• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.539-545
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• 2018

4-Hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione (PD1) is a synthetic phthalimide derivative of a marine compound. PD1 has peroxisome proliferator-activated receptor (PPAR) ${\gamma}$ agonistic and anti-inflammatory effects. This study aimed to investigate the effect of PD1 on allergic asthma using rat basophilic leukemia (RBL)-2H3 mast cells and an ovalbumin (OVA)-induced asthma mouse model. In vitro, PD1 suppressed ${\beta}$-hexosaminidase activity in RBL-2H3 cells. In the OVA-induced allergic asthma mouse model, increased inflammatory cells and elevated Th2 and Th1 cytokine levels were observed in bronchoalveolar lavage fluid (BALF) and lung tissue. PD1 administration decreased the numbers of inflammatory cells, especially eosinophils, and reduced the mRNA and protein levels of the Th2 cytokines including interleukin (IL)-4 and IL-13, in BALF and lung tissue. The severity of inflammation and mucin secretion in the lungs of PD1-treated mice was also less. These findings indicate that PD1 could be a potential compound for anti-allergic therapy.

• Journal of Chest Surgery
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• v.42 no.2
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• pp.263-267
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• 2009

A pancreatico-pleural fistula (PPF), caused by rupture of a pancreatic pseudocyststectomy or obstruction of the pancreatic duct, is a rare condition. A 48-year-old man with chronic alcoholism was admitted with a massive pleural effusion. Pleural fluid studies revealed elevated amylase and lipase. A PPF complicated by a ruptured pancreatic pseudocyststectomy was diagnosed by computerized tomography scan. Although the symptoms improved with conservative management, (chest tube drainage, NPO, total parenteral nutrition, and a pancreatic secretion inhibitor), a distal pancreatectomy, including a pseudocystectomy and thoracotomy, were performed for an increasing size of the hemorrhagic pancreatic pseudocyststectomy and a recurrent hemorrhagic pleural effusion. There were no post-operative complications and the patient was discharged on post-operative day 27.

• Tuberculosis and Respiratory Diseases
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• v.59 no.3
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• pp.306-310
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• 2005

Hyponatremia which is due to excessive sodium loss in the urine and decrease in extracellular fluid volume following an acute or chronic central nervous system injury, has been conjunctively described as cerebral salt wasting syndrome (CSWS). This syndrome is often confused with dilutional hyponatremia due to inappropriate secretion of antidiuretic hormone. Accurate diagnosis and management are mandatory for improvement of the course of the disease. This report describes a case of a 31-year-old male patient with CSWS associated with tuberculous meningitis. The patient exhibited hyponatremia, polyuria, excessive natriuresis, volume depletion, and hypotension. He was diagnosed to manifest CSWS and was treated by administration of fluids, salt, and fludrocortisone. After the respective treatments, symptoms of polyuria and hypotension were gradually resolved and hyponatremia was corrected.

• Childhood Kidney Diseases
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• v.24 no.1
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• pp.42-46
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• 2020

Disturbances in water and salt balances are relatively common in children after brain tumor surgery. However, the coexistence of different diseases of water and sodium homeostasis is challenging to diagnose and treat. The coexistence of combined central diabetes insipidus (CDI) and cerebral salt wasting syndrome (CSWS) is rare and may impede accurate diagnosis. Herein, we report the case of an 18-year-old girl who underwent surgery for a germinoma and who presented prolonged coexistence of CDI and CSWS. The patient was diagnosed with panhypopituitarism with CDI at presentation and was treated with hydrocortisone, levothyroxine, and desmopressin. Postoperatively, she developed polyuria of more than 3L/day, with a maximum daily urine output of 7.2 L/day. Her serum sodium level decreased from 148 to 131 mEq/L. Polyuria was treated with desmopressin at incremental doses, and hyponatremia was managed with fluid replacement. At 2 months after surgery, she presented with hyponatremia-induced seizure. Polyuria and hyponatremia combined with natriuresis indicated CSWS. Treatment with fludrocortisone were initiated; then, her electrolyte level gradually normalized. CSWS is self-limiting and generally resolves within 2 weeks. However, the patient in this study still required treatment with vasopressin and fludrocortisone at 16-months after surgery. Hyponatremia in a patient with CDI may be erroneously interpreted as inadequate CDI control or syndrome of inappropriate antidiuretic hormone secretion, leading to inappropriate treatment. The identification of the potential combination of CDI and CSWS is important for early diagnosis and treatment.

