• YAKHAK HOEJI
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• v.30 no.4
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• pp.198-201
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• 1986

The successful elucidation of the opiate receptor and its natural ligands has generated speculation that other drugs might interact with cellular sites designed to accommodate endogenous mediators. The properties of binding sites for the cardiac glycosides(CG), together wit the potency and specificity of the digitalis drugs suggest that CG mimic an endogenous digitalis-like factor. Recenthy, several laboratories have reported the potency in mammalian tissues and fluids of unidentified materials that share certain specific propeties of the CG. Identification of body's own digitalis might yield a natural co pound whose synthetic analogs may provide safer and more effective drugs than can be achieved by structural edification of the CG of plant origin.

• YAKHAK HOEJI
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• v.30 no.4
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• pp.169-173
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• 1986

It was carried out to detect the analgesic action of piperine by hot-plate method and to elucidate its mechanism in rats. Piperine (30mg/kg i.p.) produced profound analgesia, which was blocked by naloxone (10mg/kg). Chronic intraperitoneal administration of piperine significantly increased the contents of $\beta$-endorphin in rat midbrain. In the chronic piperine-treated groups, significant decreases of maximum opiate binding were observed. However, Kd value in these groups were not changed.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.33-44
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• 1982

The binding in vitro of an opiate agonist, $(^3H)-morphine$, was studied using rat brain slices which were incubated in the modified Krebs-Henseleit bicarbonate buffer solution containing various concentrations of electrolytes with or without morphine, naloxone or morphine+naloxone at $4^{\circ}C$ for 24 hours. The binding of $(^3H)-morphine$ may be seperated into two component; one a saturable binding and the other nonsaturable. The saturable binding may be calculated from the differences in binding observed in the absence and presence of high concentration of morphine. The maximal saturable binding and $K_D$ value in the naive preparations were $0.32{\pm}0.02\;pmole/mg$ protein and $0.75{\pm}0.07\;nM$ respectively. The saturable binding of $(^3H)-morphine$ was significantly increased by low temperature-treatment, while $K_D$ value was not changed. Morphine in the incubation media significantly increased the saturable binding of $(^3H)-morphine$ and $K_D$ value. Naloxone also increased the maximal saturable binding of $(^3H)-morphine$ and $K_D$ value of the drug. Decrease of $K^+\;and\;Mg^{++}$, and addition of $Mn^{++}$ in the incubation media significantly increased the saturable binding of $(^3H)-morphine$, but decrease of $Na^+$and increase of $Ca^{++}$ in the incubation media did not influence the binding. The increment of the saturable binding of $(^3H)-morphine$ by nonlabeled morphine in the incubation media was notaffected by decrease of $Na^+,\;K^+\;or\;Mg^{++}$, or addition of $Mn^{++}$ into the incubation media, but was inhibited by increase of $Ca^{++}$ in the incubation media, while the increment of the saturable binding of $(^3H)-morphine$ was net observed by decrease of $Na^+,\;K^+\;or\;Mg^{++}$, or increase of $Ca^{++}$ in the incubation media. The above results indicate that change of opiate binding sites in quality, i.e. affinity, and quantity, i.e. number of binding sites, may occur by low temperature-treatment in the absence and presence of morphine or naloxone and that electrolytes play role of the changes of opiate binding sites.

• Biomolecules & Therapeutics
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• v.9 no.1
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• pp.20-25
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• 2001

In this study we fed control diet and tryptophan supplemented diets containing 0.35% tryptophan to ICR mice for 2 weeks. The concentrations of serotonin and 5-HIAA were changed by injection of the serotonin synthesis inhibitor, p-CPA and the serotonin precursor, serotoninP and the change of brain serotonin concentration negatively correlated with that of pain sensitivity, and p-CPA and serotoninP also changed the analgesic effect of morphine. The injection of naloxone, the opiate antagonist, resulted in an increase in the writhing frequency, but its antagonistic effect was not significant. The concentration of 5-HIAA elevated in mice brain at least 3hr after administration of morphine hydroxide indicates that the changes in brain serotonin metabolism may be associated with the acute effects of morphine analgesia. In short, these results not only suggest that tryptophan supplemented diet suppress pain sensitivity in mice, but also indicate that at least in part analgesic mechanism of serotonin may be associated with morphine analgesia.

• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.115-122
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• 1983

The influences of diazepam and naloxone on the increase of plasma corticosterone level induced by morphine, pentazocine, ACTH, or picrotoxin were investigated in male mice. The results obtained were summarized as follows: 1) The increase induced by morphine or pentazocine of plasma corticosterone level was not affected by naloxone pretreatment but markedly suppressed by diazepam pretreatment. 2) The increase induced by ACTH of plasma corticosterone level was not affected by diazepam or naloxone pretreatment. 3) The picrotoxin markedly increased plasma corticosterone level, and the inceease was not affected by diazepam or naloxone pretreatment. This above results suggest that the increase induced by opioids of plasma corticosterone level seems to be rather related with other than opiate- or GABArerecptor.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.339.3-340
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• 2002

Capsaicin is hot taste ingredient of chili pepper and was isolated in 1876 and in 1919 its structure is sympathized compound. induces pain and when persistently dosed. the fact will bring insensible condition to other chemical and mechanical thermal stimulation by incapacitating sensory neuron is known. The analgesic effect by desensitization of such capsaicin is differ from the mechanism by analgesic action by opiate receptor of the existing analgesia or by prostaglandin mediation and the efficacy was known as similar with morphine. (omitted)

