Bone marrow-derived cells (BMCs) have abilities of cell migration and differentiation into tissues/organs in the body and related with the differentiation of teeth or periodontal tissue including fibroblasts. Then, we examined the effect of orthodontic mechanical stress to the transplanted BMC migration into periodontal tissues using BMC transplantation model.. First, a small nick is created with a needle in the epidermis on the back

First, a small nick is created with a needle in the epidermis on the back. surround and penetrate the human body”. Biofield treatment refers to. Most cases were middle-aged (mean 33 years buy provigil australia range: 4–62 years) and previously healthy; 18.4% had an underlying chronic disease, 23.7% were obese and 7.9% were current smokers. None had received the seasonal influenza vaccine; they had cough (92%), fever (86.8%), and malaise (73.7%). The median time from disease onset to hospital admission was 6 days (range 0–8 days). All were admitted to the intensive care unit with pneumonia and/or respiratory distress. Average time from disease onset to death was 8 days (range 4–18 days).. The measurement of serum OCT concentration may provide a useful marker of disease severity buy provigil australia and thus could be a useful marker for a high risk of HCC occurrence.. A total of 96 COPD cases and 33 controls were included in the study. Plasma A2M buy provigil australia CRP, and SAP levels were higher in COPD patients than in controls. Circulating concentrations of haptoglobin and tPA were found to increase in parallel with the severity of the disease. Increasing disease severity was associated with distinct intricate networks of APRs, which were especially evident in advanced stages..

Treatment of acute interstitial pneumonia is supportive and usually requires mechanical ventilation buy provigil from india often using the same methods as used for ARDS (including low tidal volume ventilation). Corticosteroid therapy is generally used, but efficacy has not been established..

This suggests that higher doses cause lesions that inhibit the expression of damage as comets, i.e., DNA-protein or interstrand crosslinks. The latter could be explained by sudden monoadduct-to-crosslink transformation due to a DNA conformational change induced by monoadduct accumulation that facilitates crosslink formation. This narrow dose-dependent transition could contribute to the narrow therapeutic window of BUS..

This study was a cross-sectional survey and was conducted between January and April 2011. Participants were 257 women between the ages of 40 and 58 years. They were recruited from the Women's Reproductive Health Programme implemented at the Adam Mickiewicz University in Poznań in cooperation with Poznań University of Medical Sciences and Medical University of Lublin. The eligibility criteria for this study were restricted to a cohort of women aged between 40 and 60 years, without a history of cancer, surgical menopause or endocrine system diseases, not pregnant, not on hormonal replacement therapy (HRT) and not using insulin. This research project was reviewed and approved by the Bioethics Committee in Poznań University of Medical Sciences and was carried out in accordance with the Declaration of Helsinki and subsequent amendments. All participants indicated informed consent by signing a form after they had been given a clear explanation of the study objectives and potential risks of the study.. For instance, in 2013, Nyberg et al. reported two patients who were treated for a DAVF and an AVM near the skull base that received a heavily parasitized supply from branches of the external carotid artery. Transarterial embolization resulted in transient cranial neuropathies, including lower facial nerve palsy in two and trigeminal nerve mandibular segment neuralgia in one of the cases. The MMA and internal maxillary arteries are common pathways that are used, and these “dangerous anastomoses” may have been the cause of cranial nerve defects in these patients [28]. In another instance, in 2000, Wang et al. reported a patient with a DAVF in the cavernous sinus that was supplied by the MMA. A choroidal infarction was observed after an embolization of the DAVF was performed through the MMA, and it was caused by the migration of the embolization agent from the MMA to the ophthalmic artery [29]. Hence, more caution should be taken when evaluating these variant collaterals, and careful angiographic monitoring and slow injection of embolization materials may help to prevent these complications.. The timing of radiotherapy after administration of the radiosensitizer was critical to achieve the maximum effect. In an in vitro study, free Dtxl had the greatest sensitization effect when radiation was given initially after drug administration, followed by a slow decrease over time, while the optimal timing of radiotherapy for FT-NP Dtxl was 24 h after drug administration, with the cytotoxicity being as effective as free Dtxl, possibly due to the delayed release of Dtxl from NPs. In an in vivo tumor model, FT-NP Dtxl produced the greatest sensitization effect when radiation was applied 12 h after systemic drug administration, and yielded better results than NP Dtxl and free Dtxl [144]. However, there was a rapid increase in tumor volume ~20 days after treatment; this is known as accelerated repopulation, due to cell-death-stimulated increased cell proliferation, which represents a serious problem in terms of tumor recurrence post-therapy [145].

