• Childhood Kidney Diseases
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• v.27 no.2
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• pp.133-138
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• 2023

Nutcracker syndrome (NCS) is a disease caused by compression of the left renal vein between the superior mesenteric artery and the abdominal aorta. Immunoglobulin A (IgA) nephropathy (IgAN) is characterized by the predominance of IgA deposits in the glomerular mesangial area. Hematuria and proteinuria can be present in both diseases, and some patients can be concurrently diagnosed with NCS and IgAN; however, a causal relationship between the two diseases has not yet been clarified. Here, we report two pediatric cases of NCS combined with IgAN. The first patient presenting with microscopic hematuria and proteinuria was diagnosed with NCS at the initial visit, and the second patient was later diagnosed with NCS when proteinuria worsened. Both patients were diagnosed with IgAN based on kidney biopsy findings and treated with angiotensin-converting enzyme inhibitors and immunosuppressants. A high index of suspicion and timely imaging or biopsy are essential for the proper management of NCS combined with glomerulopathy.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.5
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• pp.385-391
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• 2000

Using the patch-clamp technique, we investigated the alteration of 4-aminopyridine(4-AP)-sensitive, voltage-dependent $K^+$ channel (Kv) in the mesenteric arterial smooth muscle cell (MASMC) of renovascular hypertensive model, one-kidney one-clip Goldblatt hypertensive rat (GBH). To isolate $K_V$ current, internal pipette solution contained 5 mM ATP and 10 mM EGTA. Under these condition, MASMC was depolarized by 4-AP, but charybdotoxin did not affect membrane potential. Membrane potential of hypertensive cell $(-40.3{\pm}3.2\;mV)$ was reduced when compared to that of normotensive cell $(-59.5{\pm}2.8\;mV).$ Outward $K^+$ current of hypertensive cell was significantly reduced when compared to normotensive cell. At 60 mV, the outward currents were $19.10{\pm}1.91$ and $14.06{\pm}1.05$ pA/pF in normotensive cell and hypertensive cell respectively. 4-AP-sensitive $K^+$ current was also smaller in hypertensive cell $(4.28{\pm}0.38\;pA/pF)$ than in normotensive cell $(7.65{\pm}0.52\;pA/pF).$ The values of half activation voltage $(V_{1/2})$ and slope factor (k1) as well as the values of half inactivation voltage $(V_{1/2})$ and slope factor (k1) were virtually similar between GBH and NTR. These results suggest that the decrease of 4-AP-sensitive $K^+$ current contributes to a depolarization of membrane potential, which leads to development of vascular tone in GBH.

• Toxicological Research
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• v.12 no.2
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• pp.195-201
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• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.111-116
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• 1994

The role of $Ca^{2+}$/calmodulin-dependent protein kinase II in the increase of myofilament $Ca^{2+}$ sensitivity by agonist and GTP was investigated in rabbit mesenteric ${\alpha}-toxin$ permeabilized artery. $0.3{\mu}M\;Ca^{2+}$ increased myosin light chain phosphorylations monotonically. $10\;{\mu}M$ norepinephrine and $10\;{\mu}M$ GTP potentiated increase of myosin light chain phosphorylations by $0.3{\mu}M\;Ca^{2+}$, which reaches a peak at 5 min and gradually declines to the $Ca^{2+}$ alone level at 20 min. At the early phase (1 min), $10\;{\mu}M$ KN 62, the inhibitor of $Ca^{2+}$/calmodulin-dependent protein kinase II , decreased myosin light chain phosphorylation levels by $10\;{\mu}M$ norepinephrine and $10\;{\mu}M$ GTP in the presence of $0.3{\mu}M\;Ca^{2+}.\;However\;10\;{\mu}M$ KN-62 did not affect the myosin light chain phosphorylations by $10\;{\mu}M$ norepinephrine and $10\;{\mu}M$ GTP in the presence of $0.3{\mu}M\;Ca^{2+}$ at the peak (5 min) and plateau phases (20 min). From these results, the role of $Ca^{2+}$/calmodulin-dependent protein kinase II may be different depending on time, which may play a role in increase of myofilamint $Ca^{2+}$ sensitivity by norepinephrine and GTP resulting from increase of myosin light chain phosphorylations at the early phase. However, at plateau phase, $Ca^{2+}$/calmodulin-dependent protein kinase II may not be involved in the increase of myofilament $Ca^{2+}$ sensitivity by norepinephrine and GTP in rabbit mesenteric ${\alpha}-toxin$ permeabilized artery.

