• Korean Journal of Veterinary Service
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• v.36 no.4
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• pp.321-325
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• 2013

A mass of the adrenal gland was observed during a routine necropsy of a female 23-year-old Asian Water Buffalo (Bubalus bubalis) at Seoul Zoo in Gyeonggi Province, Korea. The animal showed no clinical signs but the necropsy examination revealed hydropericardium, ascites, hydrothorax and edema of the intestinal wall, lung and adrenal gland. Histopathologically, the neoplastic cells of the right adrenal gland were arranged in lobules supported by a fine fibrovascular stroma. The neoplastic cells had round hyperchromatic nuclei and granular eosinophilic to basophilic cytoplasm. Immunohistochemically, tumor cells were positive for chromogranin A and S-100 and negative for vimentin, synaptophysin and cytokeratin. Based on the above findings, this case was diagnosed as a pheochromocytoma. To the best of our knowledge, this is the first report of a pheochromocytoma in an Asian Water Buffalo (Bubalus bubalis).

• The Korean Journal of Nuclear Medicine
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• v.28 no.1
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• pp.148-152
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• 1994

The benign adrenal cortical adenoma usually secretes cortisol and its size is less than 3 cm in diameter. Though adrenal cortical carcinoma also secretes cortisol and other steroid hormones, its size is usually over 6 cm. We present a huge glucocorticoid producing adrenal cortical adenoma ($15{\times}11{\times}12 cm$), which was diagnosed by NP-59 scan and confirmed by surgery, with a review of the literature.

• Advances in pediatric surgery
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• v.6 no.2
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• pp.160-165
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• 2000

Beckwith-Wiedemann syndrome presents with multisystemic patterns of congenital anomalies and macrosomia. This syndrome was independently described by Beckwith in 1963 and by Wiedemann in 1964. There is wide spectrum of clinical manifestations, including prenatal or postnatal overgrowth, neonatal hypoglycemia, macroglossia, visceromegaly, omphalocele, hemihypertrophy and a predisposition for embryonal tumors, most frequently Wilms' tumor. We managed a case of Beckwith-Wiedemann syndrome with left adrenal cortical neoplasm of undetermined malignancy.

• Journal of Pharmacopuncture
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• v.10 no.2 s.23
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• pp.41-46
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• 2007

Effects of mahwang(Ephedrae herba) aqua-acupuncture at sinsoo (B-23)and Jisil(B-52)on adrenal cortical insufficiency were investigated in dexamethasone treated rats. Concentration of serum cortisol was decreased in dexamethasone treated rats. However, these values showed a tendency to increase in mahwang(Ephedrae herba) aqua-acupuncture groups. Concentration of serum total protein was increased in dexamethasone treated rats. However, these values were decreased by the mahwang(Ephedrae herba) aqua-acupuncture. The portion of neutrophils was decreased and the portion of lymphocytes and eosinophils were increased in dexamethasone treated rats. However, in mahwang(Ephedrae herba) aqua-acupuncture groups, the portion of neutrophils showed a tendency to increase and the portion of lymphocytes and eosinophils showed a tendency to decrease. In dexamethasone treated rats, the weight of adrenal glands were decreased, however these values were increased in mahwang(Ephedrae herba) aqua-acupuncture groups.

• The Journal of Internal Korean Medicine
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• v.29 no.2
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• pp.529-534
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• 2008

Renal cell carcinoma(RCC) is one of the major malignant renal cell tumors. Although RCC can metastasize to almost every organ, the most common metastatic sites are the lung parenchyma, the bones, the liver, and the brain. Adrenal metastasis from RCC is extremely rare. Adrenal metastasis from RCC shows poor prognosis, with little benefit from chemotherapy, radiation therapy, hormone therapy or immunotherapy. In this report, we describe a case of an RCC patient who showed lung and adrenal metastasis. The patient underwent left nephrectomy and chemotherapy(sunitinib), which were not effective. He refused further conventional medical treatment, and instead started treatment with Traditional Korean Medicine using allergen-removed Rhus verniciflua Stokes. After about 3 months of this treatment, the size of the adrenal tumor had decreased significantly with good performance status. Further study will be needed to demonstrate the tumor regression effect of allergen-removed Rhus verniciflua Stokes on patients with metastatic renal cell carcinoma.

• Korean Journal of Head & Neck Oncology
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• v.23 no.1
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• pp.50-53
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• 2007

Adrenal metastasis from papillary thyroid carcinoma is extremely rare. We present herein a patient with adrenal metastases from recurrent papillary carcinoma of the thyroid. A 54 year-old woman had received a total thyroidectomy and postoperative radioactive iodine therapy for locally advanced papillary thyroid carcinoma. One year after initial surgery, distant metastases to multiple organs including right cervical lymph nodes, left upper lung, left 2nd and 3rd ribs, 2nd thoracic vertebra and left adrenal gland were found by 18-FDG-PET-CT whole body scan. She underwent right modified neck dissection, partial resection of left 2nd and 3rd ribs, posterior arch of 2nd thoracic vertebra, left upper lobectomy of lung, and left adrenalectomy. On histologic examination, metastases to the left adrenal gland and cervical lymph nodes were papillary thyroid carcinomas, while other metastatic sites turned out to be anaplastic thyroid carcinomas. Despite aggressive surgery and postoperative adjuvant therapy, her general clinical conditions were getting worse day by day due to regrowing of the anaplastic thyroid carcinomas. To our knowledge, this is the first case reported in Korea.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.223-230
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• 2005

