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Y Kapanci

Publications and source records attributed to Y Kapanci.

At least 19 recordsLinked to original sources
PubMed1999

A case of endometrioid carcinoma of the fallopian tube mimicking an adnexal tumor of probable Wolffian origin.

We report a very uncommon case of endometrioid adenocarcinoma of the fallopian tube that mimicked, based on histology, a female adnexal tumor of probable Wolffian origin (FATPWO). We present our microscopic and immunohistochemical findings, and a review of the literature concerning these two entities. The differential diagnosis can be of great consequence, owing to the very different prognoses of the two tumors, and is based mainly on macroscopic appearance and immunohistochemical profile: epithelial membrane antigen (EMA) and CA125, generally lacking in FATPWO, are expressed in endometrioid adenocarcinoma, thus indicating the müllerian origin of this tumor.

Aged↗
PubMed1999

Beneficial effects of leukocyte-depleted blood and low-potassium dextran solutions on microvascular permeability in preserved porcine lung.

Modified Euro-Collins (EC) solution, a crystalloid intracellular-type solution, has been commonly used for pulmonary preservation. Several experimental studies have shown the advantages of using extracellular colloid-based solutions. The aim of this study was to compare the quality of preservation of two extracellular colloid solutions, leukocyte-depleted blood (BL) and low-potassium dextran (LPD) solutions, with that of EC solution. Lungs of 22 domestic pigs were flushed and preserved with EC (n = 8), BL (n = 7), or LPD (n = 7) solution. After harvesting, one of the lungs was reperfused immediately in an ex vivo circuit (control lungs), whereas the contralateral lung was reperfused after 8 h of cold (4 degrees C) storage (preserved lungs). Besides the lung function parameters (gas exchange, pulmonary hemodynamics and mechanics), the permeability of the endothelial-epithelial barrier was assessed by determining the transferrin leak index (TLI) using a double radioisotopic method, by measuring the alveolar/arterial protein concentration ratio, and by analyzing histopathologic changes. The functional quality (oxygenation, airway resistance, dynamic compliance [CL, dyn]) of both BL and LPD lungs was slightly but significantly superior to that of EC lungs. However, pulmonary vascular resistance was lower in BL-preserved than in EC- or LPD-preserved lungs. The TLI was increased in EC control and preserved lungs, whereas it was low in BL and LPD control lungs and did not increase after preservation. The alveolar/arterial protein concentration ratio was not different between control groups, but was increased fourfold in EC-preserved compared with BL- or LPD-preserved lungs. Finally, EC-preserved lungs presented a weight gain about twice that of BL- and LPD-preserved lungs. Morphologic analysis confirmed these results, because in the EC-preserved lungs, rupture of alveolar septa and severe alveolar edema and hemorrhage were observed, whereas BL- and LPD-preserved lungs showed a relatively well-preserved structure. The results demonstrate that both BL and LPD flush solutions preserve the endothelial-epithelial barrier better than does EC solution. Although the quality of preservation is similar, pulmonary vascular resistance is higher in LPD-preserved than in BL-preserved lungs.

Animals↗
PubMed1998

Metastizing low-grade clear cell leiomyosarcoma of the uterus.

An unusual case of uterine clear cell tumor is reported in a 56-year-old woman. The neoplasm was identified as a peculiar low-grade leiomyosarcoma, composed mainly of watery, clear large cells with round, fairly regular nuclei. No appreciable pleomorphism or high mitotic activity was noted. There was no necrosis. The presence of occasional areas of transition between these cells and typical spindle leiomyosarcoma cells, together with the immunohistochemical results, allowed the recognition of a smooth muscle origin of this clear cell tumor. The patient was treated by hysterectomy. Six years later she developed an inguinal metastasis resembling an hibernoma, and then later developed a large retroperitoneal metastasis, which was composed entirely of clear cells and was distinguished from a liposarcoma by immunohistochemistry.

Actins↗
PubMed1997

Phenotypic modulation of alveolar myofibroblasts in transplanted human lungs.