• The Korean Journal of Zoology
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• v.30 no.4
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• pp.341-350
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• 1987

LHRH분비와 환denylate cyclase활성에 미치는 PGE2, Opioid, 그리고 Ca2+의 영향을 흰쥐의 시상하부 조직을 사용하여 조사하였다. K+(30mM)에 의한 LHR광분비촉진은 Ca2+의존적인데 반하여, PGE2에 의해 촉진되는 LHR노 분비는 세포의 Ca2+농도에 의존하지 않았다. PGE2에 의한 LHR기 분비와 CAMP합성은 PGE2농도(1$\times$10-7M-1$\times$10-4M)에 비례하여 촉진되었으며, $\beta$-endorphin (1x10-3M)은 PGEa에 의한 LHRH 분비촉진과 CAMP합성을 공히 억제하였다. 오피오이드 수용체의 길항제인 Naloxone(Ix10-"M)은 $\beta$-endorphin에 의한 저해효과를 극복시켜서, LHR광 분비와 CAMP합성은 각각 회복되었으나, CAMP합성은 부분적인 회복을 보인 반면에, LHRH분비는 PGE2에 의한 촉진효과보다도 더 활성화되었다. 결론적으로 LHRH분비에 미치는 오퍼오이드의 억제작용은 PGE2-cAMP의 세포내 전달과정을 저해함으로써 유발되는것으로 추정 된다.정 된다.

• Journal of Hospice and Palliative Care
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• v.27 no.2
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• pp.77-81
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• 2024

This case report explores the challenges and complexities associated with opioid management of cancer pain, emphasizing the importance of early involvement of a hospice consultation team and the adoption of a multidisciplinary approach to care. A 56-year-old man with advanced pancreatic cancer experienced escalating pain and inappropriate opioid prescriptions, highlighting the shortcomings of traditional pain management approaches. Despite procedural intervention by the attending physician and increased opioid dosages, the patient's condition deteriorated. Subsequently, the involvement of a hospice consultation team, in conjunction with collaborative psychiatric care, led to an overall improvement. The case underscores the necessity of early hospice engagement, psychosocial assessments, and collaborative approaches in the optimization of patient-centered palliative care.

• Korean Journal of Biological Psychiatry
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• v.5 no.1
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• pp.34-45
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• 1998

We provide the reader with a brief introduction to the neurobiology of neuropeptides. Several comprehensive reviews of the distribution and neurochemical, neurophysiological, neuropharmacological and behavioral effects of the major neuropeptides have recently appeared. In reviews of the large number of neuropeptides in brain and their occurance in brain regions thought to be involved in the pathogenesis of major psychiatric disorders, investigators have sought to determine whether alternations in neuropeptide systems are associated with schizophrenia, mood disorders, anxiety disorders, alcoholism and neurodegenerative disease. There is no longer any doubt that neuropeptide-containing neurons are altered in several neuropsychiatric disorders. One of the factors that has hindered neuropeptide research to a considerable extent is the lack of pharmacological agents that specifically alter the synaptic availability of neuropeptides. With the exception of naloxone and naltrexone, the opiate-receptor antagonists, there are few available neuropeptide- receptor antagonists. Two independent classes of neuropeptide-receptor antagonists has been expected to be clinically useful. Naltrexone, a potent ${\mu}$-receptor antagonist, has been used successfully to reduce the need for alcohol consumption. And cholecycstokinin antagonists are now in development as a new class of anxiolytics, which would be expected to be free from tolerance and physical dependence and lack of sedation. In this review, we deal with these two kinds of neuropeptide system, the opioid system and cholesystokinins in the brain. The role of opioid systems in the reinforcement after alcohol consumtion and that of cholesystokinins in the pathogenesis of anxiety will be discussed briefly. As we know, the future for neuropeptides in psychiatry remains bright indeed.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.13 no.1
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• pp.3-14
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• 2002

Childhood psychic trauma appears to be a crucial factor in the development of serious disorders both in childhood and in adulthood. Traumatized children show strong tendency to revisualize or re-feel a traumatic events. Play and behavioral reenactments are frequent manifestations of both the single blow and the long-standing traumas in childhood. Those children who suffer the results of single, intense terror appear to exhibit detailed memory, retrospective reworkings and misperceptions. In long-standing or repetitive trauma, children would show psychic numbing, self-hypnosis, dissociation and rage. Child's brain is undergoing critical and sensitive periods of differentiation. During this time, developing central nervous system is exquisitely sensitive to stress. Stressor-activated neurotransmitters and hormones can play major roles in neurogenesis, migration, synaptogenesis, and neurochemical differentiation. Internal opiate system operates in some trauma and causes the victim to fail to respond, to avoid, to shut off feelings. Evidence is also accumulating in traumatology that dysfuntion of locus coeruleus and ventral tegmental neucleus system leads to catecholamine receptors hypersensitivity. This change result in hypervigilance, increased startle, affective lability, and increased autonomic nervous system hyperreactivity. Another site of action of trauma on the brain is hypothalamic-pituitary-adrenal axis. Individuals with PTSD do not have enough cortisol to halt the alarm reaction. When children are exposed to long-standing extreme events, massive attempts to protect the psyche and to preserve the self are put into gear. These developmental traumas mobilize various kinds of defense mechanisms. Massive denial, dissociation, self anesthesia, identification with aggressor and aggression turned against the self often lead to profound character changes in the youngsters.