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    cateye atc cc-8000 manual espa ol

    The Vectra is no longer manufactured or available, however some replacement parts still are. The basis of a real workout has always been getting your cadence steady and then increasing it's count as you continue to train. The sensor for the mileage and time functions mounts on the left rear chainstay, so it can be used on stationary trainers, for training in winter. The cadence is displayed as a whole number from 20 to 199 RPM. The Micro uses a two line Liquid Crystal Display, putting speed and cadence functions on the 10mm upper line, and all mileage and time functions, on the lower 5mm high display line. It will display both MPH or KPH. The Micro displays current speed up to 65 MPH, which is updated and displayed every second. It has a stopwatch, that increments up to 10 hours then automatically resets, so your aware of how long you've been riding.The Micro uses one CR 2032, 3 volt Lithium battery. It comes complete with all mounting hardware and has a weight on the bike of 78 grams. Black, from Japan. The Micro itself is longer manufactured. The upper line is 4mm high, the middle, (main) line of the display is 10mm high, and the lower line is 5mm high. All distance readings can be displayed in MPH or KPH. It has a switch selectable auto start function, that begins to read and record all trip functions, (elapsed time, maximum speed, average speed, trip distance) when the wheel starts to move. It will also stop each of the functions temporarily if the wheel stops moving, should you stop to rest and continue where you left off when you start to ride again. The ATC has two trip meters, displayed on the lower line, one resettable by the user, the other is a trip distance per day function that is tied to the 24 hour clock to show how far in total, you've ridden in a 0 to 24 hour period. The trip distance per day meter resets automatically each day at 12 midnight using the clock. The ATC has a 24 hour clock that is displayed at the left side of the upper line.

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    Discover everything Scribd has to offer, including books and audiobooks from major publishers. Start Free Trial Cancel anytime. Report this Document Download Now Save Save CatEye Cyclocomputer CC-8000 For Later 0 ratings 0% found this document useful (0 votes) 687 views 23 pages CatEye Cyclocomputer CC-8000 Uploaded by ourthing Description: CatEye Cyclocomputer CC-8000 Manual Full description Save Save CatEye Cyclocomputer CC-8000 For Later 0% 0% found this document useful, Mark this document as useful 0% 0% found this document not useful, Mark this document as not useful Embed Share Print Download Now Jump to Page You are on page 1 of 23 Search inside document Browse Books Site Directory Site Language: English Change Language English Change Language. It's waterproof, and has 6 functions derived from a fork mounted wheel sensor. All distance readings can be displayed in Miles Per Hour or Kilometers Per Hour, though we will speak in MPH. The Vectra uses a two line Liquid Crystal Display, the top line is 10mm high and used for speed display functions, the bottom line is used for mileage and time functions. With the Vectra your current speed, up to 65 MPH, is always displayed on the upper line, with any of the other 5 functions available simultaneously on the lower display line. Maximum and average speed are displayed to the tenth of a mile. Both of these figures, are measured and displayed for up to and within a 28 hour period, where after the a 100, 000 seconds has elapsed the counters are zeroed automatically, and it begins again. The Vectra's odometer will record total distance traveled up to 9999.9 miles and then reset to 0 or can be manually reset.The Vectra's instruction manual is printed English, French, German, Dutch, and Italian, and uses one CR 2032, 3 volt Lithium battery. It comes complete with all mounting hardware and has a weight on the bike of 71 grams. Black, from Japan.

