Microcystic stromal tumor of the ovary is a very rare ovarian tumor with distinctive microcystic histologic features and a characteristic immunophenotype of stromal tumor. However, its origin, tumor pathogenesis, and prognosis have not been well established until now. We report a very unusual case of a microcystic stromal tumor of the ovary with a mutation in exon 3 of the β-catenin (CTNNB1) gene. Macroscopically, the fragmented ovarian tumor showed a diffuse solid mass. Microscopically, the tumor had a pathognomonic histologic pattern of solid and cellular areas with microcysts and fibrous hyalinized stroma. Immunohistochemical staining with CD10, vimentin, CD99, and β-catenin showed positive expression. However, α-inhibin and E-cadherin showed negativity. Mutational analysis revealed a point mutation in exon 3 of the β-catenin (CTNNB1) gene.

OBJECTIVE:To examine the properties of mesothelial cells by measuring pleural cancer antigen 125 (CA-125) levels in different types of benign and malignant pleural effusions.DESIGN:In this retrospective study, pleural fluid was collected from 326 patients; pleural CA-125 levels were measured using radioimmunoassay. Patients were classified into five groups according to the aetiology of pleural effusions: I) tuberculosis, II) malignant, III) pyogenic, IV) congestive heart failure, and V) hepatic hydrothorax.RESULTS:CA-125 levels were significantly higher in the malignant group than in all benign groups. There was no difference in pleural CA-125 levels between transudate and exudate benign aetiologies. Although pleural CA-125 levels were significantly higher in malignant than benign effusions, about one third of malignant pleural effusions had levels of <600 U/ml. Among malignancies, there were no significant differences in pleural CA-125 levels between histological types.CONCLUSION:CA-125 levels in benign pleural effusions may not be influenced by pleural inflammation or hydrostatic or oncotic pressure changes. Pleural CA-125 levels may not be influenced by the histological type of tumour in malignant pleural effusions, suggesting that mesothelial cell properties may not be altered by these factors in the pleural space.

Malignancy represents a leading cause of morbidity and mortality in patients with a long-term surviving graft. Carcinoid tumor is a common primary endocrine tumor in the general population that is rare in transplant recipients. Our present report focused on a 48-year-old man who received immunosuppressive therapy based on cyclosporine and steroids. Twelve years after renal transplantation, he suffered watery diarrhea and abdominal discomfort. Colonoscopy showed a hard, sessile mass at 5 cm from the anal verge; endoscopic ultrasound showed a 13-mm homogenous hypoechoic mass. Upon endoscopic biopsy, the histological examination revealed a carcinoid tumor. Immunosuppresion was reduced and we performed endoscopic mucosal resection of the rectum. His clinical course has been good with no demonstrated recurrence.

OBJECTIVE:Peroxisome proliferator-activated receptor gamma (PPARgamma) is a member of the nuclear hormone receptor superfamily. Treatment of PPARgamma ligands has been shown to inhibit the growth of various human cancer cells. However, it has not been reported whether human cervical carcinoma cells express PPARgamma. In this study, we investigated the expression of PPARgamma in human normal cervix and cervical carcinoma tissues, and as well as the effect of PPARgamma ligands on cervical cancer cells survival. METHODS:Fresh cervical tissues from a study group of 10 study patients diagnosed with cervical carcinoma were analyzed for the expression of PPARgamma using real-time RT-PCR and Western blot analysis. Immunohistochemical staining for PPARgamma was also performed on the serial sections of 40 cervical carcinomas. In addition, we evaluated the feasibility of PPARgamma ligands, as a potential therapeutic drug against cervical cancer cells using MTT assay and FACS analysis. RESULTS:We found that there were lower expression levels of PPARgamma mRNA and protein in cervical carcinoma tissues than in normal cervical tissues. The extent and intensity of immunoreactive PPARgamma in normal cervix tissues were statistically much greater than those of carcinoma tissues. In order to study effects of PPAR ligand on cell proliferation, we chose ciglitizone that showed very potent growth inhibitory effects on the proliferation of two human cervical cancer cell lines (C-33-A and C-4II). C-4II cells express high expression of PPARgamma, while C-33A cells express low level of PPARgamma. Treatment with ciglitizone inhibited the growth of C-4II cells in a dose-dependent manner, while the growth inhibitory effect of ciglitizone was much less in C-33A cells. In order to test whether ciglitizone-induced growth suppressive effects on cervical cancer cell lines is PPAR-dependent, we treated cervical cancer cells with ciglitizone and/or GW9662 (a PPARgamma antagonist). No significant difference in cell survival was found in cells treated with ciglitizone alone vs. co-treated with ciglitizone and GW9662. GW9662 alone did not induce any cell growth arrest in the cells that we used (data not shown). Thus, we concluded that growth suppressive effects by ciglitizone may not be dependent upon status of PPAR expression. To clarify the mechanism by which ciglitizone inhibits the growth of cervical carcinoma cells, flow cytometry and Western blotting assay were performed. As results, we demonstrated that a large portion of C-4II cells (but not in C-33A) after ciglitizone treatment were arrest at G1 phase with the induction of p21(Cip1/Waf1) and p27(kip1) protein. CONCLUSIONS:These results suggest that PPARgamma is down-regulated in multiple human cervical cancer tissues and cell lines. Ciglitizone may suppress human cervical cancer cells in PPAR-independent manner.

