• Journal of Chest Surgery
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• v.28 no.11
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• pp.1058-1062
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• 1995

We have experienced one case of hemoptysis which developed from both upper lung fields due to pulmonary aspergilloma combined with pulmonary tuberculosis. A 48 year old female patient was admitted with 10 years history of recurrent hemoptysis. Chest X-ray film revealed moderately advanced active pulmonary tuberculosis lesion on both upper lung fields, and cresentic radiolucent space between cavity wall and round radiopaque lesion on left upper lung field. Bronchial arteriogram showed hypervascularity and extravasation of contrast media in the right lung and it was treated by bronchial artery embolization. Hemoptysis recurred 7 months after embolization and repeat examination revealed greatly increased bronchial vasculature in the left upper lobe and therefore underwent left upper lobectomy. The pathologic result was compatible with aspergillosis, and the postoperative recovery was uneventful.

• The Korean Journal of Cytopathology
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• v.9 no.2
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• pp.187-191
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• 1998

Alveolar soft part sarcoma(ASPS) is a rare malignant neoplasm with a distinct clinicopathologic entity of which fine needle aspiration(FNA) cytologic findings have been described in only a few reports. Although patients usually present with an isolated soft-tissue mass in the extremity, metastasis can occur in about 13 % of total cases and the most frequent metastatic site is the lung. We have recently experienced a FNA cytologic case of ASPS in the lung. A 23-year-old female patient was admitted to this hospital due to 2-month-history of cough She had been good in health before the visit. Chest computed tomography revealed multiple, variable sized, bilateral pulmonary nodules. Physical examination and other staging work up revealed no other lesions except for pulmonary nodules. A percutaneous transthoracic FNA was performed from the pulmonary nodules. The smear was cellular and most cells were arranged singly. In addition, a few clusters lined by thin-walled vasculature with a pseudoalveolar pattern were present. Some of the tumor cells were large and polygonal lo oval with abundant granular or vacuolated cytoplasm. Most cells were naked nuclei showing finely granular chromatin pattern with prominent central nucleoli.

• Tuberculosis and Respiratory Diseases
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• v.49 no.5
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• pp.594-600
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• 2000

Background : Positive end expiratory pressure (PEEP) ventilation is well established as an integral part of the management of patients with the acute lung injury. PEEP is a key element in the treatment of hypoxemia resulting from pulmonary edema. Pulmonary capillary pressure (Pcap) is the most important factor influencing lung edema formation, and an understanding of how Pcap is altered by variations of PEEP or pulmonary arterial occlusion pressure (PAOP) is important to improve the treatment of acute lung injury patients. This study was performed to evaluate the effects of PEEP on the pulmonary capillary pressure in acute lung injury patients. Methods : This was a prospective study of 11 acute lung injury patients. The effect of PEEP on pulmonary circulation at four different levels (0,4,8, and 12cm$H_2O$) was analyzed. Pcap was estimated visually at bed side with Swan Ganz catheters. The pulmonary vasculature was analyzed by calculating the pressure difference at the arterial and venous parts of the circulation. Results: As PEEP increased from 0 to 12 cm$H_2O$, the mean pulmonary arterial pressure (PAP) and Pcap increased respectively from $22.7{\pm}7.4$ to $25.3{\pm}7.3$ mmHg and $15.3{\pm}3.3$ to $17.8{\pm}3.2$ mmHg (p<0.05). Similarly, PAOP increased from $9.8{\pm}2.1$ to $12.8{\pm}2.1$ mmHg and the central venous pressure increased from $6.1{\pm}1.6$ to $9.3{\pm}2.3$ mmHg(p<0.05). However, the pressure gradient at the arterial (PAP-Pcap) and venous (Pcap-Pcwp) parts of pulmonary circulation remained unchanged at all evaluated PEEP levels. Conclusion : Although Pcap increased gradually with increased the pressure gradient at the arterial and venous part of the pulmonary vasculature remained unchanged at all evaluated PEEP levels in acute lung injury patients.

• Journal of the Korean Society of Radiology
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• v.84 no.4
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• pp.934-940
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• 2023

Ventriculoperitoneal shunting is the most common neurosurgical procedure for treatment of hydrocephalus. Shunt-related complications are relatively common and associated with a high rate of shunt revision. However, migration of the distal ventriculoperitoneal shunt, especially into the cardiac and intravascular regions, has rarely been reported. Awareness of this rare but potentially hazardous complication is important owing to its significant morbidity, which can be prevented by prompt management. Here, we introduce a case of a 23-year-old male with migration of the distal shunt catheter through the left internal jugular vein into the cardiac chamber and both pulmonary arteries, which occurred 2 months after receiving ventriculoperitoneal shunting. Furthermore, we discuss the possible mechanisms and management of this condition.