    There is an odometer, on the bottom line display, which shows total distance traveled since installation or last manual reset. The odometer tacks your mileage from 0 to 10,000 miles in tenths of a mile reading. It will show your maximum speed since you last reset the trip meter (which records your trip distance). Your average speed is a top line display, for any 28 hour period is always available and is resettable. So you know how long you've been riding there is a stopwatch, which is a bottom line display, that runs up to ten hours and then resets automatically. Your maximum speed for the trip is a bottom line display. After 30 minutes of dis-use the Cordless blanks out all trip and distance functions, leaving just the clock time on the display, when starting to ride again it requires that you press either of the 2 buttons to free the computer from this power saving mode. The single instruction manual is printed English, French, German, Dutch, Spanish and Italian. The transmitter should be replaced after 10,000 miles, while the computer uses less power and is good for about 2 years of average use. Made in Japan. The Original Cateye cordless has been discontinued and replaced by the Cordless 2. Occasionally, over time the bolt may back off and you may not realize and tighten it, in time before it drops off and is lost, making the computer useless. For those circumstances, we sell the Cateye original replacement wheel magnet. This is the magnet used for the magnet used Vectra, Mity 2, Micro and ATC computers. The 166-5120 wheel magnet weighs 4 grams. Accordingly, the description of the SpeedZone will be near identical to the Mity 2. The Specialized SpeedZone is their first entrant in the computer market. It small, lightweight with large paddle switches that hinge at the back and toggle downward at the front, for gloved hands. The upper and lower case pieces are ultrasonically welded together making the case weather tight.

    The last of the common functions for the ATC is Total Distance or Odometer, which is displayed on the lower line, up to 100,000 miles when it resets automatically to zero. The ATC has a multi function 10 stage memory to record the trip distance, elapsed time, and split average speed for up to ten separate legs, or splits on a ride. Because this function is unique to this computer, and so fundamental in personal training, it's worth discussing in detail. Let's assume that you're riding in a local State park each day, and you've found the course you use each day can logically be broken up into 4 stages, flat ground, hill climbing, descent, and flat ground again. The point that you begin the entire ride we will call point A, when you depart point A you press the Start button on the ATC, which starts the tripmeter and stopwatch simultaneously. One of these Memo splits can even be a break from riding, where it will recall that haven't moved an inch from the previous point, had a 0 average speed, but the passed time represents the time you rested. The Cateye ATC's instruction manual is printed English, French, German, Dutch, and Italian. The ATC uses one CR 2032, 3 volt Lithium battery. It's durable, waterproof, has an easy to read display. With all necessary hardware it weighs only 97 grams!!! The battery will generally last 3 years. Made in Japan, Black. The ATC supply is exhausted and it is no longer made. It uses a low power, broadcast transmitter on the fork mounted sensor to relay and display 7 functions, using a two line Liquid Crystal Display. The top line of the display, used for speed functions, is 10mm tall twice the height of the bottom line used for mileage and time functions. All functions are accessed through two buttons on the face of the case. All distance readings can be displayed in Miles Per Hour or Kilometers Per Hour, though we will speak in MPH.

    Variations in our DNA and differences in how that DNA functions (alone or in combinations), alongside the environment (which encompasses lifestyle), contribute to disease processes. This review explores the genetic basis of human disease, including single gene disorders, chromosomal imbalances, epigenetics, cancer and complex disorders, and considers how our understanding and technological advances can be applied to provision of appropriate diagnosis, management and therapy for patients. Keywords: cancer, genetics, genomics, molecular basis of health and disease Introduction When most people consider the genetic basis of disease, they might think about the rare, single gene disorders, such as cystic fibrosis (CF), phenylketonuria or haemophilia, or perhaps even cancers with a clear heritable component (for example, inherited predisposition to breast cancer). However, although genetic disorders are individually rare, they account for approximately 80% of rare disorders, of which there are several thousand. The sheer number of rare disorders means that, collectively, approximately 1 in 17 individuals are affected by them. Moreover, our genetic constitution plays a role, to a greater or lesser extent, in all disease processes, including common disorders, as a consequence of the multitude of differences in our DNA. Some of these differences, alone or in combinations, might render an individual more susceptible to one disorder (for example, a type of cancer), but could render the same individual less susceptible to develop an unrelated disorder (for example, diabetes). The environment (including lifestyle) plays a significant role in many conditions (for example, diet and exercise in relation to diabetes), but our cellular and bodily responses to the environment may differ according to our DNA. The genetics of the immune system, with enormous variation across the population, determines our response to infection by pathogens.