The timing of radiotherapy after administration of the radiosensitizer was critical to achieve the maximum effect. In an in vitro study, free Dtxl had the greatest sensitization effect when radiation was given initially after drug administration, followed by a slow decrease over time, while the optimal timing of radiotherapy for FT-NP Dtxl was 24 h after drug administration, with the cytotoxicity being as effective as free Dtxl, possibly due to the delayed release of Dtxl from NPs. In an in vivo tumor model, FT-NP Dtxl produced the greatest sensitization effect when radiation was applied 12 h after systemic drug administration, and yielded better results than NP Dtxl and free Dtxl [144]. However, there was a rapid increase in tumor volume ~20 days after treatment; this is known as accelerated repopulation, due to cell-death-stimulated increased cell proliferation, which represents a serious problem in terms of tumor recurrence post-therapy [145].. The methods of prevention and control of CAD are very complex and the role of the health system in their control is very limited. A participatory look, based on strong scientific documentation on the one hand, and efforts to integrate information and design long-term plans, on the other hand, should form the core of CAD management and be tried through a variety of legal instruments and diverse executive channels in different organizations and ministries to moderate the course of life with the direct participation of people..

Overall, 59% treated with 150 mg plasmin achieved the primary efficacy endpoint (>50% thrombolysis at end of treatment) without BOC (58 of 99) and with BOC (17 of 29), in contrast to 89% (8 of 9) receiving rtPA (p = 0.149) and 40% (2 of 5) receiving placebo control (p = 0.648) (Table 3, Figure 3). Thirty-three per cent (2 of 6) of the group treated with 250 mg plasmin with BOC achieved >50% thrombolysis. BOC did not improve efficacy (59% [58 of 99] without BOC vs 59% [17 of 29] with BOC, p > 0.999). Of note, 19% (4 of 21) of plasmin group C (5-h infusion at 30 mL/h without BOC) and 13% (2 of 15) of plasmin group I (5-h infusion at 35 mL/h with BOC) demonstrated >90% thrombolysis. Eighty-one per cent (17 of 21) of plasmin group C achieved >50% thrombolysis, in contrast to 40% (2 of 5) in the placebo control group. The results support an infusion rate of 30 mL/h and longer infusion duration (5 h) in administering plasmin for the treatment of aPAO.. Discovery of new components in recent years has broadened the perception beyond classic RAS. Accumulating hints have shown that ACE2-regulated Ang1-7 production represents a more effective target for the renal RAS than the circulation[6].. first 154 amino acids of AIRE followed by 48 aberrant amino acids. Secondly, inspection of Chart 1 lines 6-20 will reveal some code words. was operationally difficult (Windhoek, UNIM 2014) or slow (HAU,. If you are less confident buy provigil australia you. Criteria for extubation included an alert and hemodynamically stable patient with no excessive bleeding buy provigil australia ability of the patient to breathe through a tracheal tube (T tube) for at least 30 minutes with a fraction of inspired oxygen of less than 0.40 and a respiratory rate less than 25 breaths/min, PaO2 greater than 70mmHg, a PaCO2 less than 40mmHg and a pH greater than 7.35, with no metabolic acidosis. Other criteria included a tidal volume of 6ml/kg, a peak negative inspiratory pressure of less than -20cmH2O and a mandatory chest radiograph before extubation to rule out pneumothorax, pleural effusion and atelectasis.. and morphometric PIB parameters is expected inasmuch as the PIB. influence of both temperature and pressure on carotenoids extraction. The prospect of utilizing saliva samples in the diagnosis of AMI is appealing to a large group of scientists due to its noninvasive and economical nature. Extensive biomarker research on CVD has elucidated various proteins associated with this disease. Since approximately 27% of the whole saliva proteins resemble those found in plasma [26], similar proteins present in both saliva and plasma will be very useful to facilitate monitoring of both disease progression and therapeutic treatments among these patients. In association with AMI, some studies on plasma proteins revealed significant biomarkers involved in myocardial injury, myocardial stress, inflammation, neuroendocrine activation, atherosclerotic process, platelet activation, plaque instability, endothelial dysfunction, oxidative stress, and myocardial stretch. Out of all these proteins, natriuretic peptides, C-reactive protein (CRP), creatine kinase (CK), and cardiac troponin were included as commonly used cardiac biomarkers in acute cardiac care [27]. In a clinical setting, a kit for measuring human salivary CRP, a common biomarker related to cardiovascular inflammation, has been developed by Salimetrics®. Another recent cutting-edge technology is Oral Fluid NanoSensor Test (OFNASET) which provides portable, cheap, accurate, definitive, and quantitative results. Besides its intended use in oral cancer, this particular alternative can possibly benefit the point-of-care multiplex detection of salivary biomarkers among AMI patients [28]. Given the above-mentioned clinical benefits of saliva collection, a patient's salivary proteome should be very useful in determining heart condition of the patient in order to predict AMI. Several studies have demonstrated salivary biomarkers associated with AMI, as shown in Table 1. By comparing these salivary biomarkers with those in plasma, as elaborated by Kossaify et al. [27], CRP, CK, CD40 ligand, cardiac troponin I, cardiac troponin T, some families of interleukin (IL), tumour necrosis factor alpha, matrix metalloproteinase (MMP), and myeloperoxidase share similarities with plasma biomarkers which also play significant roles in inflammation and plaque instability (Figure 2). Although these discoveries may enlighten the diagnostic utility of salivary proteomes as biomarkers in relation to CVD, none of the salivary biomarkers listed above have been verified to predict the onset of AMI. All of these studies, as tabulated in table 1, were conducted retrospectively after the incidence. On the other hand, prospective studies should be able to alternatively facilitate the researchers to find predictive AMI biomarkers. In future, these newly detected salivary biomarkers will conceivably provide an early molecular diagnosis and eventually increase the survival rate of cardiovascular patients as opposed to that of plasma. However, more validation needs to be carried out in order to find robust and discriminatory biomarkers for this disease.

