No detectable damage

The reactions lead to a low amount of bibenzyl, except when the aromatic ring is substituted by a methyl substituent in ortho or para position. The benzylic zinc species exhibit a high stability in acetonitrile and solutions can be stored for several days, at room temperature under argon atmosphere with no detectable damage of the organozinc. Despite this stability, these organozinc species can react with aromatic aldehyde and 3-thiophene aldehyde provided use is made of chlorotrimethylsilane, which is known to activate the carbonyl function (equation 22)29. 

From the model in Scheme 10, a further prediction can be made that an even weaker oxidant than RudlDOH should be reduced efficiently in the presence of DNA with no detectable damage to the nucleic acid—i.e., only the kx pathway is operative. This prediction is confirmed by the results on Os(tpy)(bpy)0. It has been shown by X-ray crystallography that Os(tpy)(bpy)OH2 is structurally identical to the ruthenium analogue (Fig. 16), so the only difference in the complexes is the weaker oxidizing power of the osmium complex. Nevertheless, Os(tpy)(bpy)0 does not damage DNA as assessed by high-resolution electrophoresis, even though it is reduced efficiently in DNA 186). Thus, reduction of Os(tpy)(bpy)0 occurs via the kx pathway, and it is possible to use the time dependence of osmium reduction to measure kx directly. These studies show that self-inactivation of Os(tpy)(bpy)0 is catalyzed by DNA (Fig. 17). The extent of catalysis is a function of the square of the concentration of osmium bound to DNA calculated... 

At aity given time the population is exposed to the likelihood of accidents that could result in injury or even death. Fortunately, the greater majority of accidents result in no detectable damage (NDD). While mortality and morbidity rates arising out of accidents affect our hves and create high financial burdens for people, families, employers and the community, we still know little, however, about the causes of accidents. 

The accident has not changed. It remains at the point where control over the system was lost. The only change is in the exposure to the hazard and the outcome. The hazard remains the system out of control however, when the hazard met a new exposure the results are now death, injury and mayhem as opposed to the previous scenario which resulted in no detectable damage. 

Regardless of the severity of an outcome, from death at one end of the scale to no detectable damage at the other, the causation factors which gave rise to the accident and created the hazard remain unchanged. It is the information on NDD accidents that we must collect, analyse and act on if hazards and injuries are to be avoided. This is based on the principle that not all accidents result in injury. We have known for years that there is a relationship between the total ntrmber of accidents a person experiences and the number that result in injury. It could be that continued expostrre to accidents evokes the laws of probability and eventually the luck runs out. This in no way suggests that accidents are a function of luck but rather that the accident outcome may contain a component of ill fortime. The only way to ensttre the prevention of injury is to prevent the accident. 

The outcome of such an event is unlikely to have a nil result The concept of No Detectable Damage (NDD) is preferred in that if the outcome does not result in immediate direct loss, the event outcome is often quickly foigottem However, the event may have latent effects that at the time of the exposme go undetected. 

Histological examinations of lesioned animals indicated a complete bilateral depletion of granular and pyramidal cells in the dorsal hippocampi. Light microscopy failed to reveal neuronal depletion in any other region of the brain. There was no detectable damage in any region of the brain in lead-exposed animals. 

More recently, however, in cynomologous monkeys, a nonhuman primate, some limited responses to these compounds have been seen with a twofold increase in liver weight, hepatocyte hypertrophy, an increase in peroxisomes (2.7x), and an increase in mitochondria. However, no DNA damage was detected. With humans taking ciprofibrate, only limited peroxisome proliferation was seen, and there was no increase in acyl CoA oxidase. Thus, the question is, "are humans at risk " In order to understand this, the mechanism needs to be understood. 

DNA injection directly into mouse diaphragm has also resulted in luciferase expression and there appeared to be no damage to the diaphragm due to the DNA injections (Davis and Jasmin, 1993). In a related study, /3-galactosidasc ( /3-gal)-encoding pDNA injected into the articular space of rabbit knee joints resulted in /3-gal expression in the joints (Yovandich etal., 1995). In the same study, chloramphenicol acetyltransferase (CAT) encoding pDNA injected into rat knee joints also led to reporter gene expression, with peak expression 48 hours after injection and with no detectable activity 15 days later. 

