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Biomedical subjects

M Sulkowska

Publications and source records attributed to M Sulkowska.

At least 19 recordsLinked to original sources
PubMed2000

[Expression of PCNA antigen in cellular proliferative activity of cervical carcinoma].

The proliferative activity of cervical carcinoma was examined using proliferating cell nuclear antigen (PCNA) staining. Labelling index (LI) have been counted in sections of routinely processed paraffin embedded tissue blocks. Significant variation in PCNA LI were observed between study groups (p < 0.0235). The results obtained indicate that the evaluation of proliferative activity of cells expressed by high PCNA LI is assessed with worse prognosis.

Carcinoma↗
PubMed2000

[Heterogeneity of ovarian epithelial tumors in analysis of nucleolar organizer regions (NORs) expression].

Nonhistone proteins associated with the nucleolar organizer regions (NORs) can be visualized by a silver-staining technique on paraffin-embedded tissues. The number of black dots (AgNORs) appearing on the nuclei are thought to reflect cell differentiation and can be used as a measurement of cellular proliferative activity. In this study we tested AgNOR staining in ovarian epithelial tumors to evaluate its diagnostic potential in distinguishing between borderline tumors and carcinomas.

Adult↗
PubMed1999

Occlusion of pulmonary vessels by megakaryocytes after treatment with tumour necrosis factor-alpha (TNF-alpha).

Pulmonary thrombosis in the course of shock remains life-threatening, despite advances in diagnosis, prophylaxis and therapy of the disease. Tumour necrosis factor-alpha (TNF-alpha) is an important mediator of shock. The aim of this study was to analyze the morphological changes in the pulmonary capillary bed in rats after intraperitoneal administration of multiple doses of TNF-alpha (10 microg TNF-alpha/24 h for 5 days; biological activity of 2-4x10(7)U/mg of protein). Morphological investigations were undertaken by light and transmission electron microscopy with emphasis on pulmonary thrombopoiesis. The study confirmed that the lungs may be an important site of extramedullary thrombopoiesis in the course of shock. The observations also suggested that megakaryocytes shed large fragments of cytoplasm within the pulmonary capillary bed and that megakaryocytes with copious cytoplasm occlude pulmonary vessels.

Animals↗
PubMed1999

Alveolar cells in cyclophosphamide-induced lung injury. II. Pathogenesis of experimental endogenous lipid pneumonia.

An ultrastructural and histological study was made to analyse the structural and cellular features of the pulmonary lesions produced in Wistar rats by intraperitoneal (i.p.) administration of cyclophosphamide (two i.p. doses of 150 mg CP/1 kg bw/1 ml PBS). Rats exposed to cyclophosphamide (CP) developed a condition whose morphological picture corresponded to endogenous lipid pneumonia and/or pulmonary alveolar proteinosis-like changes. Damage to the endothelium and neutrophil accumulation in lung vascular bed were found to be potential initiators of endogenous lipid pneumonia-type changes. The possibility of the evolution of the acute lung injury into endogenous lipid pneumonia-type changes and into alveolar proteinosis-like changes was demonstrated. The results of the study supplement the existing theories of pulmonary alveolar proteinosis pathogenesis.

Animals↗
PubMed1999

Comparative studies on the ultrastructure of the rat lungs after intratumor treatment of Morris hepatoma with rhTNF-alpha and its muteins.

The aim of the present study was the comparative analysis of morphological changes found in the lungs of Buffalo rats in the course of Morris hepatoma 5123 after i.t. treatment with recombinant human TNF-alpha (rhTNF-alpha) and its muteins. Modification of the native TNF-alpha molecule and synthesis of mutagenized analogues can prevent undesirable symptoms observed in the case of therapeutic administration of rhTNF-alpha. TNF-alpha has been shown to interact with two distinct membrane receptors (TNF-R): p55R and p75R. Mutagenized mutein V binds selectively with p55R. Mutein VI fails to recognize either TNF-R. The cytokines were applied in a dose of 10 micrograms protein in a cycle of 8 days. The control group consisted of tumor-bearing animals which were given PBS. Ultrastructural examinations were based on transmission electron microscope (TEM). Mutein VI-receiving animals showed enhanced changes of cytotoxic nature. Severe damage to endothelial cells (necrosis inclusive) was observed. Blood vascular lumen showed accumulation of neutrophils and monocytes. Features of enhanced activity of endothelial cells were noted. Focally, within pulmonary alveoli conglomerates of fibrin and fragments of damaged cells were found, with erythrocytes, neutrophils and macrophages in their vicinity. The epithelium of pulmonary alveoli showed signs of considerable damage, including necrosis. The lumen of pulmonary capillaries in rhTNF-alpha-treated animals showed a predominance of eosinophils and monocytic cells. Features of endothelial stimulation were observed, although without a tendency to form microthrombi. Much less pronounced changes both in the lung capillary bed and in the alveolar epithelial cells were noted in the mutein V-given animals. Our findings confirm the possibility of peripheral activation of cells involved in the cytokine-induced antitumor response. Mutein V with the smallest effect on the lung tissue rebuilding seems to be a rhTNF-alpha derivative which can delimit the undesirable symptoms in the course of antitumor therapy reduced to i.t. injections.