The prospect of utilizing saliva samples in the diagnosis of AMI is appealing to a large group of scientists due to its noninvasive and economical nature. Extensive biomarker research on CVD has elucidated various proteins associated with this disease. Since approximately 27% of the whole saliva proteins resemble those found in plasma [26], similar proteins present in both saliva and plasma will be very useful to facilitate monitoring of both disease progression and therapeutic treatments among these patients. In association with AMI, some studies on plasma proteins revealed significant biomarkers involved in myocardial injury, myocardial stress, inflammation, neuroendocrine activation, atherosclerotic process, platelet activation, plaque instability, endothelial dysfunction, oxidative stress, and myocardial stretch. Out of all these proteins, natriuretic peptides, C-reactive protein (CRP), creatine kinase (CK), and cardiac troponin were included as commonly used cardiac biomarkers in acute cardiac care [27]. In a clinical setting, a kit for measuring human salivary CRP, a common biomarker related to cardiovascular inflammation, has been developed by Salimetrics®. Another recent cutting-edge technology is Oral Fluid NanoSensor Test (OFNASET) which provides portable, cheap, accurate, definitive, and quantitative results. Besides its intended use in oral cancer, this particular alternative can possibly benefit the point-of-care multiplex detection of salivary biomarkers among AMI patients [28]. Given the above-mentioned clinical benefits of saliva collection, a patient's salivary proteome should be very useful in determining heart condition of the patient in order to predict AMI. Several studies have demonstrated salivary biomarkers associated with AMI, as shown in Table 1. By comparing these salivary biomarkers with those in plasma, as elaborated by Kossaify et al. [27], CRP, CK, CD40 ligand, cardiac troponin I, cardiac troponin T, some families of interleukin (IL), tumour necrosis factor alpha, matrix metalloproteinase (MMP), and myeloperoxidase share similarities with plasma biomarkers which also play significant roles in inflammation and plaque instability (Figure 2). Although these discoveries may enlighten the diagnostic utility of salivary proteomes as biomarkers in relation to CVD, none of the salivary biomarkers listed above have been verified to predict the onset of AMI. All of these studies, as tabulated in table 1, were conducted retrospectively after the incidence. On the other hand, prospective studies should be able to alternatively facilitate the researchers to find predictive AMI biomarkers. In future, these newly detected salivary biomarkers will conceivably provide an early molecular diagnosis and eventually increase the survival rate of cardiovascular patients as opposed to that of plasma. However, more validation needs to be carried out in order to find robust and discriminatory biomarkers for this disease.. day after pm and inversely for 7 days after pm. The results showed that. The total number of co-occurrences with 5-FU was 40,284 buy provigil australia and 34,928 for capecitabine, 320 for tegafur, 1,215 for UFT, 1,422 for S-1, and 495 for doxifluridine, representing 0.183%, 0.159%, 0.001%, 0.006%, 0.006% and 0.002% of all co-occurrences in the database, respectively. In total, 864, 802, 110, 227, 246 and 168 adverse events were extracted as 5-FU- or oral fluoropyrimidine-associated adverse events with 23,690, 20,290, 200, 773, 861 and 305 co-occurrences, respectively. For each of tegafur, UFT, S-1 and doxifluridine, the total number of co-occurrences was not large enough to compare with 5-FU..

