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Biomedical subjects

E Agapitos

Publications and source records attributed to E Agapitos.

52 records · Page 3Linked to original sources

Primary causes of fetal deaths in Athens a clinicopathological study.

The authors studied 239 cases of fetal death, occurring before the 24th week of gestation, during a five-year period, from 1989 to 1993. Based on clinical information and autopsy findings, their cases were classified as follows: 1) amniotic infection syndrome; 2) congenital anomalies; 3) disorders of the placenta and adnexae, and 4) others. The causes of fetal death were determined and evaluated statistically. In 83 cases (39 %), only autopsy revealed the cause of fetal death. The correlation of clinical and pathological findings showed that autopsy constitutes an important source of information for the determination of causes of fetal death, as well as for future genetic counselling. Moreover, it can broaden our knowledge about perinatal mortality, by correctly interpreting clinical and complementary investigation data.

Abortion, Spontaneous↗

Reproductive capacity of the nucleus of the male gamete after completion of meiosis.

PURPOSE: Our purpose was to investigate the possibility of achieving fertilization and subsequent normal embryonic development by injecting round spermatid nuclei into rabbit oocytes. RESULTS: Two-to four-cell-stage embryos developed after round spermatid nuclear injections into rabbit ooplasma could further develop in vitro up to the expanding blastocyst stage or in vivo up to complete gestation. CONCLUSION: The current findings show that the haploid set of chromosomes of round spermatid can pair with the chromosomes of the ootid to participate in complete fertilization and subsequent embryonic and fetal development. In addition, we suggest that postmeiotic modifications of the round spermatid are not required for the pairing of male gamete chromosomes with those of the ootid.

Animals↗

Perinatal death and thymus gland.

Three hundred (300) cases of perinatal death were autopsied and the thymus was removed for histologic examination. The histologic findings were classified into five groups: a) normal-mature thymus, b) involutional changes--"Starry sky" pattern, c) involutional changes--intense lymphocytic depletion, d) hypoplasia--aplasia, e) agenesis. The perinatal deaths were classified into five groups according to Wigglesworth's classification: 1) normally formed macerated stillborn neonates, 2) congenital malformations, 3) conditions associated with immaturity, 4) asphyxial conditions developing in labor, 5) other specific conditions (e.g. known-beta-hemolytic streptococcal infection or a fatal inborn error of metabolism). The main objective was to identify a possible correlation between sex, gestational age, birth weight, thymus weight, histologic features of the thymus and cause of death. In conclusion, a strong correlation was found between: a) weight of thymus and gestational age, b) weight of thymus and birth weight, c) weight of thymus and its histologic features, d) histologic features of thymus and cause of death, e) weight of thymus and cause of death, f) gestational age and cause of death. No correlation was found between: a) gestational age and histologic features of thymus, b) birth weight and histologic features of thymus, c) weight of thymus and sex, d) histologic features of thymus and sex, e) cause of death and sex.

Birth Weight↗

Active and passive smoking and pathological indicators of lung cancer risk in an autopsy study.

