Acta morphologica Hungarica最新文献

To determine the role of hypoxia in the evolution of tubular damage in acute pyelonephritis (PN), the blockage of blood flow and injury to peritubular capillaries and tubules were studied morphologically in hematogenous acute E. coli PN of rats. Renal microvessels were stained by in situ intraarterial administration of Alcian blue. The non-occurrence of staining indicated blockage of perfusion. Injury to cortical capillaries and tubules was examined by electron microscope. In areas of inflammation, binding of Alcian blue did not occur in capillaries plugged by polymorphonuclear leukocytes (PMNL-s) and in the majority of glomerules. Ultrastructurally, severe injury to capillaries was found around endothelium-adhered, degranulated PMNL-s containing bacteria: the vessel wall was fragmented, the capillary basement membrane perivascular connective tissue matrix and collagen fibrils had disappeared, and fibrin had deposited intra- and extravascularly. Tubular changes varied from swelling to ischemic necrosis. The observations suggest that tubular damage was related to hypoxia due to preglomerular and capillary perfusion defects, and that PMNL-s injure capillaries via lysosomal enzymes discharged into the capillary fluid during the phagocytosis of bacteria. Since leukocyte plugs in capillaries, PMNL-dependent lytic injury to capillaries and mild ischemic tubular changes, but not ischemic necrosis, have been found in human acute PN previously, the preglomerular vasospasm may cause the tubular necrosis in experimental acute PN.

The protein synthesis inhibitor cycloheximide is widely used (in vitro or in vivo) to inhibit the autophagic degradation of endogenous cellular proteins. Circumstantial evidence has been obtained largely from in vitro experiments for a similar effect of other translational inhibitors. In the present study, the in vivo effects of cycloheximide, emetine and puromycin on autophagy in murine exocrine pancreatic and liver cells were tested using electron microscopic morphometry. The experiments were based on the assumption that the autophagic compartment will regress if the formation of the vacuoles is blocked while degradation in the pre-existing vacuoles goes on. To make the measurements easier, autophagic compartment of the cells was greatly enlarged in both cell types by administering vinblastine (10 mg/kg b. wt.) for 2 h when the inhibitors were set on for an additional 30 min. During this half-an-hour, cycloheximide (0.2 mg/g b. wt.), emetine (0.12 mg/g b. wt.) and puromycin (0.2 mg/g b. wt.), respectively caused 58.5, 35.6, and 69.5% regression of the pancreatic and 46.7, 64.2, and 54.2% of the hepatocytic autophagic vacuole compartment. Thus, similarly to cycloheximide, both emetine and puromycin have proved to be inhibitors of autophagy in vivo. The results argue for a possible relationship between the synthesis and degradation of endogenous cellular proteins.

The nervous microganglia of the thyroid gland have been studied in forty adult male rats, their morphology being analyzed by the osmium-zinc iodide technique their acetyl-cholinesterase activity (AChE) by an histochemical specific technique and their mono-amine-oxidase activity (MAO) by a tetrazolium technique. Few but constant microganglia were observed in the thyroid glands. These microganglia are formed by some 4 to 8 nerve cells. Intense mono-amine-oxidase activity (MAO) was found in the nerve cells of these microganglia, being absent in the rest of the thyroid gland. Intense specific acetyl-cholinesterase (AChE) was observed in the nerve cells scattered along nerve branches located in the connective tissue (single nerve cells or small cellular groups). AChE activity was not observed in the microganglia of the thyroid gland.

The frequency and patho-histological characteristics of pulmonary changes were studied on the autopsy material of 100 patients with rheumatoid arthritis (RA). The formal pathogenesis and different stages of vasculitis, rheumatoid nodule, interstitial pneumonia, rheumatoid pleuritis, obliterative bronchiolitis, amyloidosis and the so-called rheumatoid pneumonia in the lungs is discussed. The rheumatoid pneumonia is a disseminating inflammatory lobular-sublobular process, not described previously. The frequency of rheumatoid pneumonia was 4%. The rheumatoid pneumonia is characterized by the necrotic vasculitis, fibrinoid necrosis or thrombovasculitis of the pulmonary and bronchial arterioles, and of small arteries. Because of the diminished blood supply distal to the vascular changes inflammatory foci may develop, more or less respecting the anatomic borders of pulmonary tissue. The lobular-sublobular inflammation is basically of non haemorrhagic character. Because of the recurrent nature of vasculitis, foci of inflammation in different stages can be observed in the lungs simultaneously side by side. Clinically the rheumatoid pneumonia was accompanied by severe RA, according to the frequency and severity of acute exacerbations. In all 4 cases of rheumatoid pneumonia the pulmonary process had been proven clinically and radiologically. Rheumatoid pneumonia occurred subsequent to recurrent arthritis following steroid withdrawal, and it was resistant to antibiotics.