The robust data presented in the above work shows that co-exposure.

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Yesterday I’m walking home from school and I look up to see some strange guy in a hard hat at the far end of the block waving at me with his arm. I look around for a minute and see that there’s some kind of construction going on and I realize he wants me to cross to the other side of the street. So I do. But it miffs me a bit, because I dislike it when anyone assumes authority over me that’s not clearly theirs.

As I get near my condo, at 2529 Rio Grande, I realize what’s going on: They’re knocking down trees, and not little ones either. Just inside the stone wall which is all that remains of the seedy block of furnished apartments that used to occupy the lot immediately north of my building, stood these two proud 40-ft. oak trees, just to either side of the main gate. I don’t know how old they might have been, but I bet they predated the complex that was demolished around them. The workers have to clear the sidewalks because the branches are large and heavy and overhang them to some extent.

Now, I don’t know if it was because I was already a bit grumpy with these guys, or solely because I was offended at the casual destruction of the beautiful old trees in my neighborhood, but I decided I was going to make a hard time for these workers, if possible, and in the best situation maybe stop them from killing the trees. I’m not such a radical (or maybe brave) person as to strap myself to one of the trunks, and it didn’t really look like there would be time to make it to the hardware store and buy chain and a padlock for that purpose before they were finished, anyway.

So I did the only thing I knew to do, which was call the city. I know Austin has fairly tough municipal regulations regarding the felling of trees inside the city limits. I thought maybe I could at least verify that they had a permit to cut down these trees and get them stopped or at least fined if they didn’t. The woman who answered the city information line was confused by my request at first: “There’s a tree you want to cut down?” she said. “No,” I explained, “I’m concerned that I’m witnessing the illegal felling of a protected tree.” There was a pause, and then she said, “Hold on, I’ll have to ask about that one.” So I get the hold muzak, which is an impossibly banal counterpoint to the scene of arboreal slaughter outside my window. While I’m waiting on hold, the destruction of the first tree is completed and the excavator starts filling in the hole left by the torn-out roots.

Eventually the woman returns to the phone, and it’s clear that she now understands and appreciates my situation. “You need to speak to the City Arborist,” she tells me, and gives his name (which I never figured out how to spell, and hence will not include here), and his number, which is 512-974-1876. “I’m sorry it took so long for me to figure that out,” she says. I tell her it’s OK, and she thanks me for calling. It’s obvious at this point that she’s on my side.

I call the Arborist and get his answering machine. The excavator is now rumbling toward the second tree. I leave a rambling message about who and where I am and how they sure are beautiful trees and I just wanna make sure the workers are within their legal rights cutting them down. I am conflicted. A large part of me wants to go down and confront the workers, but I realize that will only make them defensive and will not stop them from doing what they’re doing. I pace back and forth for awhile and figure the only thing to do is take pictures so I can make sure they get punished if it turns out they’re breaking the law. So I snap a frame or two and turn back to the computer to work.

There’s a loud CRACK a minute or two later and I go back to the window and see that the excavator has broken a large limb off the second tree. About then the phone rings, and it’s the arborist, who, to my pleasure, sounds concerned and gets right to the point: “Tell me what you’re seeing,” he says. And I do. As I’m talking, the excavator repositions itself and strikes downward into the tree’s crotch, splitting the trunk, and I realize that there’s no stopping them at this point. I tell the arborist as much. “But I took pictures,” I explain, “in case it turns out that what they’ve done is illegal.”