We examined 33 successive pulmonary biopsy specimens from nine patients who underwent pulmonary transplantation; they were compared to "normal" lung tissue selected from routine transbronchial biopsy material and also to surgical biopsy specimens from a previously reported study. We used as controls the three successive biopsy specimens from Patient 7, in whom rejection reaction did not develop, and the two specimens from Patient 6, who had pneumonia caused by cytomegalovirus. The material was embedded in paraffin, and the sections were stained by hematoxylin and eosin, periodic acid-Schiff, Masson's trichrome, and Gomori's silver stains. They were also immunostained for alpha-smooth muscle actin (alpha-SMA), desmin, transforming growth factor beta1, tumor necrosis factor alpha, keratin, CD3, CD20, CD68, and HLA-dr. In all of the lung tissue from patients in whom a rejection reaction developed, alveolar myofibroblasts (MFs) expressed alpha-SMA. Sometimes, alpha-SMA expression appeared before the classical manifestations of rejection reaction. MFs labeled by alpha-SMA antibody did not express desmin; alveolar septa containing alpha-SMA-positive cells were frequently lined by transforming growth factor beta1 and, occasionally, tumor necrosis factor alpha-laden Type II pneumocytes. In lung tissue (from successive biopsies) that did not show evidence of rejection reaction, alveolar MFs did not express alpha-SMA. Our findings demonstrate that modulation of alveolar MFs is one of the manifestations of rejection in transplanted lungs; furthermore, they suggest that alpha-SMA staining might be useful in predicting rejection reaction before the classical cellular events occur.

Acute Disease↗
PubMed1995

Cytoskeletal protein modulation in pulmonary alveolar myofibroblasts during idiopathic pulmonary fibrosis. Possible role of transforming growth factor beta and tumor necrosis factor alpha.

Pulmonary biopsy specimens from ten cases of idiopathic pulmonary fibrosis (IPF) were examined using routine histological stains, including toluidine blue, and immunohistochemistry by means of specific antibodies against alpha-smooth muscle (alpha-SM) actin, desmin, keratin, TGF beta 1, and TNF alpha. The sections were compared with two cases of normal lung. As shown previously, normal alveolar interstitium did not contain alpha-SM actin positive myofibroblasts nor did the alveolar lining contain any significant number of TGF beta 1 or TNF alpha laden epithelial cells. In IPF, during the inflammatory stage, the alveolar myofibroblasts expressed alpha-SM actin and the regenerating type II alveolar epithelium staining strongly with TGF beta 1 and TNF alpha antibodies. The former cytokine was also detected in the interstitial matrix and fibroblastic cells as well as in the wall of vessels. At this stage, a manifest mast cell infiltration was noted. In very fibrotic and cystic alveolar tissue, i.e., at end stage fibrosis, the number of alpha-SM actin positive myofibroblasts as well as that of TNF alpha laden type II epithelial cells diminished, while TGF beta 1 positive cells persisted. Our findings demonstrate that during IPF alveolar type II epithelium constitutes, if not the site of synthesis, at least the main reservoir for TGF beta 1 and TNF alpha. These cytokines, besides their involvement in fibrogenesis, play probably an important role in the expression of alpha-SM actin by alveolar myofibroblasts. Our study suggests the possibility of an interaction between interstitial cells and alveolar epithelium, during IPF.

Actins↗
PubMed1995

Expression of a tumor necrosis factor-alpha transgene in murine lung causes lymphocytic and fibrosing alveolitis. A mouse model of progressive pulmonary fibrosis.