• The Korean Journal of Gastroenterology
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• v.72 no.6
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• pp.308-312
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• 2018

Percutaneous endoscopic gastrostomy (PEG) is widely used to provide nutritional support for patients with dysphagia and/or disturbed consciousness preventing oral ingestion, and PEG tube placement is a relatively safe and convenient non-surgical procedure performed under local anesthesia. However, the prevention of PEG-insertion-related complications is important. A 64-year-old man with recurrent pneumonia underwent tracheostomy and nasogastric tube placement for nutritional support and opted for PEG tube insertion for long-term nutrition. However, during the insertion procedure, needle puncture had to be attempted twice before successful PEG tube placement was achieved, and a day after the procedure his hemoglobin had fallen and he developed hypotension. Abdominal computed tomography revealed injury to a pancreatic branch of the superior mesenteric artery (SMA) associated with bleeding, hemoperitoneum, and pancreatitis. Transarterial embolization was performed using a microcatheter to treat hemorrhage from the injured branch of the SMA, and the acute pancreatitis was treated using antibiotics and supportive care. The patient was discharged after an uneventful recovery. Clinicians should be mindful of possible pancreatic injury and bleeding after PEG tube insertion. Possible complications, such as visceral injuries or bleeding, should be considered in patients requiring multiple puncture attempts during a PEG procedure.

• Proceedings of the Korean Biophysical Society Conference
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• 1999.06a
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• pp.61-62
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• 1999

;The mechanisms inducing hypertension are actively investigated and are still challenging topics. Basically hypertension must be caused by the disorder of $Ca^{2+}$ metabolism in vascular smooth muscle, such as the increase of $Ca^{2+}$ influx, the decrease of ci+ efflux, or the change of sensitivity of contractile protein etc. The one of cause of the increase of ci+ influx may be the change of ci+ channel activity. Even though the relationships of ci+ channel activity and hypertension were studied using various hypertension models, still it is not clear how much change of $Ca^{2+}$ channel activity in diabetes mellitus (DM) induced hypertension is occurred. We induced DM hypertension in SD rat and compared the $Ca^{2+}$ channel activity with age-matched normotensive SD rat. For inducing DM hypertension, left kidney was removed with 200 gm rat and, after 1 month, 60 mg/kg of streptozotocin was injected into peritoneal space to induce diabetes mellitus. Usually after 4-6 weeks, hypertension was fully induced. For isolating vascular smooth muscle cells (VSMC), we used mesenteric arteriole (3rd - 4th branch of mesenteric artery) of which diameter is below 150 urn. VSMCs were isolated enzymatically. $Ca^{2+}$ current was measured using whole cell patch clamp technique. All experiments were performed at $37^{\circ}C$. The cell membrane area of VSMC of DM hypertensive rat is larger than that of control VSMC($36.6{\pm}3.64{\;}pF{\;}vs{\;}22.4{\pm}1.29{\;}pF, {\;}mean{\pm}S.E.$) When we compared the current amplitude, the $Ca^{2+}$ current amplitude in VSMC of DM hypertensive rat is much larger than that in VSMC of normotensive age-matched rat. After $Ca^{2+}$ current amplitude was normalized by cell membrane area, the current amplitude in DM hypertension is increased to $249.1{\pm}15.9{\;}%{\;}(mean{\pm}S.E.M)$, which means the ;absolute current amplitude is about 4 times larger in DM hypertension. When we compared the steady state activation and inactivation. there were no noticeable differences. From these results. one of cause of the DM hypertension is due to the increase of $Ca^{2+}$ current amplitude. But it need further study why the $Ca^{2+}$ current is so large in VSMC of DM hypertension and how much $Ca^{2+}$ influx through $Ca^{2+}$ channel contribute to the increase of intracellular $Ca^{2+}$ and eventually contribute to development of hypertension.ypertension.

• Radiation Oncology Journal
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• v.32 no.2
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• pp.63-69
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• 2014

