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Biomedical subjects

J S Han

Publications and source records attributed to J S Han.

At least 253 records · Page 14Linked to original sources

[A study on the grief and coping pattern of mothers who have a chronically ill child].

This study was done in order to identify symptoms of grief and patterns of coping in mothers of chronically ill children. Nurses, as health professionals, must understand helpful coping methods for mothers who have chronically ill children. Based on this knowledge, nurses can develop appropriate nursing intervention strategies, and so help the mothers to develop effective ways of coping and give support to mothers with chronically ill children in process of coping with this grief. The research questions guiding this research were: 1. what type of grief does the mother have at the time of child's diagnosis and at present? 2. what are the problems confronting the mother? 3. what are the coping patterns of the mother? 4. is there a difference according to child's diagnosis in the mother's grief and coping pattern? Ths subject for this study were obtained by taking a convenience sample of 120 mothers with a chronically ill child. Interviews took place in four medical school hospitals and one medical center in Seoul from March 19th to May 16th 1990. The tools used in this study were Mcfarlan's (1983), Grief contents, Folkman & Lazarus (1983), Ways of Coping and Hymovich's (1983) the Chronicity Impact and Coping Instrument. The findings were as follows; 1. Grief items had a maximum score of three points. The highest item scores at the time of diagnosis, were in order, heart broken, talkative, and could not do anything, at the present, 'talkative', 'heart broken' and 'busy myself with other things'. 2. The problems confronting the mothers were 'worry about ill child's future', 'her responsibilities in taking care of the ill child.' 3. Most of the mothers used similar ways of coping, that is 'problem focused coping', 'detachment', 'wishful thinking', 'seeking social support' and 'focusing on the positive and hardly any of them used 'tension reduction'. 4. There was a significant difference in coping methods according to the child's diagnosis, leukemia, cancer hemophillia and nephrotic syndrome. The most frequently used coping method was detachment, especially for the mother of the child with. 5. At the time of diagnosis there was a positive correlation between the level of grief and the coping method of detachment and seeking social support.

Adaptation, Psychological↗

Analgesia from electrical stimulation of the hypothalamic arcuate nucleus in pentobarbital-anesthetized rats.

Inhibition of noxious heat-induced tail flick by electrical stimulation of the arcuate nucleus of the hypothalamus (ARH) was examined and characterized in pentobarbital-anesthetized rats. Systematic mapping studies revealed that inhibition of the tail flick reflex could be induced by stimulating widespread areas in the ventromedial parts of the hypothalamus, which include the paraventricular nucleus, ventromedial nucleus, dorsomedial nucleus, anterior hypothalamic area as well as the ARH areas. The ARH stimulation-produced tail flick suppression could be completely blocked by systemic naloxone (2 mg/kg) which shows the involvement of an opiate mechanism in this effect. Although the tail flick reflex in the lightly anesthetized state is of significantly shorter latency than in the unanesthetized state, thresholds of the ARH stimulation for suppressing spinal nociceptive reflexes in the lightly anesthetized state were not significantly different from the thresholds at the same ARH sites in the awake state.

Analgesia↗

Cholecystokinin octapeptide antagonized opioid analgesia mediated by mu- and kappa- but not delta-receptors in the spinal cord of the rat.

Intrathecal (ith) injection of cholecystokinin octapeptide (CCK-8) to the rat with single dose of 4 or 40 ng, or successive doses from 0.1 to 1 microgram at 10 min intervals produced neither analgesia nor hyperalgesia. However, the analgesia produced by ith injection of PL017, a specific mu-receptor agonist or 66A-078, a specific kappa-receptor agonist could be markedly antagonized by CCK-8 at a dose as small as 4 ng. In contrast, analgesia produced by ith injection of delta-agonist DPDPE could not be blocked by CCK-8 even at a dose as high as 40 ng. Since the effect of CCK-8 could be totally reversed by the CCK receptor antagonist proglumide, this effect is most probably mediated by CCK receptors.