“Where are you again?” he asks. “West Campus,” I tell him. “Do you know the neighborhood?” He doesn’t. “Do you have an address?” Apparently he’s got a database of some sort that lists permit-holders. I don’t know the exact address, but I can extrapolate from mine and take a guess: “Try 2601.” A minute later he comes back and says, “Yes, there’s a permit to develop that property,” which I understand from his disappointed tone to mean that there’s nothing to be done. Apparently the rule in Austin is that private homeowners need a permit to fell any tree with a diameter of 19 inches or greater, but that developers have more flexibility. The arborist can’t tell me what the specific site plan calls for with respect to these particular trees, but he can tell me that there is a plan and it’s been approved, so in all likelihood these guys are acting in accordance with it and hence within the bounds of law. I thank him and he thanks me, and before we hang up he asks me to call again any time I’m suspicious of tree-related crime, because his office depends almost completely on concerned citizens/nosy neighbors like me to catch and prevent the illegal destruction of trees. I assure him that I will.

And that’s where the story peters out. I wanted to do something but I didn’t, basically, and although I got some sympathetic voices on the phone none of it changes the basic fact of the matter, which is that there are now two muddy holes in the ground where there were once two live, beautiful, healthy trees. And I stood to one side and watched as a man with a machine tore them up. Should I have tried, physically, to intervene? Should I have obeyed that impulse to chain myself to the trunk? I don’t know the spirit of a tree, but I know how hard it was to watch them be destroyed. It was like a crime was happening out on the street, in broad daylight, and everyone was just walking by indifferently. I didn’t want to be the apathetic one; I wanted to be the one who gave a shit. But I tried to be a civilized adult about the whole thing and now I regret it. Even if I hadn’t, ultimately, saved those particular trees, a show of strength might’ve brought some attention to the subject, might’ve made the developers or the city authorities or whoever think twice the next time they decided to hire out that kind of a dirty job. But in the end I was just like everyone else: Too busy with my own concerns to take hours out of my day to worry about something as simple as the killing of a tree.

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As a chemist, I find the debate about WP as a “chemical weapon” sort of amusing. One might as well claim that we’re engaged in “chemical warfare” because the lead we use to make bullets is toxic.

It’s like that question they ask me sometimes at the post office: “Does your package contain any chemicals?” Well, OF COURSE IT DOES, because the universe is made of chemicals and if there’s any damn thing at all in the package, there’s chemicals in it. In that sense, any weapon that EXISTS is a “chemical weapon,” and the word becomes totally useless. The chemistry of WP is simply oxidation/combustion, which is the same chemistry that propels bullets and shells down gun barrels and causes fire in general, and the use of fire in warfare is as old as warfare itself. It just so happens that WP burns very hot and is self-igniting in air.

If “chemical weapons” is to remain a useable term, it’s best reserved for toxic compounds which are employed primarily to exploit their toxicology.

That being said, it seems likely to me that in the future, as war continues to be “humanized,” we will begin to see moral and eventually legal proscription of the use of burning as a means of offensive war. Destruction of uninhabited materiel or facilities is one thing, but the deliberate destruction of live human beings by combustion is pretty appalling. Think of the little Vietnamese napalm girl, or the fire-bombing of Dresden or Tokyo, or of the use of the flamethrower in trench warfare. Burning is agonizing, indiscriminate, and not terribly efficient versus shooting or blasting to bits. Burning is a frightening way to die (or, perhaps worse, to not die), and for this reason it is frequently employed as a psychological weapon.

I’m not necessarily advocating its regulation, because I think war is just nasty and efforts to “soften” it are hypocritical, but I can see it coming in the future anyway.

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Essentially, to “catastrophize” is to overreact in a negative way to a setback, such as the one who is stood up for a date and becomes upset that he or she will never find love. Broadly, catastrophization is a habit of mind that’s commonly identified in the anxious and depressed. I don’t know enough to speculate about what causes the formation of such a habit, but I can admit to recognizing it in myself. I have often characterized my depression as “an inability to control negative thoughts,” and by these negative thoughts I essentially mean overwhelming catastrophization. When I’m depressed, even the smallest and most innocous event or impression can become symbolic of my total failure as a human being.