• Journal of Chest Surgery
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• v.5 no.2
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• pp.87-96
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• 1972

Studies of blood gas and lung histopathology were done in 10 dogs after intrapericardlal aorto-right pulmonary arterial anastomosis with proximal ligation of the right pulmonary antery. Among the 5 expired during or after operation, in 3 cases, the causes of the death were due to surgical bleeding and, in 2 cases, acute cardiopulmonary insufficiency because of large anastomosis stoma measured respectively 7mm and 10mm. In the 5 of survivals, one was sacrificed because of empyema at postoperative 7 days and 2 were at postoperative one month and remained 2 at postoperative 3 month respectively. The following observations were made. 1.In every survival, continuous machinary murmur was auscultated and the angiograms of all long term survivals showed the good patency of the anastomosis stoma. 2.After the ligation of the right pulmonary artery, the values of $PO_2$ and $PCO_2$ in arterial and venous blood were generally decreased comparing with the preoperative values. The mean value of $P_aO_2$ noted $83.30{pm}11.875$[p<0.01]. After the shunts operation with ligation of the right pulmonary artery, the immediate values of PH, $PO_2$ and $PCO_2$showed no significant changes comparing with that of right pulmonary artery ligation only. In the cases of survivals more than one month, the values of $PO_2$ and $PCO_2$ in the arterial and venous blood were generally higher than that of ligation of the right pulmonary artery only. The $P_aO_2$ value noted $103.750{pm}7.395$[p<0.01]. The mean values of $P_aO_2$, $PCO_2$ and PH in the arterial and venous blood almost returned to that of preoperative studies. 3.In the specimens of lung from the cadavors expired due to acute cardiopulmonary insufficiency after the operation, there were massive congestion, hemorrhage in the alveolar spaces and bronchioles. In specimens obtained at postoperative one month, there were dilatation of alveolar spaces with partial rupture, slight congestion, and alveolar wall thickening in the lung parenchyme, but there was no significant changes in pulmonary vasculature except dilation of pulmonary capillaries. In the specimens obtained at postoperative three months, the alveolar walls were more thickened in the lung parenchyme than the finding of the specimens obtained at postoperative one month. In the wall of pulmonary capillaries, there was only slight thickening with connective tissue proliferatlon.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.6
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• pp.591-598
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• 2017

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from $10-300{\mu}m$). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations ($10-100{\mu}m$) followed by secondary relaxation (at $100-300{\mu}m$). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed $CaCl_2$-induced constriction in the 60 mM $K^+$-containing $Ca^{2+}$-free solution in a dose-dependent manner. Fluorescent imaging of $Ca^{2+}$ using fluo-4 showed that a 10 min incubation with propofol ($10-300{\mu}m$) inhibited the $Ca^{2+}$ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM $K^+$-containing $Ca^{2+}$-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

• BMB Reports
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• v.55 no.11
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• pp.565-570
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• 2022

Pulmonary arterial hypertension (PAH) is a progressive and devastating disease whose pathogenesis is associated with a phenotypic switch of pulmonary arterial vascular smooth muscle cells (PASMCs). Bone morphogenetic protein (BMP) signaling and potassium two pore domain channel subfamily K member 3 (KCNK3) play crucial roles in PAH pathogenesis. However, the relationship between BMP signaling and KCNK3 expression in the PASMC phenotypic switching process has not been studied. In this study, we explored the effect of BMPs on KCNK3 expression and the role of KCNK3 in the BMP-mediated PASMC phenotypic switch. Expression levels of BMP receptor 2 (BMPR2) and KCNK3 were downregulated in PASMCs of rats with PAH compared to those in normal controls, implying a possible association between BMP/BMPR2 signaling and KCNK3 expression in the pulmonary vasculature. Treatment with BMP2, BMP4, and BMP7 significantly increased KCNK3 expression in primary human PASMCs (HPASMCs). BMPR2 knockdown and treatment with Smad1/5 signaling inhibitor substantially abrogated the BMP-induced increase in KCNK3 expression, suggesting that KCNK3 expression in HPASMCs is regulated by the canonical BMP-BMPR2-Smad1/5 signaling pathway. Furthermore, KCNK3 knockdown and treatment with a KCNK3 channel blocker completely blocked BMP-mediated anti-proliferation and expression of contractile marker genes in HPAMSCs, suggesting that the expression and functional activity of KCNK3 are required for BMP-mediated acquisition of the quiescent PASMC phenotype. Overall, our findings show a crosstalk between BMP signaling and KCNK3 in regulating the PASMC phenotype, wherein BMPs upregulate KCNK3 expression and KCNK3 then mediates BMP-induced phenotypic switching of PASMCs. Our results indicate that the dysfunction and/or downregulation of BMPR2 and KCNK3 observed in PAH work together to induce aberrant changes in the PASMC phenotype, providing insights into the complex molecular pathogenesis of PAH.

