Human behaviour normal

A fundamental concept of ICAM is acceptance of the inevitabiUty of human error. Human factors research and operational experience has shown that human error is a normal characteristic of human behaviour, and although it can be reduced, it cannot be completely eliminated (Helmieich and Merritt, 2000). An organization cannot change the human condition, but they can change the conditions imder which humans work, thereby making the system more error tolerant (Reason, 2000). 

That we have been slow and imperfect in our efforts to match traffic law and traffic management to normal human behaviour can be illustrated through a case study of risk management at intersections in Australia." ... 

It is known that the brain is one of the most sensitive sites of action of steroids in utero, and recently there have been suggestions that EDs may affect normal brain development and behaviour. For example, it has been alleged that in utero exposure to polychlorinated biphenyl compounds (PCBs) resulted in adverse effects on neurologic and intellectual function (memory and attention) in young children born to women who had eaten PCB contaminated fish in the USA." It has also been speculated that exposure to environmental pollutants with steroidal activity may be infinencing human sexual development and sexually controlled behavioiir." ... 

All preclinical animal models of anxiety involve exposing animals (usually rats or mice) to environmental stimuli that disrupt their normal pattern of behaviour (Table 19.2). Obviously, it can never be confirmed that animals are actually experiencing the equivalent of human anxiety and so the validity of all preclinical models rests largely on confirming that the change in behaviour is prevented by drugs that have established anti-anxiety effects in humans. 

The corpus luteum arises from the ruptured follicle and secretes progesterone, which has an important role in the estrous or menstrual cycle. Luteal progesterone is also required to maintain early pregnancy in most mammalian species, including humans (Csapo Pulkkinen, 1978). Therefore, establishment and maintenance of normal corpora luteaare essential for normal reproductive function. However, with the exception of evaluations to establish their presence or absence, these structures are not evaluated in routine testing. Increased rates of follicular atresia and oocyte toxicity may lead to premature menopause in humans. Altered follicular development, failure to ovulate or altered corpus luteum formation and function can disrupt cyclicity, reduce fertility and interfere with normal sexual behaviour. Therefore, significant increases in the rate of follicular atresia, evidence of oocyte toxicity, interference with ovulation or altered corpus luteum formation or function should be considered adverse effects. 

Physiological toxicokinetic (or pharmacokinetic) models represent descriptions of biological systems and can be used to describe the behaviour of chemicals in the intact animal. Such models have been used to predict the disposition of butadiene and metabolites in rats, mice, and humans. For the case of rats and mice, these predictions can be compared with experimental data. In some cases (see below), the models successfully describe (and accurately predict) the disposition of butadiene and metabolites. Human physiological toxicokinetic model predictions normally cannot be verified due to lack of experimental data. 

Chondrocytes respond biologically to mechanical stimuli, and this is called mechanotransduction. Understanding cellular responses to mechanical stimuli and how they can be related to tissue level characteristics has many applications in biology, tissue engineering and medical science. Information about the mechanical properties of chondrocytes is fundamental to such research. Micropipette aspiration has been applied to investigate the deformation of single chondrocytes (Jones et al., 1999). It was found that human chondrocytes behave like viscoelastic solids. The Young s modulus of normal chondrocytes appeared to be very variable, but was of the order of 0.65 + 0.63 kPa. However, the viscoelastic behaviour was not quantified. 

MRS spectra from the human brain. In order to improve the robustness of the X2 minimization, an internal parameter R was used, defined by r = exp(— R ). The arctangent function, however, is preferable as it has a continuous derivative around R = 0. The equal asymptotic behaviour of this function towards 0 and 1 ensures that r remains within this valid range. We have subsequently found that using r = (arctan(7 ) + Tr/2)/n gives better performance. The fit can be conveniently performed using only the real part of the complex spectrum. Thus the normalized x2 is given by... 

Despite only a minor difference in the chemical structures of vinblastine and vincristine, the clinical effects differ considerably. Surprisingly there is no clinical evidence of cross resistance between them, or with radiation and other presently known oncolytic agents. The rise and fall of the blood activity level of vincristine is steeper than that of vinblastine.The dosage requirements of both alkaloids differ markedly the weekly intravenous dose of vinblastine for humans is 0.1—0.2 mg per kg, that of vincristine, however, is approximately one tenth of this. Concerning the side-effects, vincristine shows more neurotoxic effects and vinblastine is considered to have more potency in bone-marrow depression. This is not without consequences on human therapy therapy is limited by bone-marrow depression with vinblastine and neuromuscular effects, with vincristine. Early symptoms of side-effects are vomiting, fever, and exanthemes. Late symptoms are C.N.S. disturbances, alopecia, and leukopenia. C.N.S. disturbances are manifested by various symptoms such as paresthesias, neuritis, paresis, and muscular atrophy, accompanied by quenched reflexes. Even behaviour may be affected after a long period of treatment. But why do all these side-effects happen, when Vinca alkaloids are unable to pass the blood-brain barrier The only explanation we have at hand is that they are possibly caused by metabolites or breakdown products of the normal biochemical pathways, which are disturbed by the alkaloids. 

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