    All speed functions on the SpeedZone can be expressed in MPH or KPH, we will use MPH. The current speed is only upper line display, and is displayed continuously. There is a lower line display trip meter, that records up to 1000 miles, accurate to two decimal places, then resets, automatically. Also included is a stopwatch, on the lower line display, which shows the elapsed time between the starting point and the current point, up to 10 hours, displayed in whole seconds. You couldn't have a stop watch without a clock function, the SpeedZone has a 12 hour clock, a lower line function. To increase the useful battery life the SpeedZone has a power saving function, which after 60 minutes of in-operation blanks the display to the 12 hour clock only. To release the unit from this power saving mode requires that one of it's two buttons be pressed.The SpeedZone uses one CR 1620 or a CR 1616, 3 volt Lithium battery, with an average 3 year life. It comes complete with all mounting hardware, and has a weight on the bike of 43 grams. The SpeedZone 1, from Japan has been replaced by the SpeedZone 2 made under contract in Taiwan. We're committed to dealing with such abuse according to the laws in your country of residence. When you submit a report, we'll investigate it and take the appropriate action. We'll get back to you only if we require additional details or have more information to share. Note that email addresses and full names are not considered private information. Please mention this; Therefore, avoid filling in personal details. The manual is 0,5 mb in size. If you have not received an email, then probably have entered the wrong email address or your mailbox is too full. In addition, it may be that your ISP may have a maximum size for emails to receive. Check your email Please enter your email address. Abstract Genetics plays a role, to a greater or lesser extent, in all diseases.

    Additionally, sequence similarity between a pseudogene and its normal counterpart may promote recombination events which inactivate the normal copy, as seen in some cases of perinatal lethal Gaucher disease. Furthermore, some pseudogenes have the potential to be harnessed in gene therapy to generate functional genes by gene editing approaches. The distribution of genes between chromosomes is not equal: chromosome 19 is particularly gene-dense, while the autosomes for which trisomy is viable (13, 18, 21) are relatively gene-poor ( Table 1 ). Note that the data for the acrocentric chromosomes 13, 14, 15, 21, 22 does not include the shared ribosomal DNA array repeats present on the p arms (see Figure 2 ). Data from Ensembl, June 2018. However, if we are to describe changes to the DNA sequence, we need to describe these changes with respect to some baseline; this baseline is the human reference genome sequence. Single nucleotide variants: The most frequent variants in our genome are substitutions that affect only one base pair (bp), referred to as single nucleotide variants (SNV) or as single nucleotide polymorphisms (SNP) ( Figure 1 ) depending upon the MAF. It has been estimated that there are at least 11 million SNPs in the human genome (averaging approximately 1 per 300 bp). It also seems likely that if we sequenced the genomes of everyone on the planet, for most positions in our genome we would discover at least one individual with an SNV, wherever such variation is compatible with life. Open in a separate window Figure 1 Some types of variants found in human genomes Variation involving one or a few nucleotides are shown above the chromosome icon, and structural variants below; in each case the variants are depicted in relation to the reference sequence. For depiction of structural variants A, B, C and D represent large segments of DNA; Y and Z represent segments of DNA from a different chromosome. Abbreviation: CNV, copy number variant.