• Journal of Veterinary Clinics
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• v.34 no.4
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• pp.283-286
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• 2017

A 4-month-old, female Maltese dog was referred with continuous heart murmur. Patent ductus arteriosus was diagnosed via radiography and echocardiography. The patient was untreated because of client's refusal. After 13 months, the dog was referred again with seizure and salivation. Laboratory examination revealed increased liver enzymes, hyperammonemia and decreased total cholesterol and total protein. Microhepatica was identified on abdominal radiography. CT angiography showed a shunt vessel that originated from the portal trunk to the prehepatic caudal vena cava and patent ductus arteriosus connecting proximal descending aorta with the main pulmonary artery. No portal vasculature toward liver is observed after shunt vessel. The patient was diagnosed as concurrent patent ductus arteriosus and congenital extrahepatic portosystemic shunt with suspected portal vein aplasia. In human, cardiac malformations are frequently observed in patients with congenital extrahepatic portosystemic shunt with portal vein aplasia. This report described concurrent patent ductus arteriosus and congenital extrahepatic portosystemic shunt with suspected portal vein aplasia in a dog.

• Journal of Veterinary Clinics
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• v.30 no.2
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• pp.87-94
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• 2013

This retrospective study reviewed the clinical and diagnostic features, therapeutic outcome and compilations of interventional ductal occlusion in 37 dogs with patent ductus arteriosus (PDA). Malteses and female dogs were over-presented. Bounding pulse and left basal continuous murmur were most common findings in physical examination, while the differential cyanosis was rarely observed. Left ventricular (LV) enlargement patterns and sinus tachycardia were common in the ECG. Typical radiographic findings included LV elongation and triple bumps indicating left atrial (LA), aortic and pulmonary dilation. Echocardiographic features were typical shunt flow at the ductus arteriosus and marked LV dilation with mild to moderate mitral regurgitation (MR). The 32 of 37 dogs were interventionally treated with either thromboemolic coils (TCE) or Amplatz canine ductal occluder (ACDO). Transient hemoglobinuria caused by incomplete closure was occurred in 2 dogs treated with TCE, although the hemoglobinuria was disappeared within a week of intervention. The dislodgement of occlusion device was occurred in 2 dogs with TCE and 1 dog with ACDO. However there were no significant complications associated with this dislodgement, since those were dislodged at the lower pulmonary vasculature. We also found that no serious complications and no further medical intervention in 29 dogs having long-term follow-ups.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.360-368
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• 1998

Background: Endothelin(ET), a potent vasoconstrictor peptide produced by endothelial cells and degraded predominantly in the pulmonary vasculature, have been implicated in the development of various organ dysfunctions. Plasma concentrations of ET-1 are reported to be elevated in patients with diffuse interstitial lung disease(DILD). But, there is no study to establish the exact source and mechanisms involved in the increased plasma ET-1 concentrations in DILD patients. Methods: 12 patients with IPF, 2 patients with sarcoidosis, 2 patients with scleroderma, 1 patient with SLE and 11 healthy volunteers were studied. ET was detected by radioimmunoassay in plasma and bronchoalveolar lavage fluid(BALF) as well as in 24-hr urine specimens. For each subjects, arterial/venous(A/V) ET ratio and renal ET clearance were calculated. Results: Elevated plasma, urine and BALF ET concentrations were found in patients with DILD compared with controls. But, no significant difference was observed in ET A/V ratio and ET renal clearance between patients with DILD and controls. Conclusion: We observed that plasma ET concentrations were elevated in patients with DILD, and that the main site of ET production may be lung parenchyme.