• Asian-Australasian Journal of Animal Sciences
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• v.17 no.11
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• pp.1570-1574
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• 2004

A flock of AA breed chickens were reared in peterstme brood-vait chamber and were provided with high energy pelleted feed. At 14 d of age, a total of 350 birds were randomly divided into 3 groups as follows: 100 birds were exposed to normal ambient temperature of 20$^{\circ}C$ for control group; 150 birds were exposed to lower ambient temperature of 11$^{\circ}C$ to induce ascites (treatment I); and another group of 100 birds were exposed to lower ambient temperature of 11$^{\circ}C$ and fed diet containing 1% L-arginine for ascitic prophylactic treatment (treatment II). Samples were collected from blood and abdominal fluid of chicken at 3, 4, 5, 6 and 7 wk of age subsequently, to analysis the contents of plasma endothelin (ET-1), angiotensin II (Ang II), cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP). The results indicated that the contents of cAMP, cGMP, and Ang II in reatment I and ascitic broilers were higher than the corresponding control group (p<0.01, p<0.05), ET-1 of preascitic broilers were control group (p<0.05), while there was an insignificant difference with later ascitic broilers. The contents of cAMP and cGMP in treatment II were higher than the treatment I and control groups (p<0.01, p<0.05), whereas, the contents of Ang II were gradually decreased compared to the control group (p<0.05), the contents of ET-1 were insignificantly different. On further analysis, the increased plasma Ang II at low ambient temperature condition in broilers made endothelium cell secretion of increased ET-1, cAMP, cGMP and decreased NO. Therefore, low temperature accelerated ascites syndrome in broilers. Supplemently L-arginine can decrease ET-1, and increase cAMP and cGMP. It is concluded that cAMP mediated in broilers pulmonary hypertension syndrome.

• IMMUNE NETWORK
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• v.6 no.3
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• pp.138-144
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• 2006

Background: There are at least two different subsets of B cells, B-1 and B-2. The characteristic features and function of B-2 cells in addition to the effect of steroids on B-2 cells are well-known. Although B-1 cells have different features and functions from B-2 cells, the effect of steroids on B-1 cells is not completely understood. Therefore, this study examined the effects of dexamethasone on peritoneal (or B-1 cells) and splenic B cells (or B-2 cells). Methods: Purified B cells were obtained from the peritoneal fluid and the spleens of mice. The isolated B cells were cultured in a medium and after adding different concentrations of dexamaethasone. The cell survival rate was measured by flow cytometry using propidium iodide. The expression level of the B cell surface marker was analyzed by flow cytometry. During the culture of these cells, immunoglobulin secreted into the culture supernatants was evaluated by an enzyme-linked immunosorbent assay. Results: The survival rate of peritoneal and splenic B cells decreased with increasing dexamethasone concentration. However, the rate of peritofieal B cell apoptosis was lower than that of splenic B cells. CDS and B7.1 expression in peritoneal B cells and CD23 and sIgM expression in splenic B cells after the dexamethasone treatment were reduced. When B cells were treated with dexamethasone, the spontaneous IgM secretion decreased with increasing dexamethasone concentration. Conclusion: Dexamethasone induces apoptosis in peritoneal and splenic B cells. However, peritoneal B cells are less sensitive to dexamethasone. The dexamethasone suppressed expression of the surface markers in peritoneal B cells is different from those in splenic B cells.

• Journal of Chest Surgery
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• v.29 no.5
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• pp.581-584
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• 1996

Reexpansion pulmonary edema is a rare complication of the treatment of lung collapse secondary to pneumothordx, pleural effusion, or atelectasis but occasionally life threatening. Generally, reexpansion pulmonary edema is believed to o cur only when a chronically collapsed lung is rapidly reexpanded by evacuation or large amounts of air or fluid. This complication is heralded by tachypnea, unilateral rales, and profuse expectoration of frothy secretion within several hours of reexpansion. Increased dur- ation of pneumothorax and the use o( suction are important factors in the generation of reexpansion pulmonary edema. We had experienced 3 cases of reexpansion pulmonary edema. In the two cases the pneumothorax had been present for several days, and, after insertion of a chest tube, pulmonary edema developed unilaterally but improved with supplemental oxygen. In the third case, massive pleural effusion was present. and, after insertion of a chest tube, pulmonary edema developed unilaterally, followed by cardiac arrest. He died of pulmonary edema inspire of resuscitation.