The murine TNF-alpha gene was expressed under the control of the human surfactant protein SP-C promoter in transgenic mice. A number of the SP-C TNF-alpha mice died at birth or after a few weeks with very severe lung lesions. Surviving mice transmitted a pulmonary disease to their offspring, the severity and evolution of which was related to the level of TNF-alpha mRNA in the lung; TNF-alpha RNA was detected in alveolar epithelium, presumably in type II epithelial cells. In a longitudinal study of two independent mouse lines, pulmonary pathology, at 1-2 mo of age, consisted of a leukocytic alveolitis with a predominance of T lymphocytes. Leukocyte infiltration was associated with endothelial changes and increased levels of mRNA for the endothelial adhesion molecule VCAM-1. In the following months, alveolar spaces enlarged in association with thickening of the alveolar walls due to an accumulation of desmin-containing fibroblasts, collagen fibers, and lymphocytes. Alveolar surfaces were lined by regenerating type II epithelial cells, and alveolar spaces contained desquamating epithelial cells in places. Platelet trapping in the damaged alveolar capillaries was observed. Pulmonary pathology in the SP-C TNF-alpha mice bears a striking resemblance to human idiopathic pulmonary fibrosis, in which increased expression of TNF-alpha in type II epithelial cells has also been noted. These mice provide a valuable animal model for understanding the pathogenesis of pulmonary fibrosis and exploring possible therapeutic approaches.

Animals↗
PubMed1995

[Histologic and immunohistochemical profiles of benign granular cell tumors. Report of 41 cases].

Since the descriptions of << myoblastomas >>, later denominated granular cell tumours, many immunohistological and ultrastructural studies have been undertaken with the aim of establishing their histogenesis. Now the hypothesis of a neurogenic origin appears clear. From the large number of cases (53) diagnosed in Geneva over a period of 10 years, we decided to do a retrospective study of these tumours with regard to their immunohistological phenotypes, using the following markers: S100 protein (S100), Neuron specific enolase (NSE), Vimentin, Chromogranin, Glial fibrillary acidic protein (GFAP), Keratin, Epithelial membrane antigen (EMA), Desmin, Smooth muscle alpha actin. 100% of tumours were positive for S100, and 90% for NSE, which confirms the neurogenic origin. 70% were Vimentin positive, with however a variable intensity. All the other markers were negative. Immunohistological staining for S100 and NSE may be useful tool in the diagnosis of these tumours.

Adult↗
PubMed1994

[Endocrine tumors of the pancreas: immunohistochemical and clinical correlation].

24 out of 28 cases of pancreatic endocrine tumors were studied by immunohistochemistry. They comprised 11 insulinomas, 3 gastrinomas, 1 VIPoma, 1 glucagonoma and 8 with no endocrine syndrome. 7 patients presented metastasis by the time of diagnosis. In 14 out of 16 cases of tumors with endocrine syndrome, there was a good correlation between clinical syndrome and histological findings. Half of these neoplasms showed positivity for more than one hormone but only one cell type predominated which was responsible for the endocrine syndrome. The other hormonal stainings had no clinical expression. Bouin- or Dubosq-fixed samples allowed a better immunohistochemical analysis than for formalin-fixed tissues. Chromogranin was found to be the best general marker for endocrine tumors. Immunohistochemical staining, when positive, generally showed a diffuse coloration of the cytoplasm. Sometimes it resembled a "coup d'ongle" or a single granular staining, but its significance is still unknown.

Adult↗
PubMed1994

Morphological and immunochemical differences between keloid and hypertrophic scar.

There are two types of excessive scarring, keloid and hypertrophic scar. Contrary to hypertrophic scars, keloids do not regress with time, are difficult to revise surgically, and do not provoke scar contractures. These two lesions require different therapeutic approaches but are often confused because of an apparent lack of morphological differences. We have investigated the collagen organization and the possible presence of alpha-smooth muscle (SM) actin-expressing myofibroblasts in these conditions. Keloids contain large, thick collagen fibers composed of numerous fibrils closely packed together. In contrast hypertrophic scars exhibit modular structures in which fibroblastic cells, small vessels, and fine, randomly organized collagen fibers are present. We confirm that such nodular structures are always present in hypertrophic scar and rarely in keloid. Furthermore, only nodules of hypertrophic scars contain alpha-SM actin-expressing myofibroblasts. Electron microscopic examination supports the above-mentioned differences in collagen organization and in fibroblastic features and shows the presence of an amorphous extracellular material surrounding fibroblastic cells in keloid. The presence in hypertrophic scar myofibroblasts of alpha-SM actin, the actin isoform typical of vascular SM cells, may represent an important element in the pathogenesis of contraction. Interestingly, when placed in culture fibroblasts from hypertrophic scars and keloid express similar amounts of alpha-SM actin, suggesting that local microenvironmental factors influence in vivo the expression of this protein. Thus several morphological and immunohistochemical differences exist between hypertrophic scar and keloid that are useful for the biological and pathological characterization of the two lesions.