Purpose: To find the applicability of adjuvant radiotherapy for extrahepatic bile duct cancer (EBDC), we analyzed the pattern of failure and evaluate prognostic factors of locoregional failure after curative resection without adjuvant treatment. Materials and Methods: In 97 patients with resected EBDC, the location of tumor was classified as proximal (n = 26) and distal (n = 71), using the junction of the cystic duct and common hepatic duct as the dividing point. Locoregional failure sites were categorized as follows: the hepatoduodenal ligament and tumor bed, the celiac artery and superior mesenteric artery, and other sites. Results: The median follow-up time was 29 months for surviving patients. Three-year locoregional progression-free survival, progression-free survival, and overall survival rates were 50%, 42%, and 52%, respectively. Regarding initial failures, 79% and 81% were locoregional failures in proximal and distal EBDC patients, respectively. The most common site was the hepatoduodenal ligament and tumor bed. In the multivariate analysis, perineural invasion was associated with poor locoregional progression-free survival (p = 0.023) and progression-free survival (p = 0.012); and elevated postoperative CA19-9 (${\geq}37U/mL$) did with poor locoregional progression-free survival (p = 0.002), progression-free survival (p < 0.001) and overall survival (p < 0.001). Conclusion: Both proximal and distal EBDC showed remarkable proportion of locoregional failure. Perineural invasion and elevated postoperative CA19-9 were risk factors of locoregional failure. In these patients with high risk of locoregional failure, adjuvant radiotherapy could be considered to improve locoregional control.

• Archives of Plastic Surgery
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• v.44 no.6
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• pp.550-553
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• 2017

Esophageal perforation is a rare but potentially fatal complication of robot-assisted thyroidectomy (RAT). Herein, we report the long-term outcome of an esophageal reconstruction with a jejunal free flap for esophageal rupture after RAT. A 33-year-old woman developed subcutaneous emphysema and hoarseness on postoperative day1 following RAT. Esophageal rupture was diagnosed by computed tomography and endoscopy, and immediate surgical exploration confirmed esophageal rupture, as well as recurrent laryngeal nerve injury. We performed a jejunal free flap repair of the 8-cm defect in the esophagus. End-to-side microvascular anastomoses were created between the right external carotid artery and the jejunal branches of the superior mesenteric artery, and end-to-end anastomosis was performed between the external jugular vein and the jejunal vein. The right recurrent laryngeal nerve injury was repaired with a 4-cm nerve graft from the right ansa cervicalis. Esophagography at 1 year after surgery confirmed that there were no leaks or structures, endoscopy at 1 year confirmed the resolution of vocal cord paralysis, and there were no residual problems with swallowing or speech at a 5-year follow-up examination. RAT requires experienced surgeons with a thorough knowledge of anatomy, as well as adequate resources to quickly and competently address potentially severe complications such as esophageal rupture.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.5
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• pp.307-312
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• 2011

It has been rereported that axons which display 5-hydroxytryptamine (5-HT) immunoreactivity are abundant in the pancreas and the majority of serotonergic axons terminate within intrapancreatic ganglia, islet and acini. This histological result strongly suggests that intrapancreatic serotonergic nerves could affect to the pancreatic endocrine and exocrine secretion. Thus, this study was aimed to investigate whether intrapancreatic serotonergic nerves could affect pancreatic exocrine secretion and an action mechanism of the intrapancreatic serotonergic nerves. The rats were anesthetized with a single injection of urethane. The median line and the abdominal aorta was carefully dissected and cannulated with PE-50 tubing just above the celiac artery, and then tightly ligated just below the superior mesenteric artery. The pancreatic duct was also cannulated with Tygon microbore tubing. With the addition of serotonin, pancreatic volume flow and amylase output were significantly inhibited electrical field stimulation (EFS). On the other hand, pancreatic volume flow and amylase output were significantly elevated in EFS with the addition of spiperone. EFS application, however, pancreatic volume flow and amylase output had no significant change in cholecystokinin (CCK) alone when serotonin was applied under a 5.6 mM glucose background. Pancreatic volume flow and amylase output under 18 mM glucose background were significantly elevated in CCK plus serotonin than in CCK alone. These data suggest that intrapancreatic serotonergic nerves play an inhibitory role in pancreatic exocrine secretion and an important role in the insulin action or release.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.7 no.2
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• pp.278-283
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• 2004

Meckel's diverticulum is found in about 3% of the population, often incidentally during laparotomy or at autopsy. Over 50% of patients who develop symptoms from this anomaly are younger than 2 years of age. The most common symptom of this lesion is intestinal obstruction. Rarely Meckel's diverticulum is complicated by a mesodiverticular band, which is believed to be a remnant of a vitelline artery. We report a 11-year-old girl with small bowel obstruction because of an intestinal hernia beneath the mesodiverticular band. The causative factor was a stenotic area in the terminal ileum caused by a ringlike lipovascular mesenteric band encroaching externally on the lumen. Although the incidence of mesodiverticular bands complicating Meckel's diverticulum is quite low, the rapid clinical course and the associated high mortality rate make this an important disease.