Spontaneous cytotoxic activity of peripheral blood lymphocytes directed against chicken red blood cells has been studied in 12 healthy adults by photometric measurement of the hemoglobin released from the targets. Lymphocytes forming rosettes with chicken red blood cells (ChRBC-rosette positive lymphocytes) were separated from ChRBC-rosette negative cells by Ficoll gradient centrifugation. Isolated ChRBC-rosette positive cells were characterized as small lymphocytes with a dot like (focal) cytoplasmic acid hydrolase enzyme reaction and expression of CD 4 (helper-T-cell), CD 11b (monocyte) and CD 16 (natural killer cell) immunophenotype. In the second part of our work the spontaneous cytotoxic activity against ChRBCs of adherent cells, sheep red blood cell (SRBC) rosette negative and positive cells. IgG-Fc-receptor negative and positive lymphocyte subsets was studied simultaneously using monoclonal antibody markers and detecting immunoglobulin production and IgG-Fc-receptor positive cells ("suppressor-T-lymphocytes") had the highest ChRBC-cytotoxic-activity in parallel with their Leu 11b (CD 16) NK-cell marker positivity. The "suppressor-T-lymphocytes" and also the isolated ChRBC-rosette positive cells showed a suppressor effect on immunoglobulin production in co-cultures. ChRBC-rosette positive cells expressed significant natural killer activity against K-562 targets, but not a killer activity in ADCC assay. It needs further examinations to determine the functional role and the origin of ChRBC-cytotoxic cells with these unique immunophenotype and functional characteristics.

Tissue transglutaminase (TG) positive tumour cells in MXT mouse mammary cancer were localized by immunohistochemistry. The number of TG-positive tumour cells increased after treatment with analogs of luteinizing hormone-releasing hormone (LH-RH) and somatostatin, which inhibit tumour growth by the enhancement of apoptosis (programmed cell death). TG positivity has been previously reported to be closely linked with apoptosis. In this study, the increase in the number of TG positive tumour cells after hormonal treatment was well correlated with the augmented apoptotic index, i.e. the ratio of tumourous glandular structures which contained tumour cells showing the signs of programmed cell death. TG-positive tumour cells are, therefore, believed to be undergoing programmed cell death.

Fetuses of pregnant CD-1 Swiss albino mice, exposed to 0.1% nicotine sulphate at a dose of 1.67 mg/kg body weight from the 6th to the 15th gestational day, were compared with control fetuses to assess the effects of nicotine on first molar odontogenesis. Mothers were sacrificed on the 18th day of gestation. The 130 nicotine treated fetuses, as well as the 348 control fetuses were embedded in paraffin and sectioned in the frontal plane. The developing molars of the experimental fetuses were retarded, less differentiated, and reduced in breadth in comparison with controls. The developing molars of the control fetuses were in the bell stage of odontogenesis, whereas those of the experimental population were either in the late cap or early cap stage, depending on the absence or presence of palatal cleft, which occurred in 9.6% of the fetuses. It is suggested that nicotine, or its metabolic byproducts, interfere with normal interaction between the epithelial and mesenchymal components of the developing tooth.

The unicellular Tetrahymena first internalized, then partly released the labelled insulin. Insulin-pretreated (imprinted) Tetrahymena cells behaved differently from non-pretreated cells, in that they retained a greater part of internalized insulin in the cytoplasm. Additional exposure to excessive non-labelled (cold) insulin caused a decrease in intracellular labelled insulin retention. Internalized insulin also entered the nucleus of Tetrahymena, where it was found in a heterochromatic localization.

Fifty CFI female mice were experimentally infected with schistosomiasis mansoni (50 cercariae per mouse). This study was designed to follow the stages of structural changes that may take place in the liver of patients infected by this parasite. Histological examination of liver tissue samples were carried out weekly for ten weeks after infection with schistosomiasis mansoni cercariae. The present study suggests that the development of hepatic schistosomiasis mansoni in mice is biphasis with a first or granulomatous phase in which the morphological changes are mild and a second aggressive fibrotic phase, when hepatic collagen synthesis increases rapidly and leads to fibrotic morphological changes that are characteristic of this infection. Gross and microscopic portal fibrosis and portal vascular lesions resembled those in hepatosplenic schistosomiasis in man. The rapid production of severe hepatic fibrosis without the use of hepatotoxic compound makes this model of interest for the study of liver fibrosis and its therapy.

Adenomatoid tumors were detected as casual findings in ten uteri removed surgically for other reasons. This tumor can cause diagnostic problems in histopathological examinations. It is considered to be probably of mesothelial origin. Two forms are distinguished, in one of which smooth muscle cells participate in the growth.