OBJECTIVE: The association between involuntary smoking and lung cancer has been supported by most epidemiologic studies, but a number of authors and interest groups claim that the possibility of bias has not been excluded. Few autopsy-based studies have explored the role of active smoking and other exposures in lung carcinogenesis, and none has been previously done to examine the role of passive smoking. We have undertaken such an autopsy-based study in Athens, Greece. DESIGN: Lung specimens were taken at autopsy from 400 persons 35 years of age or older, of both genders, who had died within 4 hours from a cause other than respiratory or cancer in Athens or the surrounding area. For each person at least seven tissue blocks were taken from the main and lobar bronchi and at least five blocks from the parenchyma, including an average of about 20 smaller cartilaginous bronchi and membranous bronchioles. The specimens were examined without knowledge of the exposures of the particular subject in Turin, Italy. For 283 (71%) of the subjects the preservation of the bronchial epithelium was satisfactory for pathological examination, and for 206 among them (73%) an interview could be arranged with their next of kin, focusing on smoking habits of the deceased and their spouses, as well as other variables. The interviewers were not aware of the results of the pathological examinations. MAIN OUTCOME MEASURE: Specimens were examined for basal cell hyperplasia, squamous cell metaplasia, cell atypia, and (in membranous bronchioles and bronchiolo-alveolar airways) mucous cell metaplasia, ie, pathological entities that may be lung cancer risk indicators or epithelial, possibly precancerous, lesions (EPPL). The gland and wall thicknesses were also measured and their ratio calculated (Reid Index). RESULTS: In comparison with nonsmokers, EPPL values were significantly higher among current smokers and higher, but not significantly so, among former smokers. Furthermore, EPPL values were significantly higher among deceased nonsmoking women married to smokers rather than to nonsmokers. In this set of data neither occupation nor residence was associated with EPPL, but this could be due to the poor correlation of residential history with exposure to air pollution and the lack of adequate standardization of contemporary Greek occupations. The Reid Index was higher among smokers and former smokers in comparison with nonsmokers, among subjects with mainly urban residence in comparison with those with mainly rural residence, and among nonsmoking women married to smokers in comparison with those married to nonsmokers, but none of these differences was statistically significant. CONCLUSION: These results provide support to the body of evidence linking passive smoking to lung cancer, even though they are based on a study methodologically different from those that have previously examined this association.

Adult↗

Correlation of early pathological lesions in the bronchial tree with environmental exposures: study objectives and preliminary findings.

Lung specimens were taken at autopsy from 214 subjects aged 35 years and over who had died from nonpulmonary causes in Athens or the surrounding countryside. The samples were coded and examined for entities thought to be linked to environmental exposures, reflecting epithelial, possibly precancerous, lesions, as well as for morphological features, which were summarized using Reid's index. Of the 214 specimens, 142 were suitable for pathological examination. Next-of-kin of 101 of the dead people were identified and asked about the subject's exposure to active smoking, passive smoking, possible occupational hazards, dietary factors and proxy indicators of air pollution (residence). Preliminary analysis, controlling for age and sex, indicates that active smoking is related, although not statistically significantly, to both the Reid index (difference, 0.28, corresponding to a one-tailed p value of 0.07) and epithelial, possibly precancerous lesions (difference, 16.7, corresponding to a one-tailed p value of 0.09). Nonsignificant differences were found in the preliminary analysis of this ongoing study with respect to the other environmental factors examined.

Adult↗

[Primary angiosarcoma of the spleen. Apropos of a new case].

The authors report a new case of primary angiosarcoma of the spleen and, after a review of the literature, they discuss its clinical, diagnostic and therapeutic problems. Primary angiosarcoma of the spleen is a very rare tumor. The diagnosis should be suspected in the case of a patient with splenomegaly and unexplained anemia, with no evidence of lymphoma, leukemia or myelofibrosis. In 30% of cases, the tumor presents in the form of spontaneous rupture of the spleen. The prognosis is very poor, as it is a highly malignant tumor, even more so in the presence of early metastases with or without spontaneous rupture of the organ. Splenectomy prior to rupture could increase the survival. Patients with or without metastatic disease may be treated by combination chemotherapy, which still remains empirical and palliative.

Hemangiosarcoma↗

An immunohistochemical study of normal human neonate and adult parotid gland tissue. Detection of lysozyme, lactoferrin, a1-antichymotrypsin, a1-antitrypsin and carcinoembryonic antigen.