Recognizing the process as a habit, as something that can be lost or changed or replaced like any other habit, is itself very valuable to me. Even the simple fact that there exists a word to describe the phenomenon brings me considerable comfort–in the first place, it shows that I’m not alone in experiencing it, and in the second, well…everyone knows that to name a thing is to have power over it. The next time I begin to “catastrophize,” the word itself will occur to me, and in matching the sign to the signified I will be reminded that the catastrophe I perceive is in my head and not in the world. Maybe, in time, I’ll even be able to laugh about it, to find some humor in the extent to which I can blow things out of proportion, but of course there’s a fine line to be walked here. I can already hear myself thinking: “I’m catastrophizing again. It’s so like me to do that. No wonder I’m a such a TOTALLY WORTHLESS LOSER.”

As in learning to meditate, the trick to changing habits of mind like catastrophization is probably to avoid trying too hard. Instead of recognizing catastrophic thoughts and working really hard to stop, it’s probably better to just recognize those thoughts, release them, and then casually replace them with something else. Those three Rs could become a mantra: Recognize your negative habits, Release them in the moment, and Replace them with something more constructive. Perhaps there’s even a fourth R: Repeat the process until they change.

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This week my father preserved for me a series of editorials from the Wall Street Journal by Charles Murray, of The Bell Curve fame, arguing his thesis for the reality of g, which he identifies as an inherent and inherited “intelligence factor” that differentiates the smart from the dumb. Distribution of g in the population follows a normal, or “bell,” curve, and he points up many of the oft-touted depressing statistics of U.S. public education and explains them–convincingly, in my view–in terms of the normal statistical distribution of intelligence in our population. He revives the spectre of the IQ score, and although he acknowledges quibbles about the accuracy of the tools used to measure it, he also advocates its phenomenological legitimacy. He deals summarily with Gardner’s multiple intelligences theory, citing relatively convincing evidence that g is a real phenomenon and can’t be wished away by egalitarian reformers. He recognizes how the notion of uneven distribution of g chafes agains our ideals of equality and the political difficulties attendant to making policy decisions based on a worldview which is in this sense elitist.

I see Murray as one of a small but growing vocal minority of intellectuals who are prepared to acknowledge that human beings are in most meaningful ways determined by their genes. As biology and neurobiology advance, we come to understand more and more how even very complex human behaviors can be predicted genetically. This is certainly not the first time in history that a deterministic elitist movement has surfaced, but it may well prove to be the first time that the unpleasant awareness of genetic determinism is answered by an ethical technical solution. Before long, it seems obvious to any scientifically-informed observer, biochemistry will allow human beings to achieve meaningful control of their genetic destinies, at which point a political battle will ensue between the forces that advocate non-intervention in genetic fate and those who recognize biochemical eugenics as an escape from determinism.

Brief meditation on human nature leads me to predict that the battle will be a short one. Voices in favor of accepting determinism–such as Murray, et. al.–run up against the ubiquitous phenomenological fact of choice: Whether it is real or not, human beings experience a process of decision making that causes them to behave as if they have some measure of control over their fates. Although most rational adults can be persuaded to admit, if pressured, that there are things in life over which they have no control, most of them would also prefer that it not be so. If offered a choice between the certainty of a brilliant and beautiful and happy child and the luck of the draw, which of us would leave it to fate?

Practical eugenetic technology is not with us now, and may well not materialize until twenty years hence. Even if it takes that long, however, it still seems likely that we will find ourselves living with a technology that can correct our genes before we find ourselves living in a political culture prepared to accept that they determine our fates. In that most probable case, Murray’s arguments, though convincing, come too late on the scene. Even if we begin now to implement the policy regime he advocates, it’s likely that by the time reforms come into place the biology on which they are founded will become subject to the same socioeconomic pressures which corrupt the system now. Western culture has lived in denial of biological determinism for decades now, and in resentment of it for millenia–are we going now to give in and accept it on the very eve of our liberation? Better now to begin preparing for that future culture of eugenetic control, to begin steering now toward’s Keillor’s Lake Wobegon, where all the children are above average, and away from Huxley’s Brave New World, where minds are manufactured to meet the demands of industry.