Animals↗
PubMed1999

The effect of pentoxifylline on ultrastructure and antioxidant potential during cyclophosphamide-induced liver injury.

The aim of this study was to evaluate the effect of pentoxifylline (PTXF) (30 mg/kg b.w. for 10 days) on the antioxidant potential in the rat liver after single intraperitoneal (i.p.) cyclophosphamide (CP) administration (150 mg/kg b.w.) and to draw a correlation between the morphological changes and biochemical findings. Morphological examinations were based on ultrastructural analysis in the transmission electron microscope. It was found that single i.p. CP administration caused destructive changes, particularly within mitochondria and in the smooth endoplasmic reticulum of hepatocytes. The changes were accompanied by an increase in the MDA (malondialdehyde) level in liver tissue homogenates. The animals receiving PTXF + CP showed no normalization of MDA level, the same damage of the liver as those given CP, and marked statistically significant decrease in the activity of GSH/Px (glutathione peroxidase) compared to CP-receiving animals. No statistically significant differences were revealed in the activity of Cu,Zn-SOD and GSSR (superoxidase dismutase, glutathione reductase) both between control animals and CP- or CP + PTXF-receiving groups, or between CP and CP + PTXF groups.

Animals↗
PubMed1999

Gap junctional intercellular communication and carcinogenesis.

Intercellular communications are indispensable for the maintenance of homeostasis in the multicellular organisms. Gap-type junctions are one of the most common and perhaps most interesting intercellular connections. Of various communication systems gap junctional intercellular communication is the only means for cells to directly exchange signals. Substantial progress has recently been made in the studies on the role of gap junctions both in experimental and human tumorigenesis. The present study is a review of the potential mechanisms associated with gap junctional cellular communication included in non-genotoxic tumorigenesis.

Animals↗
PubMed1999

[Immunohistochemically expression of the protein p53 evaluated in invasive squamous cell carcinoma of the cervix].

The p53 protein expression in the invasive squamous cell carcinoma of the cervix was evaluated immunohistochemically. Its predictive role in the correlation with histological grading and staging was analyzed. 13.7% of examined cases (10/73) presented positive protein expression. There was no correlation between the intensified protein p53 expression and particular prognostic histological factors.

Adult↗
PubMed1998

Cyclophosphamide-induced generation of reactive oxygen species. Comparison with morphological changes in type II alveolar epithelial cells and lung capillaries.

Cyclophosphamide (CP) causes lung toxicity in animals and humans. The mechanisms of pulmonary damage caused by CP are not fully understood. Possibilities include direct toxicity to pulmonary tissue or indirect toxicity through activation of pulmonary inflammatory cells. The aim of the present study was the ultrastructural analysis (in transmission electron microscope) of the changes following CP administration within the structures forming the interalveolar septum of the lungs, particularly type II epithelial cells. An attempt was also made to reveal a correlation between the morphological changes, intensity of lipid peroxidation in lung tissue homogenates and blood serum collected from the left ventricle of the heart and the alterations in the activities of superoxide dismutase (Cu, Zn-SOD) and glutathione reductase (GSSG-R). The experiment used 40 male Wistar rats of 160-180 g body weight (b.w.). The animals were divided into two groups. Group I - (20 animals) were given single intraperitoneal (i.p.) dose of 150 mg CP/1 kg b.w./1 ml PBS. Group II - (20 animals) were given single i.p. dose of 1 ml PBS. All experimental animals were sacrificed after 1 (subgroups I, II-1) and 7 (subgroups I, II-7) days of CP (or PBS) treatment. I.p. administration of CP caused an increase in lipid peroxidation products (MDA-malondialdehyde) in lung tissue homogenates especially in subgroup I-1 (p = 0.00174). No statistical differences, however, were noted in the blood serum MDA levels, although a statistically significant decrease was found in GSSG-R (p = 0.00174) and SOD (p = 0.00174) activities in the serum. The paper discusses a potential link between the findings of biochemical analysis and the morphological changes found within lung tissue. Pulmonary trombopoesis was indicated as a possible mechanism preventing a decrease in blood platelet count following CP administration.

Animals↗
PubMed1998

The effects of cyclophosphamide on pulmonary thrombopoiesis in rats.

