Grażyna Nowaczyk

Immunolocalization and Expression of Kallistatin and Tissue Kallikrein in Human Inflammatory Bowel Disease

The distribution of tissue kallikrein (TK) and its plasma inhibitor, kallistatin in plasma and intestinal tissue, was studied in patients with active ulcerative colitis (UC) and Crohns disease (CD). TK was localized to goblet cells and kallistatin to epithelial cells of normal human intestine. Both proteins are visualized in macrophages inside granulomas in CD as well as in plasmocytes in both CD and UC. Intestinal tissue kallikrein (ITK) and kallistatin are significantly decreased in inflamed intestine compared to noninflammatory controls. TK mRNA is significantly decreased in intestinal biopsy samples from active UC patients compared with inactive patients or controls. Immunoreactive TK is present in plasma in very low concentrations in patients and did not differ in normal subjects. Plasma kallistatin was significantly decreased in patients with active disease compared to normal controls. Our data suggest that release of TK during inflammation plays a role in inflammatory bowel disease.

A new outside stent – does it prevent vein graft intimal proliferation?

OBJECTIVE The saphenous vein subjected to arterial pressure stretches to its elastic limits and constitutes intimal hyperplasia. Sheathing of the vein graft with pressure-resistant tubing might prolong vein graft patency. METHODS Twenty-one sheep received radial vein grafts or hybrid grafts composed of radial vein, collagen fibrin glue and highly flexible torlen/dacron mesh tubing transplanted into the carotid artery position. Veins were examined with the use of light and electron microscopy. Proliferating cell antigen (Ki-67) stains served as markers of proliferation. RESULTS The mean wall thickness of both intimal and medial layers was evaluated. The mean intimal wall thickness was 19+/-11 microm in hybrid grafts vs. 24+/-7 microm in unsheathed grafts (P<0.001); 22+/-6 vs. 26+/-10 microm (P<0.001); 23+/-8 vs. 52+/-15 microm (P<0.001); 37+/-21 vs. 90+/-31 microm (P<0.001); 57+/-31 vs. 104+/-28 microm (P<0.001); 58+/-21 vs. 133+/-32 microm (P<0.001); and 72+/-22 vs. 244+/-100 microm (P<0.001) after respectively 5 days, 9 days, 4 weeks, 6 weeks, 8 weeks, 10 weeks and 12 weeks from implantation. Electronic microscope examination of hybrid grafts revealed a smooth endothelial layer with intact nuclei and an intima composed of layers of collagen and muscle fibers. In unsheathed grafts endothelial edema and nuclear destruction were observed. CONCLUSIONS The external vein graft support with mesh tubing reduces intimal and medial layer thickening and cell proliferation in composite vein grafts transplanted in the arterial position.

Glucose-6-phosphatase and age: biochemical and histochemical studies

Glucose-6-phosphatase catalyzes the final reactions in both gluconeogenesis and glycolysis. It occurs mainly in glycogenic tissues, such as the liver, where it plays an important role in the synthesis of glucose, a carbohydrate essential for tissue functioning. The effect of age on liver glucose-6-phosphatase activity was evaluated in male Wistar rats treated with mixed function oxidase system (MFO) inducers. The rats were divided into the following age groups: 0.5, 1, 2, 4, 8, 12, 20 and 28 months of age. Glucose-6-phosphatase activity was evaluated biochemically and histochemically. Biochemical glucose-6-phosphatase activity increased up to the 20th month of rat life and then decreased rapidly. A similar tendency was observed in inducer-treated groups, though only dexamethasone stimulated this enzyme activity in all age groups studied. Histochemical glucose-6-phosphatase activity was strongest in the periportal zones. Glucose-6-phosphatase activity decreased significantly at month 8 and then it increased significantly until month 20. In the oldest age group, glucose-6-phosphatase activity decreased again. On histochemical analysis, the inducers used variably affected glucose-6-phosphatase activity.

Processes of apoptosis and cell proliferation in uterine myomas originating from reproductive and perimenopausal women

We studied uterine myomas originating from females of reproductive age and from females of perimenopausal age. Uterine myomas represent benign tumors of the myometrium, and they develop frequently in women of reproductive age. The frequency of uterine myomas increases with age until women reach the menopause. The study included patients with a myomatous uterus, in the reproductive age or peri-menopausal age, independently evaluating small and large myomas. Myometrial alterations in their direct vicinity were evaluated independently of the myomas. The study included evaluation of immunolocalization of two index proteins which participate in myoma cells growth control: Ki-67 nuclear antigen and caspase 3. In women of reproductive age, both in small and large myomas, elevated immunostaining of Ki-67 was noted in parallel to low levels of caspase 3 staining, which indicated the ongoing process of proliferation. In women of peri-menopausal age with small or large myomas, no Ki-67 immunostaining was detected, while staining of caspase 3 manifested low levels. Proliferation in reproductive age women myomas is higher than in the peri-menopausal age.

The aromatase expression in myomas and myometriums of women in reproduction and perimenopausal age.

Uterine myomas represent one of the most common female pathologies. Uterine smooth muscle myomas or fibromas are benign tumours which respond to hormones and their etiology induces wide interest. The myomas were found to contain aromatase and, in addition, cells of the myomas were found to synthesize estrogen. This study was conducted on patients with the myomas, in either generative age or in the perimenopausal period. Expression of aromatase was detected in patients of various age, with large or small uterine myomas, using an immunohistochemical technique. In addition expression of the enzyme was examined at the periphery of every myoma.

Expression of Estrogen Receptors in Placentas Originating from Premature Deliveries Induced by Arterial Hypertension

Till the end of 1980s transmission of the message carried by the hormone was thought to be mediated by a single estrogen receptor only. In the mid 1990s studies were published which described the discovery of a new estrogen receptor in both animals and humans [4-7]. The new estrogen receptor, ER-proved to be highly homologous to the classical estrogen receptor, ER- Functional differences at the molecular level between ER- and ER- are of principal importance for the body. Just as importantly, in the case of estrogen receptors the same ligand may play role of either an agonist or antagonist, depending on whether it binds to ER- or ER-. Therefore, following binding of the ligand ER- and ER- may induce distinct biological effects, linked to conformational changes of the receptor [8].