    Chromosome ideogram from NCBI Genome Decoration Page. Insertions and deletions (indels): Insertions or deletions of less than 1000 bp are also relatively common in the human genome, with the smallest indels being the most numerous. Structural variants: Structural variants are defined as variants affecting segments of DNA greater than 1000 bp (1 kb). They include translocations, inversions, large deletions and copy number variants (CNV). CNVs are segments of our genome that range in size from 1000 to millions of bp, and which, in healthy individuals, may vary in copy number from zero to several copies ( Figure 1 ). By analysis of many human genomes it is apparent that CNV exists for approximately 12% of the human genome sequence. The largest CNVs may contain several entire genes. Where the population frequency of a CNV reaches 1% or more, it may be referred to as a copy number polymorphism (CNP). Repeat variations: Human genomes contain large numbers of repetitive sequences. The number of repeats in each array can vary, generating multiple alleles, so that these loci have high variability within the population, and can be used in identifying individuals (see below). Although generally inherited stably (i.e. with the same number of repeats) from parent to child, expansions in some microsatellites are associated with disease. Variation between healthy individuals Given that no two individuals look exactly alike (apart from identical twins) it will come as no surprise that this is reflected in our DNA. What is surprising is the amount of variation between us. Looking at any one human genome, compared with the reference sequence, we would find approximately 3 million SNPs, and approximately 2000 structural variants. The genomes of any two unrelated individuals will differ in approximately 0.5% of their DNA (approximately 15 million bp), and most of this variation can be attributed to CNVs and large deletions.

    Furthermore, most cancers result from an accumulation of genetic changes that occur through the lifetime of an individual, which may be influenced by environmental factors. Clearly, understanding genetics and the genome as a whole and its variation in the human population, are integral to understanding disease processes and this understanding provides the foundation for curative therapies, beneficial treatments and preventative measures. With so many genetic disorders, it is impossible to include more than a few examples within this review, to illustrate the principles. For further information on specific conditions, there are a number of searchable internet resources that provide a wealth of reliable detail. In this review, an understanding and knowledge of basic principles and techniques in molecular biology, such as the structure of DNA and the PCR will be assumed, but explanations and animations of PCR (and some other processes) are available from the DNA Learning Center ( ). The focus here will be on human disease, although much of the research that defines our understanding comes from the study of animal models that share similar or related genes. The human genome and variation The human genome and the human genome reference sequence The complete instructions for generating a human are encoded in the DNA present in our cells: the human genome, comprising roughly 3 billion bp of DNA. Genome sequence information for humans and many other species is freely accessible through a number of portals, including the National Center for Biotechnology Information (NCBI; ) and Ensembl ( ), which also provide a wealth of related information. The majority of our DNA is present within the nucleus as chromosomes (the nuclear DNA or nuclear genome), but there is also a small amount of DNA in the mitochondria (the mtDNA or mitochondrial genome).

    Most individuals possess 23 pairs of chromosomes ( Figure 2 ), therefore much of the DNA content is present in two copies, one from our mother and one from our father. Open in a separate window Figure 2 Giemsa banding (G-banding) to form a karyogram ( A ) Metaphase spreads like this are obtained from cultured cells arrested in metaphase using colcemid, followed by Giemsa staining to create characteristic light and dark bands. Generally the dark bands represent regions which are AT-rich and gene-poor. ( B ) The chromosomes from the spread are arranged in pairs to view the karyotype, often using specialist software like Cytovision. ( C ) Diagrammatic representations of the G-banding patterns, called ideograms, are used as a reference. In fact the p arms of the acrocentric chromosomes (13, 14, 15, 21, 22) all have very similar content, which includes the nucleolar organiser regions or NORs. Each NOR contains a tandem repeat of ribosomal DNA (rDNA) which encodes the rRNAs. Chromosome ideograms from NCBI Genome Decoration Page. The human nuclear genome encodes roughly 20000 protein-coding genes, which typically consists of both protein-coding (exon) and non-coding (intron) sequences. Our genome also contains roughly 22000 genes that encode RNA molecules only; some of these RNAs form components of the translation machinery (rRNA, tRNA) but there are many more that perform various roles within the cell, including regulation of expression of other genes. In fact it is now believed that as much as 80% of our genome has biological activity that may influence structure and function. Although originally considered as evolutionary relics, there is now evidence that some may be involved in regulating their protein-coding relatives, and in fact dysregulation of pseudogene-encoded transcripts has been reported in cancer.

