Photokina 2002: Kodak has announced the new 14 megapixel DCS-14n. This new digital SLR is even more remarkable for its capture device, a 13.89 megapixel full-frame (36 x 24 mm) CMOS sensor. The magnesium-alloy body is built around a Nikon F100/F80, has a built-in portrait grip and is notably smaller than any previous Kodak DCS D-SLR. The camera is powered by a Lithium-Ion battery, takes Compact Flash (Type I/II) and SD/MMC storage, supports JPEG-ERI (higher dynamic range JPEG) and also features an orientation sensor. The camera should be available in December with an expected street price of US$4,000.
The camera captures images at about two frames per second. Images can be saved as DCR raw files or Kodak Professional Extended Range Imaging (ERI) JPEG files. Kodak ERI-JPEG files serve as another form of picture protection for photographers, especially in situations where re-shooting is inconvenient. Kodak ERI-JPEGs are created by and stored in-camera on removable media for later color correction or manipulation, and provide two-stops of exposure latitude and extended color space within a JPEG workflow, a benefit no other competitor offers. The ERI-JPEG format provides professional photographers ease-of-use of JPEG files with the image quality and color/exposure control of Kodak's highly regarded DCR format raw camera files, to create the best quality images.
Heeding photographers' calls to simplify the transition to digital photography, the DCS Pro 14n includes features for new and more advanced digital shooters. The camera operates in two user modes: basic and advanced. The camera defaults to the basic setting and offers a very intuitive, simple interface. In the advanced mode, the user can adjust many more capture, resolution and storage settings, among others.
"The digital camera learning curve has been sharply reduced with the DCS Pro 14n. Novices and advanced users will be equally at home with the camera's user-friendly functionality," said Kelbley. "As Kodak continues to lead the industry in digital capture, we design our cameras to grow with the photographer. Whether it's a beginner or experienced digital photographer ready to move up to a pro series camera, the DCS Pro 14n will help users explore new territory and upgrade along the way."
The camera includes a power source in the form of a single rechargeable Li-Ion battery pack, or by an accessory AC adapter. Photographers may select NTSC or PAL video formats for image review. In NTSC mode, the color LCD and the video output are enabled simultaneously, a feature particularly useful for portrait photographers preparing set-ups. Using a video monitor, photographers can "play back" images captured during a shoot as a preview and potential sales opportunity with customers.
Family moments are precious and sometimes you want to capture that time spent with loved ones or friends in better quality than your phone can manage. We've selected a group of cameras that are easy to keep with you, and that can adapt to take photos wherever and whenever something memorable happens.
The camera captures images at about 1.7 frames per second. Images can be saved as DCR raw files, normal JPEG files or ERI-JPEG files. The ERI-JPEG files serve as another form of picture protection for photographers, especially in situations where re-shooting is inconvenient. They provide two stops of exposure latitude and extended color space within a JPEG workflow - a benefit no competitor offers. Images are stored via COMPACTFLASH and/or MMC/SD memory cards. Images can be written to each card type simultaneously in any combination of the three available formats. In addition, FIREWIRE connectivity - at a transfer rate of up to 12 MB per second - adds speed to the photographers' workflow.
The DCS Pro SLR/c camera includes features for both new and more advanced digital shooters. The camera operates in two user modes: basic and advanced. It defaults to the basic setting and offers a very intuitive, simple interface. In the advanced mode, the user can access and adjust a host of capture, resolution, storage and other settings.
What were you shooting with in 1997? One of the cameras I had in my hand was a Kodak DC20. This primitive digital camera could hold 8 shots of sub-VGA resolution images (493 x 373). It had no LCD finder, so you had to upload the images via a serial port before you could even see what you had shot. It was focus-free, automatic exposure, ISO 800-1600. And I was fascinated with it.
In this podcast, I pull the DC20 out of the closet, put a battery in it, and connected it to an old PowerBook 1400 that has a serial port and Mac OS 9, which supports the camera software. Why? Because by doing so, I'm able to actually step back into the history of personal digital photography.
The rapid progression of infection and the extensive and persistent pulmonary replication of the virus are accompanied by viremia and detection of virus in extrapulmonary sites, suggesting that other factors may contribute to the increased pathogenicity of the MA15 virus. A prolonged viremic state or a secondary viremia is seen in mice infected with MA15 and rMA15 that is not observed following infection with the recombinant SARS-CoVs (Urbani), rMA15SM, or rMA15ORF1ab. The MA15 virus model captures viremia and multi-organ involvement noted in human SARS patients . However, as in all SARS cases, the primary site of infection is the lung.
