Y2K Interruption: Can the Doomsday Scenario Be Averted?

The management philosophy until recent years has been to replace the workers with computers, which are available 24 hours a day, need no benefits, no insurance and never complain. But as the year 2000 approached, along with it came the fear of the millennium bug, generally known as Y2K, and the computers threatened to strike!!!! Y2K, though an abbreviation of year 2000, generally refers to the computer glitches which are associated with the year 2000. Computer companies, in order to save memory and money, adopted a voluntary standard in the beginning of the computer era that all computers automatically convert any year designated by two numbers such as 99 into 1999 by adding the digits 19. This saved enormous amount of memory, and thus money, because large databases containing birth dates or other dates only needed to contain the last two digits such as 65 or 86. But it also created a built in flaw that could make the computers inoperable from January 2000. The problem is that most of these old computers are programmed to convert 00 (for the year 2000) into 1900 and not 2000. The trouble could therefore, arise when the systems had to deal with dates outside the 1900s. In 2000, for example a programme that calculates the age of a person born in 1965 will subtract 65 from 00 and get -65. The problem is most acute in mainframe systems, but that does not mean PCs, UNIX and other computing environments are trouble free. Any computer system that relies on date calculations must be tested because the Y2K or the millennium bug arises because of a potential for “date discontinuity” which occurs when the time expressed by a system, or any of its components, does not move in consonance with real time. Though attention has been focused on the potential problems linked with change from 1999 to 2000, date discontinuity may occur at other times in and around this period.

The “broken escalator” phenomenon: Vestibular dizziness interferes with locomotor adaptation

BACKGROUND: Although vestibular lesions degrade postural control we do not know the relative contributions of the magnitude of the vestibular loss and subjective vestibular symptoms to locomotor adaptation. OBJECTIVE: To study how dizzy symptoms interfere with adaptive locomotor learning. METHODS: We examined patients with contrasting peripheral vestibular deficits, vestibular neuritis in the chronic stable phase (n = 20) and strongly symptomatic unilateral Meniere’s disease (n = 15), compared to age-matched healthy controls (n = 15). We measured locomotor adaptive learning using the “broken escalator” aftereffect, simulated on a motorised moving sled. RESULTS: Patients with Meniere’s disease had an enhanced “broken escalator” postural aftereffect. More generally, the size of the locomotor aftereffect was related to how symptomatic patients were across both groups. Contrastingly, the degree of peripheral vestibular loss was not correlated with symptom load or locomotor aftereffect size. During the MOVING trials, both patient groups had larger levels of instability (trunk sway) and reduced adaptation than normal controls. CONCLUSION: Dizziness symptoms influence locomotor adaptation and its subsequent expression through motor aftereffects. Given that the unsteadiness experienced during the “broken escalator” paradigm is internally driven, the enhanced aftereffect found represents a new type of self-generated postural challenge for vestibular/unsteady patients

Simultaneous irradiation of fibroblasts and carcinoma cells repress the secretion of soluble factors able to stimulate carcinoma cell migration.

Stroma mediated wound healing signals may share similarities with the ones produced by tumor's microenvironment and their modulation may impact tumor response to the various anti-cancer treatments including radiation therapy. Therefore we conducted this study, to assess the crosstalk between stromal and carcinoma cells in response to radiotherapy by genetic modulation of the stroma and irradiation. We found that fibroblasts irrespective of their RhoB status do not modulate intrinsic radiosensitivity of TC-1 but produce diffusible factors able to modify tumor cell fate. Then we found that Wt and RhoB deficient fibroblasts stimulated TC-1 migration through distinct mechanisms which are TGF-β1 and MMP-mediated respectively. Lastly, we found that simultaneous irradiation of fibroblasts and TC-1 abrogated the pro-migratory phenotype by repression of TGF-β and MMP secretion. This last result is highly relevant to the clinical situation and suggests that conversely to, the current view; irradiated stroma would not enhance carcinoma migration and could be manipulated to promote anti-tumor immune response

Geometry of Valley Growth

Although amphitheater-shaped valley heads can be cut by groundwater flows emerging from springs, recent geological evidence suggests that other processes may also produce similar features, thus confounding the interpretations of such valley heads on Earth and Mars. To better understand the origin of this topographic form we combine field observations, laboratory experiments, analysis of a high-resolution topographic map, and mathematical theory to quantitatively characterize a class of physical phenomena that produce amphitheater-shaped heads. The resulting geometric growth equation accurately predicts the shape of decimeter-wide channels in laboratory experiments, 100-meter wide valleys in Florida and Idaho, and kilometer wide valleys on Mars. We find that whenever the processes shaping a landscape favor the growth of sharply protruding features, channels develop amphitheater-shaped heads with an aspect ratio of pi