Actins↗
PubMed1993

Rat alveolar myofibroblasts acquire alpha-smooth muscle actin expression during bleomycin-induced pulmonary fibrosis.

The majority of fibroblasts in alveolar septa are characterized by the presence of cytoplasmic bundles of microfilaments that contain cytoplasmic actin isoforms; these cells have been named contractile interstitial cells or V-type myofibroblasts. In the rat, they express desmin as intermediate filament protein. In this study, we explored the possibility that modulation and replication of such septal fibroblasts result in the appearance of alpha-smooth muscle (alpha-SM) actin-positive myofibroblasts, typical of lung fibrosis. Experimental pulmonary fibrosis was produced by a unique intratracheal instillation of bleomycin to 28 rats. Eight additional rats used as controls received the equivalent volume of saline. Paraffin and frozen sections of lungs were examined at days 1, 3, 5 and 7 after treatment. Microfilaments and intermediate filaments were stained using antibodies against total actin, alpha-SM actin, desmin, vimentin, keratin, and SM myosin. Electron microscopic labeling of desmin and alpha-SM actin using immunogold technique was done on Lowicryl K4M resin-embedded specimens. alpha-SM actin appeared in desmin-positive alveolar fibroblasts as early as 24 hours after intratracheal bleomycin instillation; the modulation of alpha-SM actin in these cells was preceded by a lymphomonocytic infiltration of alveolar septa. Twenty-four hours to 3 days after bleomycin administration, a proliferation of alveolar myofibroblasts occurred. Fibrosis with laying down of collagen fibers took place after the above mentioned cellular modifications. Our results support the view that septal fibroblastic cells can modulate into typical alpha-SM actin-containing myofibroblasts during experimental bleomycin-induced pulmonary fibrosis. In such a modulation a possible role of cytokines, particularly of transforming growth factor-beta, is considered.

Actin Cytoskeleton↗
PubMed1993

Expression and localization of tumor necrosis factor-alpha and its mRNA in idiopathic pulmonary fibrosis.

The expression of tumor necrosis factor alpha and its mRNA was investigated in surgical biopsies from idiopathic pulmonary fibrosis by immunohistochemistry, in situ hybridization, and Northern blotting. Normal areas of lungs resected for cancer were used as controls. Tumor necrosis factor alpha mRNA levels were higher in idiopathic pulmonary fibrosis than in normal lungs as determined by Northern blots. In normal lungs, tumor necrosis factor alpha and its mRNA were identified in alveolar and interstitial macrophages. In fibrotic lungs, tumor necrosis factor alpha was detected in macrophages and, to a greater extent, in epithelial cells (presumably type II cells) lining the thickened septae. Tumor necrosis factor alpha mRNA was found only in some interstitial cells and some of the cells lining the alveolar septae. An elevated concentration of tumor necrosis factor = alpha, particularly within the alveolar epithelium, might contribute to the alveolar damage and proliferation of interstitial cells in idiopathic pulmonary fibrosis.

Adult↗
PubMed1992

Hepatitis B virus, alpha-fetoprotein synthesis, and hepatocellular carcinoma in Zaire.