    Although much of the variation in our genome lies within the non-coding DNA, we now know that, on average, each individual has several hundred variants that are either known, or predicted, to be damaging to gene function, including roughly 85 variants that lead to truncated (incomplete) protein products. Furthermore, the total number of functional genes per human genome may vary by up to 10% between individuals as a consequence of CNVs, large deletions and loss-of-function variants. Clearly there is no requirement for all of our genes to be functional: for many genes only one working copy is required, and in other cases there appears to be a level of redundancy or plasticity built into the system. However it is becoming increasingly apparent that some of the variations in our genomes may lead to higher susceptibility to common diseases. Variation between populations The greatest amount of variation is found within populations of African ancestry, which is consistent with initial migration out of Africa, with each group of migrants taking subsets of variants with them. Common variants tend to be shared between all populations, whereas rare variants are more likely to be specific to particular populations or related populations. Some of the differences will be related to environmental adaptation, for example skin pigmentation or enzymes to detoxify dietary plant toxins. These same enzymes are also responsible for the metabolism of many pharmaceutical (and recreational) drugs; genetic variants may lead to some individuals being ultrarapid metabolisers or poor metabolisers, which may translate into poor drug response or adverse side effects. For example, deficiency in dihydropyrimidine dehydrogenase, leading to a toxic response to the cancer treatment 5-fluorouracil, is two to three times more common in African-American populations than in Caucasians. Forensic DNA profiling in the U.K.

    currently analyses 16 microsatellites from across the genome, together with a region from the amelogenin gene present on both X and Y chromosomes that is 4 bp different in size between them, allowing gender identification. The process is similar to QF-PCR for prenatal aneuploidy testing, which will be discussed later. On the other hand, if the two samples do not match, it can be concluded that the crime scene sample was not from the suspect. Likewise, in paternity testing, DNA profiling can exclude a man as the father of a child, but cannot prove he is the father with absolute certainty. DNA profiling is also useful in helping to identify human remains, for example where decomposition makes physical identification difficult. The fact that certain variants (including microsatellite alleles) are more frequently found in populations of particular ancestry means that the capability already exists to make some inferences on likely ancestral origin based on only a DNA sample and research is underway to establish whether particular features (for example, eye colour, hair colour and even facial characteristics) can be predicted from DNA. Thus the DNA profiling of the future may generate an identikit image of a wanted individual. De novo mutations and mosaicism Most of the variants in our genome were inherited from one of our parents. However, our DNA is constantly bombarded with DNA damaging agents and furthermore every time a cell’s DNA is replicated prior to division there is opportunity for errors. Microsatellites have a relatively high mutation frequency, with gain or loss of a repeat unit occurring in roughly 1 per 1000 microsatellites per gamete per generation. In contrast with aneuploidy, which is most often a consequence of meiotic error during oocyte generation, new mutations are almost four times more common in the male germline than the female germline, which is likely to relate to the high number of cell divisions during spermatogenesis.

    For both sexes the new mutation rate increases with age, though again, the increase is more marked in the male germline. Most new mutations will have little or no effect on health, particularly those outside coding sequences, but some are associated with disease. If a new mutation occurs during embryogenesis or development this can lead to mosaicism, where some cells in the individual have that new variant while others do not. New mutations occurring during embryogenesis and development also generate a few differences between the genomes of identical twins. Very rarely fusion of two embryos will generate a chimera: an individual that has two genetically distinct cell lines present. Where the same sex chromosome constitution is present in both cell lines chimerism might only come to light with the observation of apparent non-maternity or non-paternity amongst offspring (where one cell line predominates in the gonads and the other predominates in blood cells). Fusion of two embryos of different sex can lead to characteristics of both genders being present, and chimerism is found in approximately 13% of cases of hermaphroditism. Summary The massive amount of variation between individual human genomes can make it very difficult to determine which variants are benign and which might be associated with a disease. Thus it will become increasingly common to investigate wider genomic influences when considering contribution of variants to disease. Note that several scientific conventions are used when referring to chromosomes, genes, proteins and variants affecting them; these ensure unambiguous communication between scientists and health professionals. International System for Human Cytogenetic Nomenclature (ISCN) is used for describing karyotypes and changes at the chromosomal level. Individual loci and genes, for which there are often multiple different historical names, have now been assigned specific unique names by the HUGO Gene Nomenclature Committee (HGCN) ( ).

