The Norwegian Term
Bank is now completing the final phases of its work on the Norwegian version
of ICD-10, a statistical classification system for illnesses, injuries
and causes of death. The project has stretched over several years and is
the most comprehensive since the Term Bank produced Norwegian terms for
the oil industry in the 1980s.
ICD-10 is originally an English-language classification system that acts as a tool for coding various illnesses in health institutions, making statistical processing of data material easier. The Term Bank was made responsible for the translation and organization of the Norwegian version.
– This has been time-consuming and extremely comprehensive work, says Kai Innselset at the Term Bank. – The actual translation of ICD-10 was just the first stage of the project. Our suggested translations were then sent to a number of specialist organizations for their comments. They submitted their own suggestions, and the health authorities in collaboration with the Term Bank then made their decision.
Some of the specialist groups wanted mainly to use Latin terms, while others wanted more Norwegian terms, Innselset said.
– In the final version of ICD-10 we tried to comply with as many wishes as possible by covering the medical terms in Norwegian, Latin and Norwegianized Latin versions. The electronic edition includes a wide range of synonyms to cover most of the options we imagined the doctors might search under. In the printed edition, we were naturally enough not able to make such extensive use of synonyms, but we are now in the process of preparing an index which will simplify the use the coding system here too.
Both the electronic and the printed Norwegian version of ICD-10 will be ready for use from 1 January next year.
How do we remember? Why do we sleep? Questions that any child can ask, and that scientists put years of effort and millions of kroner into answering. A scientist at the University of Bergen'ss Dept. of Physiology has been looking at changes in the way that brain cells communicate. This could turn out to be an important piece of the jigsaw of answers to such important questions.
A peculiarity of human beings is our tendency to describe ourselves and our own intellect via tags such as our ability for language and abstract thought, and the brain - a highly complex, highly tuned machined. The sheer breadth of such generalities reveals their limitations, and raises the question of whether they really mean anything. Paradoxically, our lack of understanding becomes most evident when we realise how little we actually know about the brain. Is our insight into ourselves limited by the inability of the brain to understand its own structure?
While we can't say how well individuals understand themselves, revealing the functions of the brain is a legitimate field of research, and one in which real progress is being made, says Clive Bramham, Research Council of Norway Research Fellow at the Dept. of Physiology. Last November, he chaired a symposium on this topic at the Annual Meeting of the Society for Neuroscience, in San Diego, California.
Bramham does research on plasticity, i.e. variations in the way that signals are transmitted between the neurons (nerve cells) in the hippocampus. Such cells communicate via very complex networks, sending a stream of impulses through the system via synapses, the switches that link the axons of each cell with the dendrites of perhaps hundreds of its neighbours.
When the transmitter cell is electrically stimulated, an immediate increase can be seen in the activity of the receptord cell, a rise that may persist for weeks. This reaction is known as long-term potentiation or LTP, and scientists believe that this is the process that comes into operation when the brain stores memories.
The hippocampus is essential for short-term memory, since it receives complex processed information from the cortex. What we are trying to find out is how the hippocampus passes information on to long-term memory, and we believe that LTP has an important role to play here. LTP takes place at the level of the individual synapse, and although we used artificial stimulation in our experiments, we believe that these studies reflect a natural process. What we need to know is how LTP functions in the living brain, explains Bramham.
One interesting aspect of our results is that the potential for inducing LTP is switched on and off according to how wakeful we are. If we stimulate our subjects electrically while they are in deep sleep, there is no measurable change in the activity of the receptor cells. If we give them identical stimulation while they are dreaming, we see strong LTP. So what is happening, and why? What we need to do is map the activity of the brain during wakefulness and sleep, and to find out why it switches itself on and off, says Bramham, who has been collaborating on these studies with Associate Professor Bolek Srebro, also at the Dept. of Physiology.
One theory is that spontaneous LTP depends on interaction between the activity of the brain in its sleeping and waking states; the basic idea is that the brain picks up information while we are awake, and puts it into more permanent storage while we sleep.
This problem touches on one of the basic questions about the physiological function of sleep. Why do we spend one third of our lives sleeping? It is clear that it has some sort of effect. Something is taking place during sleep; but just what is it?
Bramham has been studying a new type of LTP, in which the information in the transmitter cells consists of two types of chemicals; glutamate and opioid peptides (also known as endorphins). Scientists have long been aware of the presence of peptides in the brain without knowing why they are there. Bramham has found that they are only released as a result of high-frequency stimuli, such as he uses to induce LTP in his experiments. This is the first evidence of a connection between opioid peptides and variations in neural transmission processes in the brain.
We already knew that opioid peptides are the body's natural pain-killers, and that drugs like morphine and heroin create dependence precisely because they mimic these peptides. In fact, treating drug dependence is the most obvious clinical application of our research, says Bramham.
His own results were discussed at the Society for Neuroscience symposium in the context of a wide range of other work. What emerged was a state-of-the-art report on the effects of opioid peptides on LTP that confirmed the importance of the phenomena being studied in Bergen. The positive reception his work was given made it clear that working far from other major centres of brain research need not be a drawback. In fact, being less influenced by scientific fashion, we may be able to do more independent thinking here, he says.
The experimentBramham's studies of the role of opioid peptides in long-term potentiation were carried out in two stages. The first experiments, on anaesthetized rats, started by selectively stimulating nerve pathways that run on such peptides. Bramham then injected naloxone, which blocks the effects of opioids, into the hippocampus, and found that this did not affect ordinary neural communication, which is mediated by the other transmitter, glutamate. However, naloxone did selectively block the development of long-term potentiation, suggesting that opioid peptides play an important role in improving the ability of neurons to communicate. The second phase of the experiments used slices of living hippocampal tissue, in which the specific types of opioid receptors involved had been identified. As well as finding selective blocking, as in the first experiments, the researchers showed that the effects of opioid receptors are mediated indirectly via GABA, a transmitter on small interneurons that usually inhibit neural communication. When the GABA receptors were blocked, LTP was no longer dependent on activating the opioid peptides. Bramham says that it is now essential to map out the natural pattern of neural activity that induces LTP in living animals, and to identify how LTP at single synapses alters the patterns of communication in large neural networks. This will give us a better basis for understanding memory. [Back] |
The hippocampusThe hippocampus (which rather resembles a sea-horse Ñ hence the name) store memory traces for several weeks, before moving them gradually over to other specific areas of the brain. The illustration shows how neural impulses are first transmitted to the visual cortex and then to the hippocampus, where they remain for some weeks before they are transmitted back to the long-term memory cortex. [Back] |
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