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Research in informatics ranges from fundamental computer science to applied informatics cheap super cialis 80 mg without a prescription. Several definitions of medical informatics take both the scientific order super cialis 80mg without prescription, fundamental aspect and the applied generic 80 mg super cialis free shipping, pragmatic aspect into account purchase super cialis 80mg overnight delivery. Shortliffe super cialis 80 mg lowest price, for example, provides the following definition: “Medical Information Science is the science of using system-analytic tools … to develop procedures (algorithms) for management, process control, decision-making and scientific analysis of medical knowledge. Medicine identifies the area of research; informatics identifies the methodology used. In medical informatics, we develop and assess methods and systems for the acquisition, processing, and interpretation of patient data. If the medical informatics research is applied, the objective is to develop a computer system that will be used by healthcare professionals, for example 168 DIAGNOSTIC DECISION SUPPORT research aimed at the development of electronic medical records. If the research is more fundamental, the computer plays a role as an experimental environment for models that are developed; the objective is not to build a system, but to verify a hypothesis or to investigate the limitations of models. Some research in the area of artificial intelligence in medicine, for example, fits this last category. Applying ICT to a given medical domain is not merely adding a new technique: ICT has the potential to radically change processes in that domain. When introduced into an environment, ICT will initially often emulate or resemble the already existing processes. When workers and researchers in that domain begin to appreciate the potential of ICT, this initial stage is followed by more fundamental changes in that domain that take advantage of the potential of ICT. Electronic communication, for example, is a relatively simple technology. The contents of a message may be structured (that is, contain a predefined set of data) or free text. When introduced into the healthcare process, electronic communication is used to replace existing paper documents. The names of the first electronic messages often even carry the names of their paper counterpart: electronic discharge letter, electronic prescription, etc. At first glance, little has changed compared to the previous paper based communication, except the speed of delivery. At this stage, the infrastructure (for example computers, lines) required for ICT has been installed, but its impact on the processes is still very limited. Subsequently, however, the ability to send data using electronic communication is used to support new forms of collaboration between healthcare professionals. At present, the emphasis has shifted from replacing paper documents to sharing data between colleagues. As clinicians increasingly share data, issues such as the standardisation of the content of medical records are becoming important areas of research. In addition, the fact that data can be transferred easily over distances enables clinicians to interpret data while the patient is located miles away (resulting in, for example, the so-called “telediagnosis”), or to communicate with patients over longer distances using, for example, the internet. In this chapter we will focus on the contribution of medical informatics to diagnostic decision support. We believe that the use of ICT in the domain of diagnostic decision support is still in an early stage. Although in a few specialties (for example radiology), ICT is used extensively for decision support, most clinicians have little or no experience with decision support systems. Many researchers argue that the fundamental enabling technology is the introduction of electronic medical records. Once electronic medical records are available, they argue, we will witness a rapid increase in the use of diagnostic decision support systems. The entries in the record enabled the clinician to recall previous episodes of illness and treatment. In recent years, however, medical records have been used increasingly for other purposes: they are used as a data source for purposes ranging from billing the patient to performing epidemiological studies, and from performing quality control to defending oneself against legal claims. One of the major barriers for using the data in such ways is the inaccessible and often unstructured nature of the paper record. The introduction of computer based medical records to a large degree, removes that barrier. Recent decades have seen a rapid increase in the role of computers in medical record keeping, and professional organisations have started to play an active role in the introduction of electronic records. For example, in 1978 the first Dutch general practitioners started using personal computers in their practices. In 1990, 35% of Dutch GPs were using one or more computer applications; although the majority of these are administrative, an increasing number of clinicians use computer stored medical records.