Animals↗

Diencephalon as a cardinal neural structure for mediating 2 Hz- but not 100 Hz-electroacupuncture-induced tail flick reflex suppression.

Transections at two levels of the forebrain were undertaken in the rat to investigate the neural structures indispensable for the mediation of tail flick reflex suppression (TFRS) induced by low (2 Hz) and high (100 Hz) frequency electroacupuncture (EA) stimulation. Removal of the telencephalic structures did not affect TFRS produced by high frequency EA, although a mild and temporal attenuation was observed for low frequency EA-induced TFRS. Ablation of the whole forebrain (the telencephalon and diencephalon) resulted in a total abolishment of 2-Hz EA effect as measured 5, 24 and 72 h after surgery. In the meantime there was a moderate attenuation (-32.8%, P less than 0.05) of 100-Hz EA effect, which appeared 5 h after the operation and recovered after 24 h. The results indicate that (1) high frequency EA effect persisted in animals devoid of the whole forebrain structures; (2) an intact diencephalon is indispensable for the neural circuitry controlling low frequency EA-induced TFRS.

Animals↗

A technique for temporal bone sections using non-decalcified frozen guinea pig cochleas: a study of succinic dehydrogenases.

We have developed a technique for sectioning temporal bones and have studied non-decalcified frozen guinea pig cochleas to localize succinic dehydrogenases. The technique is simple and practicable. The 6-microns sections used preserve both fine cochlear structure and satisfactory histochemical localization for identifying the succinic dehydrogenases. The technique can also be extended to immunological test, detecting transmitters and investigating enzymes in the cochlea.

Animals↗

Naloxone-reversible analgesia produced by microstimulation of the arcuate nucleus of the hypothalamus in pentobarbital-anesthetized rats.

Suppression of the tail flick response to noxious heat and paw withdrawal response to noxious pressure were produced by electrical stimulation of arcuate nucleus of the hypothalamus (ARH) in pentobarbital anesthetized rats. Systemic administration of naloxone (2 mg/kg) greatly antagonized the ARH stimulation-produced inhibition of both algesic reflexes. The thresholds of stimulation for inhibition of two spinal nociceptive reflexes in the lightly anesthetized state were not significantly different from the thresholds of stimulation at the same ARH sites in the awake state in the same animals. These findings provide evidence establishing the (1) usefulness of the anesthetized rat model for investigation of antinociceptive mechanisms; (2) the involvement of endogenous opioid mechanisms in mediating ARH stimulation-produced analgesia.

Analgesia↗

Phorbol ester suppression of opioid analgesia in rats.

Protein kinase C (PKC) has been shown to be an important substrate in intracellular signal transduction. Very little is known concerning its possible role in mediating opiate-induced analgesia. In the present study, 12-O-tetradecanoylphorbol 13-acetate (TPA), a selective activator of PKC, was injected intrathecally (ith) to assess its influence on the analgesia induced by intrathecal injection of the mu opioid agonist PL017, the delta agonist DPDPE and the kappa agonist 66A-078. Radiant heat-induced tail flick latency (TFL) was taken as an index of nociception. TPA in the dose of 25-50 ng, which did not affect the baseline TFL, produced a marked suppression of opioid antinociception, with a higher potency in blocking mu and delta than the kappa effect. In addition, mu and delta agonists induced remarkable decreases in spinal cyclic AMP (cAMP) content whereas the kappa effect was weak. The results suggest a cross-talk between the PKC system and the signal transduction pathway subserving opioid analgesia.

Analgesia↗

Lumbar intrathecal administration of naloxone antagonizes analgesia produced by electrical stimulation of the hypothalamic arcuate nucleus in pentobarbital-anesthetized rats.

