Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 25% of U.S. women over age 50 will suffer one or more vertebral compression fractures related to osteoporosis. Vertebral fractures may be biconcave, anterior wedge, or crush deformities. A fracture is most often precipitated by putting a load on outstretched arms (eg, while raising a window). Back pain is usually incapacitating for a few weeks, then diminishes in severity but remains intense for 2 to 3 months. Acute complications include transient ileus, urinary retention, or (rarely) cord compression. Long-term effects include kyphosis, deconditioning, insomnia, and depression. Initial treatment includes bed rest, pain management with local and systemic analgesia, bracing to improve comfort, and patient reassurance. Long-term management includes spinal stretching exercises, walking, and treatment of underlying osteoporosis with calcitonin or estrogen in selected patients.
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PMID:Vertebral compression fractures: how to manage pain, avoid disability. 802 Jul 59

Interleukin-1beta (II-1beta) is a cytokine known to have somnogenic properties. We have previously shown that II-1beta decreases food intake when injected into the lateral part of the paraventricular nucleus of the hypothalamus (PVH), and, because food intake and sleep are closely related behaviors, we tested the hypothesis that II-1beta could alter sleep when injected into the lateral PVH area. We compared the effects of II-1beta with those of two other peptides involved in feeding behavior and known to act in the PVH area, the corticotropin-releasing factor (CRF) and salmon calcitonin (sCT). The EEG of rats was recorded for 48 h after the injection. The results showed that CRF had no effects, II-1beta reduced significantly sleep duration during the first 5 h following the injection, and sCT profoundly affected sleep cycles, producing an almost 30-h long insomnia, with a major reduction of slow wave sleep and a long period of alternation of REM sleep and wakening. It is concluded that (i) the area between the lateral part of the PVH and the fornix is a brain site involved in sleep regulation, (ii) II-1beta, a peptide generally considered as somnogenic, decreases sleep when administered in this area, and (iii) sCT is an extremely potent suppressor of slow wave sleep.
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PMID:Interleukin-1beta and calcitonin, but not corticotropin-releasing factor, alter sleep cycles when injected into the rat hypothalamic lateral paraventricular area. 1032 98

The extinction of a conditioned fear response is of great interest in the search for a means of ameliorating adverse neurobiological changes resulting from stress. The discovery that endocannibinoid (EC) levels are inversely related to the extent of such stress, and that the amygdala is a primary site mediating stress, suggests that ECs in this brain region might play a major role in extinction. Supporting this are the observations that the basolateral complex of the amygdala shows an increase in ECs only during extinction and that early clinical trials indicate that cannabinoid-like agents, when taken orally by patients suffering from post traumatic stress disorder (PTSD), reduce insomnia and nightmares. In order to optimize the potential of these agents to ameliorate symptoms of PTSD four important questions need to be answered: first, what is the identity of the cells that release ECs in the amygdala during extinction; second, what are their sites of action; third, what roles do the ECs play in the alleviation of long- depression (LTD), a process central to extinction; and finally, to what extent does brain derived neurotrophic factor (BDNF) facilitate the release of ECs? A review of the relevant literature is presented in an attempt to answer these questions. It is suggested that the principal cell involved in EC synthesis and release during extinction is the so-called excitatory extinction neuron in the basal nucleus of the amygdala. Furthermore that the main site of action of the ECs is the adjacent calcitonin gene-related peptide inhibitory interneurons, whose normal role of blocking the excitatory neurons is greatly diminished. The molecular pathways leading (during extinction trials) to the synthesis and release of ECs from synaptic spines of extinction neurons, that is potentiated by BDNF, are also delineated in this review. Finally, consideration is given to how the autocrine action of BDNF, linked to the release of ECs, can lead to the sustained release of these, so maintaining extinction over long times.
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PMID:Regulation of fear extinction by long-term depression: The roles of endocannabinoids and brain derived neurotrophic factor. 2786 1