Cyclophosphamide (CP), an antineoplastic and immunosuppressive agent, even when administered in large doses, slightly affects the quantity of blood platelets. The aim of the present study was to analyse the effect of single intraperitoneal administration of CP (150 mg/kg b.w.) on the quantitative changes in platelets obtained from the left and right ventricle of the heart, as well as to evaluate the occurrence of megakaryocytes in lung tissue depending on the period of time that passed from CP administration. In control subgroups, fewer platelets were found in the blood collected from the RV compared with the left ventricle at all time intervals. After 1 and 3 days following i.p. administration of CP, a decrease was observed in the number of platelets both in the blood from the right ventricle and left ventricle when compared with control. However, after 14 days, the number of platelets in the blood from the left ventricle was higher, compared with the left ventricle and right ventricle of control animals, and significantly higher (p < 0.001747), compared with their number obtained from the right ventricle of CP-receiving animals. Simultaneous ultrastructural examinations with transmission electron microscopy revealed the increased number of platelets in the lung vascular bed of CP-receiving rats at all time intervals. However, megakaryocytes were found 7 and 14 days after administration of CP. The findings clearly indicate that the lungs could be a major place of thrombopoiesis following therapy with a single large dose of CP.

Animals↗
PubMed1998

Alveolar cells in cyclophosphamide-induced lung injury. An ultrastructural analysis of type II alveolar epithelial cells in situ.

Recent studies have brought rich evidence in favour of the significant contribution of the surfactant system-forming structures to morphogenesis of many pulmonary disorders. The aim of this study was to evaluate the effect of intraperitoneal cyclophosphamide administration on changes within this system. The experiments used 40 Wistar rats, of 170 g body weight. The animals were divided into two experimental groups. Group I animals were given cyclophosphamide (Endoxan-ASTA) in a single intraperitoneal dose of 150 mg/1 kg b.w./1 ml PBS/. Group II (control) received 1 ml PBS. All the animals were sacrificed after 1, 3, 7 and 28 days following intraperitoneal cyclophosphamide or PBS administration. Morphological examinations of pulmonary tissue were based on ultrastructural analysis in the transmission electron microscope. The study revealed that a single intraperitoneal cyclophosphamide injection caused damage to all elements forming the surfactant system, particularly to type II alveolar epithelial cells. Rebuilding processes in pulmonary tissue, coexisting with destructive changes, occurred with a significant contribution of type II alveolar epithelial cells. These cells are likely to take an active part in pulmonary fibrosis processes observed after the action of cyclophosphamide.

Animals↗
PubMed1998

Apoptosis-like changes in the lungs induced by cyclophosphamide and papain. I. An ultrastructural study.

An ultrastructural study was made to analyze the structural and cellular features of the pulmonary lesions produced in Wistar rats by the administration of cyclophosphamide (CP) and/or papain (P). Combined administration of cyclophosphamide and papain caused severe damage to lung tissue including necrosis, particularly to alveolar epithelial and endothelial cells. Some of the damaged type II cells showed nuclear and cytoplasmic features that are considered indicative of apoptosis. Apoptosis-like changes were also observed in endothelial and mesenchymal cells in the interstitium of interalveolar septa. Phagocytosis of apoptotic bodies by macrophages was found too. Apoptosis-like changes were not revealed in those areas of lung tissue where fibroplasia processes prevailed. Nor were they observed in the animals receiving papain only. Occasionally apoptosis-like changes were found in type II cells and in endothelial cells in rats given cyclophosphamide only. The results obtained also suggest the possibility of active participation of type II alveolar epithelial cells in the fibroplasia process in the course of lung rebuilding in acute lung tissue damage induced with simultaneous administration of cyclophosphamide and papain.

Animals↗
PubMed1998

[Chronic cor pulmonale--a disease of the right or both ventricle(s) of the heart?].

Some aspects of the development of chronic cor pulmonale have been presented. Special attention has been paid to the possibility of simultaneous formation of changes in the muscle of both ventricles of the heart and to an increase in the number of capillaries in the myocardium in the early stage of this disease. Angiogenesis, the role of hypoxia and endothelins in the pathogenesis of these changes have been discussed.

Chronic Disease↗
PubMed1998

Alveolar cells in cyclophosphamide-induced lung injury. The effect of pentoxifylline on BAL-isolated cells.

The present study provides the evaluation of pentoxifylline (PTXF) effect on quantitative and morphological changes of cells isolated from the lungs by BAL method in animals given cyclophosphamide (CP). CP was administered once, intraperitoneally, on the 7th day of the experiment, in a dose of 150 mg/kg b.w. PTXF was administered in drinking water in a dose of 30 mg/kg b.w./24 h for 14 days of the experiment. Morphological examinations of the isolated cells were performed using the scanning electron microscope (SEM). An attempt to identify type II alveolar epithelial cells was also undertaken. A single CP dose caused a significant rise in the total number of cells isolated from the lungs of the animals 7 days following CP administration. At the same time, a fall was noted in the percentage of neutrophilic granulocytes. No significant quantitative changes were observed in the population of cells isolated after 1, 3 and 28 days following CP administration. PTXF, in doses applied, did not significantly affect quantitative changes and morphological picture of the isolated cells. Our observations suggest that none of the methods applied for identification of type II pneumocytes are completely specific. At the same time they stain type II cells and subpopulations of alveolar macrophages heavily loaded with phagocytized surfactant. However, those methods are simple and enable an approximate evaluation of damage and regeneration processes in the extracellular alveolar lining layer and epithelium.

Alkaline Phosphatase↗