In lightly pentobarbital-anesthetized and acutely-prepared rats, electrical stimulation within the arcuate nucleus of the hypothalamus consistently inhibited the tail-flick responses to noxious heating of the tail. The opioid receptor antagonist, naloxone hydrochloride applied intrathecally at the lumbar level, at dose of 20 micrograms, reversed this inhibition without affecting the baseline pain threshold. The same dose of naloxone, applied to the cervical subarachnoid space, had no effect on the inhibitory modulation by the arcuate nucleus. Naloxone, at doses 2- to 4-fold greater than the intrathecal dose, did not modify the suppression of the tail-flick, when given systemically. With the doses ranging from 5 to 40 micrograms, naloxone showed a dose-dependent blockade of the inhibition produced by stimulation of the arcuate nucleus. These results indicate that an endogenous opioid system is most likely involved in the descending inhibition of spinal nociceptive reflexes, resulting from stimulation of the arcuate nucleus of the hypothalamus.

Analgesia↗

Modification by cholecystokinin octapeptide of the binding of mu-, delta-, and kappa-opioid receptors.

Previous study has shown that cholecystokinin (CCK) octapeptide (CCK-8) suppressed the binding of opioid receptors to the universal opioid agonist [3H]etorphine. In the present study, highly selective tritium-labeled agonists for the mu-[(tryrosyl-3,5-3H][D-Ala2,MePhe4,Gly-ol5]enkephalin ([3H]DAGO], delta- ([tyrosyl-3,5-3H][D-Pen2,5]enkephalin ([3H]DPDPE], and kappa- ([3H]U69,593) opioid receptors were used to clarify which type(s) of opioid receptor in rat brain homogenates is suppressed by CCK-8. In the competition experiments, CCK-8 suppressed the binding of [3H]DAGO and [3H]U69,593 but not that of [3H]DPDPE to the respective opioid receptor. This effect was blocked by the CCK antagonist proglumide at 1 mumol/L. In the saturation experiments, CCK-8 at concentrations of 0.1 nmol/L to 1 mumol/L decreased the Bmax of [3H]DAGO binding sites without affecting the KD; on the other hand, CCK-8 increased the KD of [3H]U69,593 binding without changing the Bmax. The results suggest that CCK-8 inhibits the binding of mu- and kappa-opioid receptors via the activation of CCK receptors.

Animals↗

Hemorrhagic fever with renal syndrome: MR imaging of the kidney.

Magnetic resonance (MR) imaging of the kidneys was performed in 14 patients with a severe form of hemorrhagic fever with renal syndrome (HFRS), a major public health problem in Far Eastern Asia. To the authors' knowledge, this is the first report of renal assessment with MR imaging in HFRS. Three MR imaging studies were done while patients were in the oliguric phase, 19 were done during the diuretic phase, and three were done during the convalescent phase. The authors differentiated the cortex and the medulla in all 21 T1-weighted examinations and all 25 T2-weighted examinations. Seven T1-weighted examinations (33%) and 20 T2-weighted examinations (80%) showed low signal intensity along the outer portion of the medulla, which thus enabled differentiation from the inner medulla. Low signal intensity along the medulla (especially the outer medulla) on T2-weighted images, possibly representing medullary hemorrhage, is fairly constant and characteristic on MR images of the kidneys in patients with HFRS.

Adult↗

Toxic acute renal failure and hepatitis after ingestion of raw carp bile.

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.

Acute Kidney Injury↗

The role of periaqueductal gray in mediation of analgesia produced by different frequencies electroacupuncture stimulation in rats.

The marked suppression of noxious heat-evoked tail flick reflex was produced in conscious rats by low (2 Hz) or high (100 Hz) frequency electroacupuncture (EA) stimulation at acupoints S36 and Sp6. Electrolytic and kainate lesions in the ventral periaqueductal gray (vPAG) led to significant attenuation of the low and high frequency EA analgesia as measured 4 and 6 days following the lesion. In sham-operated animals, analgesia induced by either low or high frequency EA remained intact. The role of vPAG in organization of different EA analgesia is discussed in detail.

Analgesia↗

Habenula as a relay in the descending pathway from nucleus accumbens to periaqueductal grey subserving antinociception.