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Roots were separated from the bulb and fixed in a mixture of glacial acetic acid - ethanol (3:1 v/v). Afterward, the meristematic tissues were dehydrated in serial alcohol concentrations (50º, 75º, 95º and 100º), stained by the Feulgen technique and extended in monolayer on glass slides.
The eukaryotic cells in proliferation possess a safety mechanism that interrupts their passage from G2 to mitosis if the DNA has not been totally replicated or repaired (Murray, 1992; Park and Lee, 2003). This negative control is blocked when DNA base analogs are used which can cause cell pass to mitosis with alterations in its genetic material (Lydall and Weinert, 1995; Nigg, 2001; Robinson et al., 2001). The use of these analogs, 5AU and caffeine, disable these safety mechanisms either in animal (Malumbres et al., 2000) or plant cells (Murakami and Nurse, 2000). The existence of these controls during the cellular cycle assumes that the cells can recognize damage in its DNA and impede the beginning of replication or mitosis. Genetic experiments in exposed bacteria to UV radiations (Selby and Sancar, 1990), and biochemical studies on DNA replication and repair (Tobey, 1975; Forrest et al., 2003), have given detailed information on the events. However, the studies in eukaryotic cells have not been very successful due to the higher cell complexity and organization. The existence of a chromatin with a great structural and functional versatility determines that a genetic lesion might cause an intricate net of molecular alterations. With the purpose of studying the recovery capacity of cells in G2 as well as the passage for this phase of the cycle, two aberrant agents have been used: 5-AU and caffeine. These two clastogenic compounds, inaddition to producing chromosomic aberrations, cause a delay in the kinetics to mitosis in injured cells. The results allow for establishment that the 5-AU has two related effects: 1) it inhibits the late replication responsible for the premetaphasic synchronization which agrees with other reports (Del Campo et al., 1997) and 2) it promotes delay in the post-replicative phase due to induced genomic lesions with duration in G2 of 4 h in comparison with 2.2 h observed in controls. These values are triplicate when a secondary treatment was given with 5 mM caffeine (Table 1). The results allow to infer that the cells tried with the 5-AU presented a damage that makes them sensitive to the caffeine treatment and that an important fraction of the lesions produced by the 5-AU is repaired when the cells are in the last phase of G2. The caffeine inhibits the repair mechanisms in G2 (Del Campo et al., 2003). In presence of this drug the cells arrive to mitosis with the types of unrepaired lesions before mentioned (Table 2). As it is observed in Figure 4a, one of the nuclei suffered a premature chromosomal condensation, observed in a state similar to prometaphase, with its nuclear membrane seemingly broken. The chromosomal breaks that appear correspond to segments, replicated or not, that could eventually originate micronucleus (Marcano et al., 1999). Observation of these aneuploid nuclei and other chromosomic aberrations like breaks, anaphasic bridges, agglutinated chromosomes and left-behind chromosomes, implies the effect of the treatments on the spindle microtubules, reflected in segregation problems, as has been observed in yeasts (Lydall and Weinert, 1995). The micronucleus observation in different phases of mitosis (Fig. 5), indicates the presence of nucleolus organizing, that are able to capture the diffusible factor which trigger the entrance to replication and once the nuclei are repaired, the entrance to mitosis. Similar results have been reported in animal and plant cells (Gonzalez-Fernández et al., 1971; Rao and Johnson, 1974; Hervás et al., 1982; Del Campo, 2003). Two synergetic actions are set out during the DNA repair mechanisms: mitotic retardation associated to genomic damage and removal of the lesions with recovery of the DNA normal structure, or on the contrary, programmed cellular death when recovery is not possible. The results of the combined 5-AU/caffeine treatment, establish that the action of caffeine could reside in the existence of 2 cooperative effects: increase of the mitotic delay and inhibition of some of the repair routes. The results shown in table 1 evidence a repaired damage average of 9.2% for the case of the 5-AU treatment and of 11.35% for the double 5AU/caffeine treatment, with a residual damage of 12.8 for the first case and of 27.8 for the second one. This is why it is presumed that the damage caused by the drug is irreversible starting from the second cellular cycle. Either the 5-AU or the combined action of this one with the caffeine, alters the controller capacity of the negative regulators G2 described in different cell systems (Tobey, 1975; Murakami and Nurse, 2000; Nigg, 2001; Del Campo et al., 2003). 2b1af7f3a8