Instrumented animals may be reused after appropriate washout periods on the assumption that the compounds in the doses tested cause no reversible damage. Since the cardiovascular parameters measured are sensitive to the overall well being of the animals, changes in baseline conditions should be examined for detecting possible compound-related toxicities. Assuming such toxicities are not observed, animals can be maintained for over one year with appropriate care. 

The unmonochromated x-ray source was Mg Ka. To minimize x-ray damage to the PTFE specimen (10), the source was operated at only 7.5 kV and 5 mA and was retracted as far from the specimen as possible. Under these conditions, no change in the Cls line of virgin PTFE could be detected after several hours of x-ray exposure, and more importantly, there was no detectable outgassing of the specimen at the 1x10 mbar level. 

For non-transparent specimens, as shown by Bucknall and Stevens useful information relative to the deformation mode can be obtained by recording hysteresis loops as a function of cycles. Figure 6 shows hysteresis loops obtained at 0.2 Hz at various N values for PS tested at a stress amplitude of 24.1 MPa and Fig. 7 for HIPS tested at 17.2 MPa. For PS, with Nf = 1,451 cycles, there is no detectable change in loop area at this stress amplitude up to the final cycle. This illustrates the highly localized nature of the fatigue-induced damage zone in PS and indicates that, for this polymer, hysteresis loop observations are not an effective method for detecting craze... 

The action of ONOO on DNA rather than deamination is oxidative and ONOO addition leads to more damage than treatment with an equivalent amount of NO. The spectrum of ONOO" damage is also increased over NO, which is probably accounted for by their relative reactivity. The addition of ONOO to naked plasmid DNA can cause strand breaks using as little as 2-5 pM compared to no detectable strand breaks in NO treated plasmids at millimolar concentrations [132,133]. 

Cystatin C is nearly completely metabolized by proximal renal tubular cells. As a consequence, under ordinary circumstances there is little to no detectable cystatin C present in the urine. Thus, a true clearance of cystatin C cannot be determined. However, in the presence of tubular damage, cystatin C may be detected in the urine [147,148] and may be more sensitive to early and mild changes of kidney function compared with creatinine [149,150]. In this regard, elevation in serum cystatin C consistent with AKI, defined by at least a 50% increase from baseline, was evident 1-2 days prior to changes in SCr [151]. Finally, in patients with AKI, elevated urinary cystatin C was highly predictive of subsequent need for acute renal replacement therapy and outperformed several other urinary biomarkers in some studies [152]., but not in others [152a]... 

The ceramic filter showed good filtration efficiency, with stable pressure drop. However, after more than 1200 hours of trouble free operation suddenly two ceramic candles broke. The difficulty to detect a relatively small failure in a hot gas filter was then noticed in practice even though no serious damage was caused. 

Elevations in cTnl and cTnT are highly specific for myocardial injury. However, in individuals without myocardial disease, their levels are very low to undetectable. This is in contrast to the low but measurable concentrations of CK-2 and myoglobin detected in serum from skeletal muscle turnover in patients with noncardiac-related diseases and in normal individuals. Therefore release of cTnl or cTnT from myocardium into the blood following AMI and after the washout that accompanies successful reperfusion generates an excellent signal compared with no detectable baseline levels before myocardial damage. The initial rapid release of cardiac troponin subunits I and T following successful reperfusion is most hkely derived from the soluble cytosolic myocardial fraction (6% cTnT 3% cTnl). 

Since 1999 specially trained dogs, so-called mold sniffer dogs, have been used for the rapid detection of hidden mold damage. They detect damage in areas not only at their level but also on indoor ceilings. Their usefulness has not been scientifically evaluated, but there are reports on their successful use in such procedures [67]. No decisions about rehabilitation should be made solely on the basis of detection by the sniffer dog [14]. Odor perceived by humans is not a quantitative measure for microbial damage because the quantity of typical odorous substances does not necessarily correlate with the biomass or the area... 

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