This study explored the possibility of a relay at habenula for the descending neural pathway of antinociception. The latency of the escape response elicited by radiant heat on the snout of the rabbit was taken as index of nociception. (1) Microinjection of 20 micrograms of morphine into nucleus accumbens resulted in a one-fold increase in nociceptive threshold 20-40 min after the injection. This effect of morphine was markedly attenuated by naloxone or met-enkephalin antiserum administered to the nucleus habenula, suggesting that the release of met-enkephalin in habenula is essential for the antinociception induced by morphine injected into nucleus accumbens. (2) Injection of 10 micrograms of morphine into habenula produced a significant increase in escape response latency 20-40 min after the injection. This antinociceptive effect of morphine was attenuated by naloxone or muscimol, and enhanced by bicuculline methochloride administered to periaqueductal grey, suggesting that morphine may act on habenula to activate a descending neural pathway extending to periaqueductal grey to induce an antinociceptive effect, which seems to utilize endogenous opioid peptides and gamma-aminobutyric acid as its mediators. Taking together, the results suggest that habenula is an important relay in the descending neural pathway from nucleus accumbens to periaqueductal grey subserving antinociception.

Animals↗

[Stressful life events, health symptoms, social support and coping in early adolescents].

Numerous research reports have substantiated the role of stressful life events in relation to the onset of health changes. The relationship tends to hold across different age groups. Theoretically, adolescence has been considered a developmental crisis period of great stress, impoverished coping skills and high vulnerability to biological, social and psychological demands. The research problem addressed by this study was to examine the relationships between stressful life events and health symptom patterns, and the effect of two variables, coping and social support, theoretically considered to mediate the relationship between stress and health symptoms in adolescents. The following five hypotheses were tested in this research: 1. Health symptoms are positively related to stressful life events in adolescents, 2. Health symptoms are negatively related to coping in adolescents, 3. Health symptoms are negatively related to social support in adolescents, 4. When coping is controlled, the relationship between health symptoms and stressful life events will decrease, and 5. When social support is controlled, the relationship between health symptoms and stressful life events will increase. The study subjects consisted of 1090 high school students of the metropolitan city of Seoul. The following sampling procedure was used: 1. Of the 169 high schools in nine school administrative districts in the city, a proportional sample of ten schools was selected. 2. One class from each of the freshman and sophomore was randomly selected and all the students who were in the sampled class were used as the study sample. The study was limited to freshman and sophomore adolescents, aged 15 to 18 (mean = 16.6). Of the 1090 subjects 688 (63%) were boys and 402 (37%) were girls. An Adolescent Inventory of Stressful Life Events, a Health Symptom Questionnaire and an Adolescent Coping Inventory were adapted for this study. The Norbeck Social Support Questionnaire was utilized to collect the data on perceived social support. Five high school teachers in the areas of school health and counselling reviewed the items of each questionnaire for content validity. A pilot study was undertaken to ascertain reliability. Fifty three high school students responded to the questionnaires and gave their opinions on the items. For stressful life events, health symptoms, coping, and social support, the Cronbach's alpha's on the study were .70, .94, .77, and .76, respectively. Research assistants attended all the sampled classes with the school proctor to explain the purpose and procedures of the study to the students. The questionnaires along with a ballpoint pen were distributed to the students who were asked to complete each item.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Psychological↗

[Cholecystokinin octapeptide (CCK-8) antagonized analgesia mediated by mu and kappa opioid receptors].

CCK-8 has been shown to antagonize the analgesia produced by morphine or endogenous opioid peptides. The present study was performed to clarify the interaction between CCK-8 and different opioid ligands. Analgesia produced by intrathecal (I.T.) injection of the specific mu receptor agonist PL017 10 ng or kappa receptor agonist NDAP 500 ng can be antagonized by I.T. injection CCK-8 at a dose as small as 4 ng. In contrast, analgesia produced by I.T. injection of the delta receptor agonist DPDPE (6.5, 13 and 26 micrograms) was not blocked by CCK-8 (4 ng or 40 ng, I.T.). The antagonistic effect of CCK-8 on PL017 and NDAP could be completely reversed by proglumide (3 micrograms, I.T.). I.T. injection of CCK-8 (4 or 40 ng single dose or cumulative dose of 0.1, 0.2, 0.5 and 1.0 microgram at 10 min intervals) produced neither analgesia nor hyperalgesia. In conclusion, CCK-8 preferentially antagonizes opioid analgesia mediated by mu and kappa receptors, and this antagonistic effect is mediated by CCK receptors.