The immunohistochemical detection and distribution of lysozyme (Ly), Lactoferrin (Lf), a1-Antichymotrypsin (a1-AChy), a1-Antitrypsin (a1-AT) and Carcinoembryonic antigen (CEA) were studied in neonate and adult parotid gland tissue, using the peroxidase-antiperoxidase (PAP) method. Ly stain in neonates extended into acini, intercalated ducts and occasional cells of large ducts, whereas in adults Ly was usually confined to the intercalated ducts. The distribution pattern of Lf in neonates varied considerably between individual glands showing three staining patterns. Most of the intercalated ducts, some groups of acini and rare striated duct cells were positive for Lf in adults. a1-AChy and a1-AT in neonates were positive mainly in the large ducts, whereas staining for a1-AChy and a1-AT in adults frequently extended into some intercalated duct cells, although less intensively. Finally, CEA in neonates was localized in the lumina and luminal membranes of the acini, in intercalated ducts, and less frequently in the large ducts. In adults CEA was present predominantly in the lumina and luminal membranes of the intercalated duct cells. These differences may suggest an immunohistochemical postnatal differentiation of the parotid gland.

Adult↗

[Comparative immunohistochemical study of lysozyme and lactoferrin in human neonate and adult parotid glands].

Lysozyme and lactoferrin, substances of the non-specific defense system of the salivary glands, were studied in normal human parotid glands of neonates and adults using the immunoperoxidase method. To our knowledge, the immunohistochemical detection and distribution of lysozyme and lactoferrin in neonate parotid glands have not been previously reported. In neonate parotid glands, a monotonous positive reaction for lysozyme was found in the acini, in the intercalated ducts and in a few cells of large ducts. On the contrary, lysozyme was observed mainly in the intercalated ducts of the adult parotid glands. Three staining patterns for lactoferrin were found in neonate parotid glands. The first pattern was identical to that of lysozyme in neonates, the second was similar to that of lactoferrin in adults, and in the third extremely few acinar and intercalated duct cells were positive. In adult parotid glands, lactoferrin was detected in groups of acini and intercalated ducts and rarely striated duct cells. In adult parotid glands, our findings are discussed in correlation with those of other investigators. The results of our study indicate that lysozyme and lactoferrin have an important role in the defense mechanism of neonate parotid gland. There is also a distinct immunohistochemical difference between neonate and adult parotid gland. Since it is known that there is a morphological differentiation of the parotid gland postnatally, it is presumably suggested that an immunohistochemical differentiation also occurs.

Adult↗

Primary causes of perinatal death. An autopsy study of 556 cases in Greek infants.

The primary causes of death in 556 autopsy cases of perinatal death during the six years from 1979 through 1984 are discussed. On the basis of the clinical data and gross and microscopic findings, each case was assigned to one of the following categories of primary causes of death: a pulmonary hyaline membrane disease, infection, malformation, anoxia, immaturity, maternal causes, other causes, and unaccounted for Definitions of perinatal infant diseases, essential points of diagnosis, and statistics relating to perinatal infant death are also discussed.

Autopsy↗

Association of single umbilical artery with congenital malformations of vascular etiology.

The possible association of a single umbilical artery (SUA) with malformations of vascular etiology is investigated in this study. Four hundred twelve fetal and embryonic autopsies showing one or more congenital malformations, collected over 7 years, were reviewed. Microscopic confirmation of a SUA was evident in 20 cases (4.85%). The two subgroups with 2 (nA = 20) or 3 umbilical vessels (nB = 392) were compared with each other, in relation to the frequency of malformations per organ system. In the group of fetuses with congenital malformations, no association was observed between SUA and the incidence of CNS, cardiac, pulmonary, or genital malformations. However, there was a significantly higher incidence of atresia of hollow organs (P = 0.003), renal aplasia (P = 0.034), and limb reduction defects (LRD) (P = 0.0383) when only a single umbilical artery was present. This suggests a possible etiopathogenetic association of SUA with congenital malformations of vascular etiology. Furthermore, the findings of our study suggest that prenatal identification of a SUA warrants a thorough search for atresias, renal aplasia, and LRD-type malformations.

