to 768x1024 at 90 degrees rotation, AcquireNextFrame returns a 1024x768 surface with the desktop image rotated within it. Here are some rotation examples.
The alpha-synuclein gene (SNCA) has been implicated in autosomal dominant forms of Parkinson's disease. We screened 119 individuals from families with this rare form of the disease for SNCA duplications by semiquantitative multiplex PCR. Two patients had duplications, which were confirmed by analysis of intragenic and flanking microsatellite markers. The phenotype in both patients was indistinguishable from idiopathic Parkinson's disease and no atypical features were present, by contrast with reports of families with triplication of the same gene. These results indicate that SNCA is more frequently associated with familial Parkinson's disease than previously thought, and that there is a clear dosage effect according to the number of supernumerary copies of this gene.
Diploid and stable karyotypes are associated with health and fitness in animals. By contrast, whole-genome duplications-doublings of the entire complement of chromosomes-are linked to genetic instability and frequently found in human cancers1-3. It has been established that whole-genome duplications fuel chromosome instability through abnormal mitosis4-8; however, the immediate consequences of tetraploidy in the first interphase are not known. This is a key question because single whole-genome duplication events such as cytokinesis failure can promote tumorigenesis9. Here we find that human cells undergo high rates of DNA damage during DNA replication in the first S phase following induction of tetraploidy. Using DNA combing and single-cell sequencing, we show that DNA replication dynamics is perturbed, generating under- and over-replicated regions. Mechanistically, we find that these defects result from a shortage of proteins during the G1/S transition, which impairs the fidelity of DNA replication. This work shows that within a single interphase, unscheduled tetraploid cells can acquire highly abnormal karyotypes. These findings provide an explanation for the genetic instability landscape that favours tumorigenesis after tetraploidization.
The spinal muscular atrophy (SMA) region on chromosome 5q13 contains an inverted duplication of about 500 kb, and deleterious mutations in the survival motor neuron 1 (SMN1) gene cause SMA, a common lethal childhood neuropathy. We have used a number of approaches to probe the evolutionary history of these genes and show that SMN gene duplication and the appearance of SMN2 occurred at very distinct evolutionary times. Molecular fossil and molecular clock data suggest that this duplication may have occurred as recently as 3 million years ago in that the position and identity repetitive elements are identical for both human SMN genes and overall sequence divergence ranged from 0.15% to 0.34%. However, these approaches ignore the possibility of sequence homogenization by means of gene conversion. Consequently, we have used quantitative polymerase chain rection and analysis of allelic variants to provide physical evidence for or against SMN gene duplication in the chimpanzee, mankind's closest relative. These studies have revealed that chimpanzees have 2-7 copies of the SMN gene per diploid genome; however, the two nucleotides diagnostic for exons 7-8 and the SMNdelta7 mRNA product of the SMN2 gene are absent in non-human primates. In contrast, the SMN2 gene has been detected in all extant human populations studied to date, including representatives from Europe, the Central African Republic, and the Congo. These data provide conclusive evidence that SMN gene duplication occurred more than 5 million years ago, before the separation of human and chimpanzee lineages, but that SMN2 appears for the first time in Homo sapiens. 041b061a72