We investigated the epidemiology of hepatocellular carcinoma (HCC) in Zaire, and evaluated the association between exposure to hepatitis B virus (HBV) and the development of HCC. Two hundred and twenty-three consecutive cases of HCC diagnosed over 19 years (1966-1985) were reviewed. HCC represented 8.32% of all carcinomas and 5.56% of all cancers. Frequency was higher in males (75.7%) than in females (24.3%); a sex ratio of 3/1. The majority (82.1%) of patients were aged 14 to 55 years with a peak occurrence in the fourth decade (28.6%). The mean age in males (41.27 +/- 17.5 years) and females (37.40 +/- 15.16 years) was significantly different (p < 0.02). Sera from 40 patients and 68 age and sex-matched controls were analyzed for markers of HBV infection: patients and controls had comparable rates of exposure (96% vs 72.1%, respectively). However, patients had significantly higher HBsAg carrier rates (56.7% vs 7.35%; p < 0.001), and lower anti-HBsAg seroconversion rates (25% vs 63.2%, p < 0.05). Using immunohistochemical analysis, the livers of patients were evaluated for HBsAg and HBcAg. These HBV antigens were more frequent in non-tumourous hepatocytes (53.3% vs 23.3%, respectively) than in HCC cells (13.3% vs 3.3%). Serum alpha-fetoprotein (AFP) was abnormal (> 20 ng/ml) in 90% of patients. The geometric mean (GM) AFP was 7273.8 ng/ml. AFP levels were significantly higher in HBsAg-positive HCC cases (GM: 19,322.6 ng/ml; 95% confidence interval (CI): [3639.2, 102,565.2]) than in antigen negative cases (GM: 1939.5 ng/ml; 95% CI: [182.8, 19,952.6]), but did not correlate with HBV replication. Immunohistochemical detection of AFP revealed a similar correlation between AFP and HBsAg. Neither AFP level nor HBsAg production correlated with cellular atypia or tumor grade.

Adolescent↗
PubMed1992

Cytoskeletal features of alveolar myofibroblasts and pericytes in normal human and rat lung.

Frozen or paraffin-embedded human and rat lung specimens were stained with antibodies against total actin, alpha-smooth muscle (SM) actin, vimentin, desmin, or gelsolin. Alveolar interstitial myofibroblasts [i.e., contractile interstitial cells (CIC)] were labeled by total actin antibody but not by alpha-SM actin antibody. They stained for vimentin and gelsolin and, in rat lungs, most of them for desmin. Pericytes located around venules at the junction of three alveolar septa were always positive for alpha-SM actin and never for desmin. Tissue samples were also immunostained by an alpha-SM actin antibody and studied by electron microscopy. With this technique we confirmed that cells, identified as pericytes on the basis of their location, were intensely labeled by alpha-SM actin antibodies, whereas alveolar myofibroblasts were not. We conclude that in the lung interstitium pericytes and alveolar myofibroblasts have distinct cytoskeletal features, alpha-SM actin antibody staining being a simple method to distinguish between them. Furthermore, it appears that alveolar myofibroblasts have a peculiar pattern of cytoskeletal protein composition which, in the rat, is similar to that previously described for stromal cells in uterine submucosa, liver sinusoids (Ito cells), or the core of intestinal villi.

Actins↗
PubMed1991

[Primary malignant non-Hodgkin lymphomas of the digestive tract: the role of surgery].

Forty-two patients with non-Hodgkin's malignant lymphoma (NHML) of the gastrointestinal tract were operated on between 1971 and 1989. NHML was located in the stomach in 23 (55%), in the small bowel in 16 (38%), and in the colon in 3 (7%). One-fourth of patients were hospitalized with an acute abdomen and had to undergo emergency surgery. Preoperative diagnosis was obtained in 40% of cases only. Since 1986, however, and thanks to immunohistochemistry, gastroscopy was able to diagnose gastric NHML in 10 of 11 cases. Twenty-six patients (62%) underwent curative surgery. Operative mortality was 11.9%, 42% in case of emergency surgery, but mortality was nil after elective procedures. Half the patients had no further treatment. Five-year survival was 67%. Except for the mucosa associated lymphoid tissue (MALT) tumors, histopathological characteristics had less influence on prognosis than expected. On the other hand, prognosis was significantly better after curative surgery (p less than 0.001).