    Sequence variants are described according to Human Genome Variation Society (HGVS) guidelines ( ) for both DNA and proteins. Finally, since the same names are applied to genes and the proteins they encode, italics are used to refer to the gene, with standard font used when referring to the protein. Chromosome structure and chromosomal disorders Introduction Almost every human cell contains a full diploid genome, consisting of 2 metres of DNA arranged into 46 chromosomes: 22 homologous autosomal pairs, and the sex chromosomes comprising two X chromosomes in females and an X and a Y in males. The exceptions are anucleate cells like erythrocytes (red blood cells), cell fragments (platelets) and haploid germline cells (sperm and eggs) which contain 23 chromosomes. Although mechanisms have evolved which ensure that during cell division, daughter cells will inherit a complete genome, those mechanisms occasionally make mistakes. This can lead to cells with chromosomal abnormalities, which can be categorised as numerical abnormalities, i.e. the resulting daughter cell contains too many or too few chromosomes, or structural abnormalities, where more complex rearrangements of the genome have taken place. The normal chromosome complement of a species (i.e. the number, size and shape of chromosomes) is called its karyotype. Human chromosomes consist of DNA which is wrapped around a core of histone proteins to form chromatin. Most of the time, chromatin exists in a diffuse form within a cell’s nucleus, however, during metaphase of the cell division cycle, the chromosomes condense. It is these condensed chromosomes which can be stained with a variety of chemicals, and which can then be observed under a light microscope, to reveal the characteristic banding patterns. The bands reflect regions of chromatin with different characteristics, and therefore different functional elements.

    A photographic representation of a person’s metaphase chromosomes, arranged by size, may be referred to as a karyogram or karyotype ( Figure 2 A,B) and a graphical representation is called an ideogram ( Figure 2 C). The available stains for chromosomes differ in their chemical properties and consequently in the resulting banding pattern. The most commonly used stain is called Giemsa after the chemist who developed it in 1904; the resulting banding pattern of chromosomes is referred to as G-banding. The microscopic analysis of stained chromosomes is termed cytogenetics. When viewing condensed metaphase chromosomes under a microscope, some key features can be identified ( Figure 3 ). All mammalian chromosomes have a centromere, which appears like a narrow waist, here proteins attach for separation of chromosomes during cell division. In some species such as the mouse, the centromere is located at one end of the chromosome, termed as telocentric. In humans, chromosomes 1, 3, 16, 19 and 20 are metacentric, chromosomes 13, 14, 15, 21, 22 and Y are acrocentric, while the remainder are submetacentric. Open in a separate window Figure 3 Chromosome structure and band nomenclature This ideogram of the complete chromosome 8 illustrates the general structure of all human chromosomes: short (p) and long (q) arms, joined at the centromere. Each chromosome has a characteristic G-banding pattern, with each band annotated, for example p22 or q23. The approved way of stating the location q21.1 is q-two-one-point-one ( not q-twenty-one-point-one). Telomeres, with a shared structure, are present at both ends of each chromosome. Each telomere is composed of arrays of TTAGGG repeats, followed by a subtelomere, which is formed of repetitive sequences which can be similar between several telomeres. Numerical abnormalities An abnormality where a cell contains more than two complete sets of the human haploid genome (69 chromosomes or more) is termed as polyploidy.


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