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I propose the prefix “cylo-” to describe all matters pertaining to “cylon biology,” in other words that “cylo-” be used analogously to “bio-” to describe any subject pertaining to cylon biology rather than normal human biology. The show, after all, has established that cylon biology (“cylology,” under my new system), although generally indistinguishable from human biology at the macro-level, is chemically distinct. Which explains how Dr. Baltar can build a cylon detector and how cylons, though histologically identical to humans, can exhibit all the unique characteristics that they do, i.e. running for days without tiring, spinal bioluminescence, group consciousness, unusual RF susceptibility, etc. Thus “cylo-” can be assumed to denote that aspect of cylon physiology which is analogous to, but not identical with, human physiology.

Which gives us all kinds of great new words like “cylogenetic,” “cylochemistry,” “cylological,” “cylonic,” “cylosphere,” “cylome,” “cylophysics,” and my personal favorite, “cylohazard.”


In honor of this last term, I’ve made up a “cylohazard symbol,” which is derived from the analogous human biohazard symbol, differing in that it is based on a five-fold axis of radial symmetry, instead of a three-fold axis. This decision is in keeping with the established significance of the pentagon and the nested pentagon as a symbol of cylon hegemony in both the old and the new Battlestar Galactica series. Material which is infectious of cylons, such as samples of the “cylon plague” from Season 3, would rightly bear the cylohazard symbol, regardless of whether or not it was also infectious of humans. Material which is infectious of both species should properly bear both symbols.

Someday I might write a buy brand provigil “ANSI standard” from the BSG universe describing the layout and appropriate use of the cylohazard symbol by itself or in conjunction with the biohazard, chemohazard, and or radiological hazard signs.

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There is a road that begins, in my heart. with the general disdain I feel for most specimens of homo sapiens, and ends, in my spleen, with the blackest hate that one man can feel for another, the kind of hate most people, including myself, are fortunate enough never to experience, the kind reserved for a villain who has destroyed a loved one and witnessed by actions of murderous revenge. Arrayed along this road, like Burma-Shave ads on the highway to Abilene, are signposts, behaviors, that mark the boundaries between the states of disdain and dislike, dislike and loathing, loathing and hate.

It is somewhere around Wichita Falls, by my reckoning, that the countries of true hate begin. In mapping these infernal regions, I have found it useful to apply what I call “the sweve test,” which is really a pair of tests: Driving along, I mount a rise to discover the person of my enemy, standing in the road a short distance ahead, and put to myself the question, “Do I swerve to avoid him?” If the answer is yes, then he has not yet passed into the territory of loathing; if no, then the second test must be applied: Mounting a second rise, I discover the person of my enemy standing beside the road a short distance ahead, and put to myself the question, “Do I swerve to hit him?” If no, he is loathed; if yes, hated.

The swerve test has much to recommend it. First, it is accurate: In the best tradition of Skinner, it avoids murky subjectivity by addressing only behavior. While my own estimation of the extent of my distaste for a particular person may vary with the weather, the proximity of my next meal or the quality of my last, or whether or not I remembered to take my medication that morning, the volition to actually effect his destruction, either passively or actively, is much less mutable.

Second, the swerve test is precise: We may imagine the swerve as a kind of behavioristic quantum–the smallest act measurable as evidence of intent. Here is a heavy mass, moving with great speed, having tremendous inertia, and by a small motion of my hand I can deflect its course and thereby choose to spare or destroy my enemy. In the first test, I must expend this minimum effort to save him, and in the second, to destroy him. The two outcomes differ only by a quantum.

Third and finally, the results of the test are easy to interpet: At the end of the day, the subject of the swerve test, like Schrodinger’s cat, is either alive or dead.

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I’m imagining a portable device that integrates a global-positioning system (GPS) receiver with a short range (say 25m) LIDAR (laser imaging detection and ranging) system that could be used to map the street-level topography of the earth–buildings, rooms, trees, streetsigns–as the user moves through it. I’m imagining a built-in-panoramic video camera that can be used to map textures onto all the surfaces. I’m imagining an internal hard-drive and/or cellular modem so that all this mapping information can be uploaded, sooner or later, to a central server that compiles location-mapping correlation data from multiple users to create an immersive 3D simulation of the real surface of the earth. I’m imagining stores and businesses and schools having sales, conducting meetings, and teaching classes at virtual locations inside the virtual earth at the same time they happen in the real earth, or even in lieu thereof. I’m imagining mappers competing to be the first to scan the inside of Kitum cave, or the top of Mt. Everest, or the basement of the Pentagon. I’m imagining that we’ll see it happen within 15 years. I’m imagining that the first people to make it work are going to be very, very rich.