Female↗
PubMed1990

Histopathologic features of hepatocellular carcinoma in Zaire.

The pathology of hepatocellular carcinoma (HCC) was studied based on 223 Zairian HCC cases registered from 1966 to 1985. The observations included the following: (1) hepatitis B surface antigen (HBsAg) status, (2) histologic types, (3) degree of cellular differentiation, and (4) frequency and types of the accompanying cirrhosis. Serum HBsAg was positive in 56.7% of HCC patients and 5.7% of controls (P less than 0.001). Immunohistochemical localization of HBsAg was positive in 53.3% in normal hepatocytes and in 10% in neoplastic cells. Morphologically, mixed type HCC (48.4%), trabecular (31.4%), and compact variants (13.5%) were predominant. Clear cell and pseudoglandular variants were rare (less than 1%). The majority of tumors (83%) were poorly differentiated HCC (Grades: 2-3, 3, 3-4, and 4). Well-differentiated HCC were extremely rare (0.5%). Fifty percent of HCC arose in a cirrhotic liver, predominantly of the macronodular (67.4%) inactive (55%) type. The micronodular cirrhosis was very uncommon (1.1%). These findings clearly show the excess of poorly differentiated HCC in African patients and suggest a possible link between the morphologic features of HCC in Africa and its extraordinary fast-running course.

Adolescent↗
PubMed1990

Modulation of actin isoform expression in alveolar myofibroblasts (contractile interstitial cells) during pulmonary hypertension.

Lungs of 37 patients with pulmonary hypertension (PHT), 5 normal human lungs, and 30 normal rat lungs, were studied using immunohistochemical stainings for actin, alpha-smooth muscle (alpha-SM) actin and desmin. The type of PHT was determined on clinicopathologic grounds (in 17 cases by catheterism); 20 patients had precapillary and 17 postcapillary PHT. In normal lungs, myofibroblasts, ie, contractile interstitial cells (CIC), distributed in alveolar septa, were not stained by alpha-SM actin antibodies. Only around the venules, were cells labeled by this antibody present. Furthermore, there were bundles of alpha-SM actin-positive cells around the openings of air sacculi into the alveolar ducts. In precapillary PHT, the distribution and immunostaining properties of interstitial cells remained unchanged; alpha-SM actin-positive cells were observed in thickened arterial intima and in plexiform lesions. In postcapillary PHT secondary to heart failure, to mitral stenosis, or in veno-occlusive disease, many interstitial cells in the alveolar septa were decorated by alpha-SM actin antibodies but not with desmin. The authors propose that, in postcapillary PHT, mechanical stretch due to capillary congestion may be responsible for the generation of cells that express an actin isoform associated with smooth muscle.

Actins↗
PubMed1989

Tumor necrosis factor/cachectin plays a key role in bleomycin-induced pneumopathy and fibrosis.

The role of TNF-alpha/cachectin in the pneumopathy elicited by bleomycin has been investigated. After a single intratracheal bleomycin instillation, an increase of the lung TNF-alpha mRNA level was evident, from days 5 to 15, as shown by Northern gel analysis of whole lung RNA. In contrast, lung IL-1-alpha and GM-CSF mRNA were not detectable. In mice passively immunized with rabbit anti-mouse TNF-alpha IgG, the bleomycin-induced collagen deposition, evaluated by the total lung hydroxyproline assay on day 15, was prevented. Depletion of the CD4 and CD8 T lymphocytes by an in vivo treatment with mAb prevented the bleomycin-induced increase of TNF mRNA level and fibrosis. After an administration of bleomycin in continuous intraperitoneal perfusion, the diffuse alveolar damage observed by light and electron microscopy was almost completely prevented by anti-TNF antibody. These results indicate that in response to bleomycin, the T lymphocytes induce, by an undefined mechanism, an increase of the pulmonary TNF production, which leads to alveolar damage, growth of fibroblast, and collagen deposition.

Animals↗