The purpose of the present study was to examine the effect of naltrexone, an opioid antagonist, on secretion of catecholamines (CA) evoked by cholinergic nicotinic stimulation and membrane-depolarization from the isolated perfused rat adrenal gland and to establish the mechanism of its action. Naltrexone $(3{\times}10^{-6}M)$ perfused into an adrenal vein for 60 min produced time-dependent inhibition in CA secretory responses evoked by ACh $(5.32{\times}10^{-3}M)$ , high $K^+$ $(5.6{\times}10^{-2}M)$ , DMPP ($10^{-4}$ M) and McN-A-343 $(10^{-4}M)$ . Naltrexone itself did also fail to affect basal CA output. In adrenal glands loaded with naltrexone $(3{\times}10^{-6}M)$ , the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}-ATPase$, were also inhibited. However, in the presence of met-enkephalin $(5{\times}10^{-6}M)$ , a well-known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Collectively, these experimental results demonstrate that naltrexone inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that this inhibitory effect of naltrexone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• Archives of Pharmacal Research
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• v.28 no.6
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• pp.699-708
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• 2005

The present study was designed to investigate the effect of naloxone, a well known opioid antagonist, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal glands, and to establish its mechanism of action. Naloxone ($10^{-6}\~10^{-5}$ M), perfused into an adrenal vein for 60 min, produced dose- and time-dependent inhibition of CA secretory responses evoked by ACh ($5.32\times10^{-3}$ M), high K+ ($5.6\times10^{-2}$ M), DMPP ($10^{-4}$ M) and McN-A-343 ($10^{-4}$ M). Naloxone itself also failed to affect the basal CA output. In adrenal glands loaded with naloxone ($3\times10^{-6}$ M), the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$-ATPase, were also inhibited. In the presence of met-enkephalin ($5\times10^{-6}$ M), a well known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Taken together, these results suggest that naloxone greatly inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that these inhibitory effects of naloxone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• Biomolecules & Therapeutics
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• v.9 no.3
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• pp.201-208
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• 2001

The present study was conducted to examine the effects of cholinergic stimulation and membrane depolarization on secretion of epinephrine (EP) and norepinephrine (NE) in the perfused model of the rat adrenal gland and to investigate the effect of bromocriptine on secretion of EP and NE evoked by these secreta-gogues. Acetylcholine (ACh, 5.32 mM), high $K^{+}$(56mM), 1.1-dimethyl-4-phenyl piperazinium iodide (DMPP, 100 $\mu$M for 2 min), (3-(m-cholro-phenyl-carbamoyl-oxy)-2butynyl trimethyl ammonium chloride (McN-A-343, 100 $\mu$M for 2 min), cyclopiazonic acid (10 $\mu$M for 4 min) and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl) -pyridine-5-carboxylate (Bay-K-8644, 10 $\mu$M for 4 min) evoked a 1.3~5.3-fold greater secretion of EP than NE in the perfused rat adrenal gland. The perfusion of bromocriptine (1-10 $\mu$M) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in secretion of EP and NE evoked by ACh, high $K^{+}$, DMPP, and McN-A-343. Moreover, under the presence of bromocriptine (1~10 $\mu$M), releasing responses of EP and NE evoked by cyclopiazonic acid and Bay-K-8644 were also greatly reduced. Taken together, these results suggest that cholinergic stimulation and membrane depolarization enhance more release of EP than NE in the perfumed rat adrenal medulla, and that bromocriptine inhibits the release of EP and NE evoked by stimulation of cholinergic receptors as well as by membrane depolarization. It seems that this inhibitory effect of bromocriptine is associated with inhibition of calcium channels through activation of dopaminergic D2-receptors located in the rat adrenomedullary chromaffin cells.lls.

• Biomolecules & Therapeutics
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• v.8 no.1
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• pp.13-21
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• 2000

The present study was designed to investigate the effect f quinidine on catecholamine (CA) secretion evoked by ACh, high $K^{+}$, DMPP, McN-A343, cyclopiazonic acid and Bay-K-8644 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. The perfusion of quinidine (15-150 $\mu$M) into an adrenal vein for 60 min produced relatively dose- and time-dependent inhibition in CA secretion evoked by ACh (5.32$\times$10$^{-3}$ M), high $K^{+}$ (5.6$\times$10$^{-2}$ M), DMPP (10$^{-4}$ M for 2 min), McN-A-343 (10$^{-4}$ M for 2 min), cyclopiazonic acid (10$^{-5}$ M for 4 min) and Bay-K-8644 (10$^{-5}$ M for 4 min). Furthermore, in adrenal glands pre-loaded with quinine (5$\times$10$^{-5}$ M), CA secretory responses evoked by veratridine (10$^{-4}$ M) was time-dependently inhibited. Also, in the presence of lidocaine (10$^{-4}$ M), which is also known to be a sodium channel blocker, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclo-piazonic acid were also greatly reduced in similar fashion to that of quinidine-treatment. Taken together, these results suggest that quinidine causes greatly the inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization, indicating strongly that this effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells. Furthermore, these findings indicate strongly that this inhibitory action of quinidine appears to be associated to the blocking action of sodium channels at least in CA secretion from the rat adrenal gland.and.