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Webster &2001 John Wiley & Sons Ltd 478 NEUROTRANSMITTERS purchase super cialis 80mg without a prescription, DRUGS AND BRAIN FUNCTION body temperature does not follow the change in the sleep±waking cycle order super cialis 80 mg free shipping. Generally discount super cialis 80mg overnight delivery, it becomes shorter (to as little as 20 h) generic super cialis 80 mg with mastercard, rather than longer super cialis 80mg without a prescription, which suggests that these cycles are regulated in different ways. Entrainment has also been shown in aplysia which, after exposure to a normal dark±light cycle, retains a cyclic pattern of activity for a number of days even if subjected to continuous light. These genes have been studied most extensively in insects but they have also been found in humans. Their protein products enter the cell nucleus and regulate their own transcription. This feedback process is linked to exposure to light and so it is not surprising that visual inputs are important for maintenance of circadian rhythms. However, it is not the reception of specific visual information, transmitted in the optic nerve to the lateral geniculate nucleus (LGN) and visual cortex (i. The fibres conveying this sensation arise in the retina but diverge from the optic nerve and travel in the retinohypothalamic tract (RHT) to innervate the suprachiasmatic nucleus (SCN), a small nucleus which is found in the anterior hypothalamus above the optic chiasma (Fig. A deficit in information carried in this pathway could help to explain why the blind often suffer from disrupted sleep patterns. Another prominent input to the SCN comes from the intergeniculate leaflet (in the lateral geniculate nucleus (LGN) complex) via the geniculohypothalamic tract (GHT) and, whereas the retinohypothalamic pathway seems to be essential for light-entrainment of the circadian rhythm, the LGN seems to be influenced by rhythmic variations in non-photic inputs such as changes in motor activity. Of course, the LGN is obviously influenced too by visual inputs and, together with the GHT projection to the SCN, can be regarded as an indirect retino- hypothalamic pathway which appears to be inhibitory on SCN neurons. A neuronal input to the SCN from 5-HT neurons in the median Raphe nucleus is another possible route for setting the circadian clock (entrainment) by non-photic stimuli (Fig. Destruction of the SCN, the target of all these pathways, abolishes the synchronised circadian rhythms in locomotor and autonomic function which clearly points to this nucleus as a crucial centre for the control of cyclic function. However, there seems to be some topographical organisation of the neurons in the SCN in respect of their function and the transmitters they release. Whereas those in the dorsomedial zone of this nucleus (or nuclei, since it is paired) contain arginine vasopressin (AVP) or angiotensin II and GABA, neurons in the ventrolateral zone contain vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP) and GABA. It is these latter neurons which form the core of the nucleus and show rhythmic pacemaker function. In fact, when maintained in culture, they even display a metabolic rhythm which has the same phase as that of SCN neurons in vivo. Unfortunately the presence of GABA in these neurons means that they must be inhibitory and so could not directly stimulate any brain function when activated, e. Neurons within the SCN innervate those hypothalamic areas which have a crucial role in the regulation of the reproductive cycle, mood and sleep/arousal, as well as regions such as the basal forebrain and the thalamus which help to determine the state of arousal. They also project to the pineal gland to govern the synthesis and release of SLEEP AND WAKING 479 Figure 22. Other inputs derive from the lateral geniculate complex and the serotonergic, Raphe nuclei and help to reset the SCN in response to non-photic stimuli. Neurons in the SCN project to the hypothalamus, which has a key role in the regulation of the reproductive cycle, mood and the sleep±waking cycle. These neurons also project to the pineal gland which shows rhythmic changes in the rate of synthesis and release of the hormone, melatonin the hormone, melatonin, which is another factor involved in the control of the 24-h cycle. Despite its trivial name, the pineal gland does not contribute to discriminative vision and its role is merely to detect changes in light intensity so that, in animals with a clear photoperiod, it couples physiological rhythms with the length of the day±light cycle. In mammals, the pineal is not exteriorised but it persists as a brain appendage for the secretion of the hormone, melatonin. Melatonin is not a normal metabolite of neuronal 5-HT but it is synthesised from that amine in the pineal gland by the enzyme, 5-hydroxytryptamine N-acetyltransferase. This is a rate-limiting process that shows a circadian rhythm with maximal activity occurring during darkness. The product of this reaction, N-acetyl 5-hydroxytryptamine, is methylated, to form melatonin, by the enzyme hydroxyindole-O-methyltransferase. The rate of melatonin synthesis is controlled primarily by the release of noradrenaline from sympathetic fibres originating in the superior cervical ganglion. The activity of these neurons and, consequently, the synthesis and release of melatonin, follows a circadian rhythm such that sympathetic input and melatonin synthesis are both increased in the dark. This coupling with the light cycle certainly involves the SCN since destruction of this nucleus greatly reduces the fluctuations in melatonin production. Moreover, retrograde transneural tracing has shown that there is a neuronal pathway 480 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION Figure 22. The effect of noradrenaline on melatonin synthesis appears to be mediated through b-adrenoceptors, using cyclic AMP as their second messenger, although studies on cultured pinealocytes suggest that this process is potentiated by activation of a1-adrenoceptors (see Hagan and Oakley 1995).