Essential thrombocythemia (ET) is a chronic myeloproliferative disorder (MPD) of insidious onset and characterized by regulatory defect in stem cells. It is possible that ET can induce autonomous megakaryocyte (MK) growth. The physiology of megakaryocytopoiesis was not well defined, and, as a consequence, the pathophysiology of ET characterized by excessive platelet production was poorly understood. Secondary thrombocytopenia, especially post-transplantation, could be fatal so there were many trials to overcome this problem. This experiment was designed to test the effect of cytokines on ex vivo expansion of MK progenitor cells from ET. The MK colony forming unit (CFU-MK) expansion degree according to single or combination cytokines were analyzed in normal person and ET patients. Mononuclear cells were isolated from bone marrow aspiration and then cultured in serum-free medium (MegaCult™) supplemented with SCF, G-CSF, TPO, IL-11 and 3 types of cytokine combination. After 14 days of ex vivo expansion and then the CFU-MK were counted by microscope. In the absence of cytokines, CFU-MK of ET significantly expanded than normal (p<0.05), which represented autonomous CFU-MK formation. There were significantly increased mixed CFU-MK of ET in SCF, G-CSF and TPO (SGT) combined cytokine added well (p<0.05) but pure and total CFU-MK of SGT added well did not show significant expansion. When the effect of cytokines were compared between normal and ET, all of the cytokines significantly expand CFU-MK in ET (p<0.05) than normal and especially in pure CFU-MK. In summary, autonomous MK growth was shown in ET and SGT can be relatively effective cytokine combinations in ex vivo CFU-MK expansion. Further investigation will be needed to find out the most effective culture system and cytokine combination for ex vivo MK progenitor expansion.

PURPOSE:Though nitric oxide has many favorable protective effects on donor lungs, it may also have cytotoxic side effects. In this regard, we investigated whether administration of nitroglycerine, a nitric oxide donor, could minimize ischemia-reperfusion injury in an isolated rat lung reperfusion model.MATERIALS AND METHODS:Thirty-five Sprague-Dawley rats were used for this experiment. The nitroglycerine (NTG) group (n = 18) received the drug intravenously and the 17 control group hosts were treated with the same amount of normal saline. The heart-lung block was retrieved, weighed, and maintained in University of Wisconsin solution for 24 hours at 10 degrees C. Reperfusion was performed using human blood diluted in Krebs-Hensleit solution for 60 minutes. Peak inspiratory pressure, pulmonary artery pressure, and blood gas analysis were performed. After 60 minutes of reperfusion, the amount of protein in bronchoalveolar lavage (BAL) fluid and the myeloperoxidase (MPO) activity in the lung were measured.RESULTS:There were no major statistical differences between the two groups in peak inspiratory pressure and pulmonary artery pressure, but the NTG group maintained lower pulmonary artery pressure during the whole period of reperfusion. Oxygen tension in the NTG group was significantly higher, whereas there were no differences in carbon dioxide tension, BAL fluid, protein, or MPO activity.CONCLUSION:Administration of NTG before donor lung preservation resulted in better lung protection, a possible strategy for clinical application.

The purpose of this study was to compare canine sequential bilateral lung transplantation (SBLT) with left single lung transplant (LSLT) models. After 24 hours of lung preservation with low potassium/dextran glucose (LPDG) solution, seven SBLT procedures were performed using mongrel dogs. The comparative group including nine cases of LSLT. After completion of each transplant, the dogs were maintained on a ventilator for 3 hours. Thereafter serial hemodynamics were evaluated with recipients with chest X-ray, computed tomography, and lung perfusion scan checked at 2 hours after transplantation. Pathological evaluations were also performed. Five of seven SBLT successfully completed the whole assessment, all LSLT survived. In SBLT, pulmonary arterial pressure and pulmonary vascular resistance were significantly elevated, but recovered 3 hours after reperfusion. The ultrastructural aspects of alveolae and pulmonary artery endothelium showed a reversible mild injury 24 hours after lung preservation and reperfusion. The present study suggests that the canine SBLT model using LPDG solution provides an excellent preservation effect and is more physiological as the dog is completely dependent on the function of the transplanted lung.

Aim of Study. Nitric oxide (NO) has been reported as a favorable protective supplement in donor lung preservation, but related ultrastructural studies are rare in the literature. This study was performed to assess the ultrastructural changes and to evaluate the protective effect of NO as donor nitroglycerin (NTG) treatment of ischemia-reperfusion injury in rat lungs.Materials and Methods. Fifteen Sprague-Dawley rats weighing 300 to 350 g were used in this study. The NTG group (n = 5) used intravenous administration followed by mixture in the University of Wisconsin (UW) solution. For the non-NTG group (n = 5), we injected the same amount of normal saline intravenously followed by admixture in the UW solution. The heart-lung blocks were removed, weighed, and kept in UW solution for 24 hours at 10degreesC. Reperfusion using human blood diluted in Krebs-Hensleit solution was done for 60 minutes. For the control group (n = 5), we injected the same amount of normal saline intravenously, and removed the lungs with no preservation and reperfusion procedures.Results. The non-NTG group showed multiple patchy areas of alveolar collapse with marked swelling and destruction of type I epithelial cells, loss of type 11 cell surfactant granules, endothelial swelling and papillary projection, interstitial edema, and alveolar macrophages with active phagocytosis of the destroyed materials. The NTG group showed similar ultrastructural changes, but in a lesser severity compared with the non-NTG group.Conclusion. Administration of the NTG reduced the ischemia-reperfusion injury in the rat donor lungs. Ultrastructural examination was an effective tool to evaluate the protective effect of NTG in ischemia-reperfusion procedures of donor lungs.