Analgesics↗

[Effects of dynorphin A and CCK-8 on synaptosomal 45Ca uptake of the rat spinal cord].

Cholecystokinin octapeptide (CCK-8) and angiotensin I (AI) have been shown in behavioral studies being endogenous antiopioid substrates (AOS). To assess their antiopioid mechanism at postreceptor level, we observed the effects of the three opioids and the two AOS on 45Ca uptake of the rat spinal synaptosomal preparations. Morphine, Dyn A and DPDPE at concentrations of 10 nmol/L to 1 mumol/L, produced a mild suppression of 45Ca uptake of synaptosomal preparations from ventral spinal cord. CCK-8 showed a mild suppression only at a concentration of 1 mumol/L. In synaptosomes prepared from dorsal spinal cord, Dyn A but not morphine or DPDPE, produced a strong inhibition of 45Ca uptake which was blocked by nor-BNI, a kappa receptor antagonist, at 1 mumol/L. While CCK-8 (10 nmol/L to 1 mumol/L) also suppressed 45Ca uptake, it could antagonize the suppressive effect induced by Dyn A. In contrast to CCK-8, AI (10 nmol/L to 1 mumol/L) influenced neither on synaptosomal 45Ca uptake, nor on Dyn A suppression of 45Ca uptake. The results presented above fit very well with our behavioral studies, i.e., CCK-8 antagonized opioid analgesia in both the brain and the spinal cord, whereas AI antagonized opioid analgesia in the brain but not in the spinal cord. It is therefore concluded that antagonism of the opioid suppression of synaptosomal 45Ca uptake might be one of the mechanisms for the antiopioid activity of CCK-8 and AI.

Animals↗

[The neural pathway from nucleus accumbens to amygdala in morphine analgesia of the rabbit].

The purpose of this study was to explore possible neural connections between the nucleus accumbens and amygdala involved in analgesia. The latency of the escape response elicited by radiant heat applied on snout of the rabbit was taken as an index for nociception. It was found that: (1) the analgesic effect elicited by intra-accumbens injection of morphine was attenuated dose-dependently by intra-amygdala administration of opioid antagonist naloxone, or antisera against met-enkephalin (ME) or beta-endorphin (beta-EP), suggesting the involvement of ME and beta-EP in the accumbens-amygdala connection; (2) the analgesia produced by intra-amygdaloid injection of morphine was not affected by naloxone administered to nucleus accumbens, suggesting a one-way connection between the two nuclei; (3) the analgesia of intra-accumbens injection of morphine was significantly attenuated by muscimol, the GABA receptor agonist, and enhanced by bicuculline methochloride, the GABA receptor antagonist injected into the same site where morphine was administered. The results suggest that the analgesic effect of morphine administered to the nucleus accumbens is mediated by the suppression of the GABAergic inhibitory neurons located within the nucleus.

Amygdala↗

Simultaneous electric activities of pain-excitation and pain-inhibition neurons in nucleus parafascicularis of thalamus in rats during acute morphine tolerance.

When acute morphine-tolerated rat was administered by ip morphine (10 mg/kg) which was effective before the acute tolerance to morphine, both the inhibitory effect of morphine on the electric discharges of pain-excitation neurons (PEN) in nucleus parafascicularis (PF) and the excitatory effect of morphine on the electric activities of pain-inhibition neurons (PIN) were simultaneously weakened, or even vanished. If a large dose of morphine (20 mg) was given ip, the modulating action of morphine on simultaneous electric discharges of PEN and PIN reappeared. It is obvious that the phenomenon of acute morphine tolerance and the antagonism to morphine tolerance can be explicitly expressed on the level of central neurons.

Animals↗