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Distinct anatomical pathways have not been identified since there is no specific enzyme involved in their synthesis that can be used for immunohistochemistry generic super cialis 80 mg without a prescription, and they are not sufficiently concentrated for ordinary histofluorescence buy generic super cialis 80 mg. TRYPTAMINE Although tryptamine can be detected in brain there has been much debate over whether it exists separately from 5-HT or merely co-exists with it buy 80mg super cialis with visa. Specific high-affinity binding sites have been demonstrated for tryptamine in rat cortex generic super cialis 80 mg with mastercard. These appear to be different from 5-HT sites but until appropriate antagonists are found it remains possible that they form a subset of the ever-increasing number of 5-HT receptors (see Chapter 9) buy super cialis 80mg with mastercard. The behavioural response in rats to tryptophan plus a MAO inhibitor (Grahame-Smith 1971) is accompanied by an elevation of brain tryptamine as well as 5-HT and is less marked if the synthesis of tryptamine is reduced by a decarboxylase inhibitor that does not have a significant effect on 5-HT levels. In fact after a MAOI, tryptamine produces a behavioural response in rats similar to that of tryptophan apart from the absence of certain features like tremor and wet-dog shake. The complexity of the situation is illustrated by studies of the effect of intra-hypothalamic injections of 5-HT and tryptamine on rat body temperature (Cox, Lee and Martin 1981). In these it was shown that 5-HT decreased temperature while tryptamine actually increased it but it was not possible to block one effect preferentially with a whole range of antagonists, despite 278 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION Figure 13. These are all formed by decarboxylation rather than hydroxylation of the precursors of the established monoamine neurotransmitters, dopamine and 5-HT. Also although it was the tryptamine and not the 5-HT response, which was abolished after destruction of 5-HT neurons with 5,7- dihydroxytryptamine and implies that tryptamine was releasing 5-HT, it was found that raphe (5-HT) neuron stimulation produces hyperthermia, like tryptamine, rather than hypothermia, like 5-HT. These opposing effects of tryptamine and 5-HT are also seen when they are applied directly to cortical neurons by iontopheresis. Surprisingly, the 5-HT antagonist metergoline is more effective against tryptamine and the depressant effects. When the medial Raphe nucleus OTHER TRANSMITTERS AND MEDIATORS 279 is stimulated this produces inhibition of cortical neurons followed by excitation but it is the inhibition (tryptamine-like) that is blocked by metergoline. In keeping with this finding is the observation that depletion of 5-HT with pCPA reduced only the excitatory (5-HT) response while 5,7-dihydroxytryptamine, which destroys the neurons, abolished both effects (see Jones 1983). The inference from these studies and those on temperature is that some neurons in the raphe nucleus release something other than 5- HT. This might be tryptamine but if it is not, then its effects are presumably modified by tryptamine. Possibly there is a subclass of 5-HT receptors that would be preferentially activated by tryptamine if its endogenous concentrations were ever adequate. PHENYLETHYLAMINE The relationship of phenylethylamine to dopamine is not unlike that of tryptamine to 5- HT. Present in low concentrations in the brain there is some evidence for distinct binding sites but not for specific neurons. When injected icv it causes stereotyped behaviour similar to, but more marked than, that seen with amphetamine. These effects are blocked by neuroleptics (DA antagonists) and since phenylethylamine does not bind directly to DA receptors it is assumed to release DA, like amphetamine. This is substantiated by the fact that in rats with unilateral 6-OHDA lesions of the SN its systemic administration causes ipsilateral rotation like amphetamine (see Chapter 6). Phenylethylamine certainly increases the overflow of [3H]-DA from striatal synapto- somes and slices and of endogenous DA in vivo, but part of this may be due to block of DA uptake. In any case such effects only occur with concentrations of 5  10À5 M, which are not likely to be encountered in vivo and it is not Ca2‡-dependent. Peripherally phenylethylamine causes contractions of the rat fundus just like amphetamine, tryptamine and 5-HT. These are reduced by some 5-HT antagonists, like methysergide, but not by DA antagonists. Thus some of its central effects may be mediated through a tryptamine receptor. Needless to say, the DA and amphetamine-like activity and structure of phenylethylamine, together with the facility for its synthesis in the CNS, has led to unproven suggestions of its involvement in schizophrenia. In fact there is some evidence for increased excretion of its metabolite (phenyl acetic acid) in the subgroup of paranoid schizophrenics. TYRAMINE p-Tyramine is produced by decarboxylation of tyrosine and is present in the CNS in higher (threefold) concentrations than m-tyramine, the hydroxylated derivative of phenylethylamine. In the periphery p-tyramine is easily hydroxylated to octopamine, which has some direct effects on a1 adrenoceptors, unlike tyramine which functions by releasing NA. When tested on central neurons tyramine always produces the same effects as NA but they are slower and less marked, implying an indirect action. By contrast octopamine often produces the opposite effect to NA and it is probable that octopamine may have a functional role in the invertebrate CNS where it is found in higher concentrations (5 mg/g) than in the mammalian brain (0.

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