• The Journal of Internal Korean Medicine
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• v.30 no.1
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• pp.9-23
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• 2009

Objectives : Asthma is a chronic inflammatory disorder of the airways by many cells such as mast cells, Th2 lymphocytes and eosinophile. The present study was aimed to evaluate the effects of Salviae miltiorrhizae (SM) on T cell cytokine production, mast cells. and eosinophils, Methods : We screened 13 herbs to find compounds with potential to control Th cytokine production. using concanavalin A (con A)-activated splenocyte cultures. Con A-activated $IFN-\gamma$ and IL-4 levels in supernatants of splenocyte cultures. Bone marrow derived mast cells (BMMC) were incubated with SM and then the expressions of membrane proteins of BMMC were analyzed by fluorescence activated cell sorter (FACS). BALB/c mice sensitized to ovalbumin (OVA) were challenged with aerosolized OVA for 6 weeks. During the last weeks some mice were treated with SM. Then eosinophils in bronchoalveolar lavage fluid (BALf) were counted and pathologic changes of lung tissue were observed with hematoxylin-eosin stain. Results : SM increased $IFN-\gamma$ level on splenocyte culture significantly. but had no significant effects on expressions of ICAM-1, CD62L, integrin $a_4$. c-kit, IL-3 receptors. CD11a, or IgE receptors of BMMC. SM treatment significantly inhibited eosinophil infiltrates in BALf and peribronchial lung inflammation. Conculusions : The present data suggested that SM may have an effect on Th cytokine secretion and eosinophils associated with asthma responses. Therefore SM might be of therapeutic value in treating asthma.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.6
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• pp.555-564
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• 2021

We investigated the effects of naringenin and morin on IL-5 and ROS production in PMA+ionomycin-treated EL-4 cells with the corroboration of their antioxidant and anti-inflammatory properties using an asthma-induced mouse model. The EL-4 cell line was used to study the outcomes of naringenin or morin, followed by cell viability studies. Western blot analysis and ELISA test were used to determine Th2 mediated cytokines. In vivo studies were carried out on BALB/c mice to induce allergic asthma using ovalbumin administered intraperitoneally. Intracellular ROS was determined using 2',7'-dichlorodihydrofluorescein diacetate, followed by serum enzymatic (AST and ALT) estimations and inflammatory cell count in the bronchoalveolar lavage fluid (BALF) and lung tissues. Histopathological studies were conducted to examine lung tissue-stained architecture. Our findings suggested that naringenin and morin significantly suppressed IL-5 and ROS production via various pathways. Interestingly, by reducing NFAT activity, naringenin and morin stimulated HO-1 expression, thereby suppressing IL-5 secretion due to regulating the transcription factor Nrf2 via P13/Akt or ERK/JNK signalling pathways in EL-4 cells, demonstrating the involvement of HO-1 expression in inhibiting asthmatic inflammation. The increased inflammatory cells in the BALF were substantially decreased by both naringenin and morin, followed by inhibition in the elevated Th-2 cytokines levels. The TNF-α protein levels in an allergic asthma mouse model were significantly reduced by suppressing Akt phosphorylation and eosinophil formation. Recent findings confirmed that naringenin and morin possess the potential to control asthma-related immune responses through antioxidant and anti-inflammatory properties, indicating potential therapeutic agents or functional foods.

• BMB Reports
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• v.54 no.3
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• pp.182-187
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• 2021

Leukotriene B4 (LTB4) is a lipid mediator of inflammation that is generated from arachidonic acid via the 5-lipoxygenase pathway. Previous studies have reported that the receptors of LTB4, BLT1, and BLT2 play mediatory roles in the allergic airway inflammation induced by ovalbumin (OVA). However, considering that house dust mites (HDMs) are the most prevalent allergen and well-known risk factor for asthmatic allergies, we are interested in elucidating the contributory roles of BLT1/2 in HDM-induced allergic airway inflammation. Our aim in this study was to investigate whether BLT1/2 play any roles in HDM-induced allergic airway inflammation. In this study, we observed that the levels of ligands for BLT1/2 [LTB4 and 12(S)-HETE (12(S)-hydroxyeicosatetraenoic acid)] were significantly increased in bronchoalveolar lavage fluid (BALF) after HDM challenge. Blockade of BLT1 or BLT2 as well as of 5-lipoxygenase (5-LO) or 12-lipoxygenase (12-LO) markedly suppressed the production of TH2 cytokines (IL-4, IL-5, and IL-13) and alleviated lung inflammation and mucus secretion in an HDM-induced eosinophilic airway-inflammation mouse model. Together, these results indicate that the 5-/12-LO-BLT1/2 cascade plays a role in HDM-induced airway inflammation by mediating the production of TH2 cytokines. Our findings suggest that BLT1/2 may be a potential therapeutic target for patients with HDM-induced allergic asthma.