Abnormalities, Multiple↗

Atherosclerosis of the carotid artery: absence of evidence for CMV involvement in atheroma formation.

Several studies suggest that certain viral and bacterial pathogens may contribute to the process of atherogenesis. However, this relation between infectious agents and atherosclerosis has not yet been established with certainty. The aim of this study was to investigate the presence of CMV in carotid endarterectomies from 40 patients suffering from atherosclerosis using immunohistochemistry and the polymerase chain reaction (PCR). None of the specimens examined gave a positive result, indicating absence of CMV particles or CMV DNA sequences in the walls of carotid arteries. This finding suggests it is possible that CMV infection may not play a major role in the formation of atheroma. Therefore, further investigation is required in order to clarify the etiology of atherosclerosis.

Aged↗

Expression of PDGF-A, TGFb and VCAM-1 during the developmental stages of experimental atherosclerosis.

PURPOSE: A considerable number of growth factors, cytokines, and adhesion molecules are implicated in the development of atherosclerotic lesions. These molecules interact in a complex network influencing the evolution of several processes, such as lipid metabolism, cellular proliferation and tissue repair. The aim of this study was to evaluate the expression of the growth factors PDGF-A, and TGFb, and the adhesion molecule VCAM-1 in the sequential steps of experimental atherogenesis. METHODS: Forty-two New Zealand white male rabbits were divided into 4 groups. The group A rabbits (n = 8) received normal diet and served as control animals. The remaining groups were fed with a diet enriched with 1% cholesterol and 6% corn oil. The rabbits of group B (n = 9) were sacrificed 1 month after the beginning of the study, of group C (n = 15) after 2 months and of group D (n = 10) after 3 months. In tissue sections of the aortic arch the antibodies of the prementioned factors were detected immunohistochemically. RESULTS: In group A only TGFb and PDGF-A were detectable. In lesions of the first month PDGF-A expression was high but declined towards the third month. VCAM-1 expression was getting more intense up to the second month and subsided thereafter. TGFb expression intensified towards the third month. Changes in the expression of these factors were statistically significant. CONCLUSION: PDGF-A, responsible for the uncontrollable growth of smooth muscle cells, and VCAM-1, regulating monocyte recruitment in the intima, acts mainly during the early stages of atherogenesis. TGFb, one of the main factors controlling the formation of connective tissue matrix, has a gradually increasing expression towards the third month contributing probably to the fibrous plaque formation.

Animals↗

Limb reduction defects--autopsy study.

We present a case-control study of limb reduction defects taken from autopsy material of the Pathology Department of the University of Athens from the year 1986 to 1990. During this period 1725 perinatal autopsies were performed, in which 34 neonates were found to have had a limb reduction defect (LRD) (1.97%). The cases were divided into five subgroups: transverse, intercalary longitudinal, split, and multiple types of LRD. Of all the cases, 44.17% involved the upper limb, 41.17% the lower limb, and 14.70% both. Coexisting nonlimb malformations were found in 17 cases (50%), 5 with recognized syndromes and 12 with other associated defects. Risk factors correlated with LRD were found to be low birth weight (2500 g or less) and threatened abortion.

Abnormalities, Multiple↗

A fatal case of diphtheria.

A fatal case of diphtheria occurred in a nonimmunized child. The child died because of the late diagnosis of the disease, which is now extremely rare.

Child, Preschool↗

Immunohistochemical detection of fibronectin in early and advanced atherosclerosis.

Fibronectin is known to be involved in the pathogenesis of atherosclerosis. We therefore applied paraffin-section immunohistochemistry, which permits detailed morphological analysis of the tissue distribution of fibronectin, in order to evaluate the alterations of fibronectin in terms of quantity and localization during the progression of atherosclerosis in humans. In 48/60 (80%) cases (p < 0.005) with early atherosclerotic lesions we found intense fibronectin staining presenting a distribution in continuous fibrils in the subendothelium around the fibrous plaque. The total amount of fibronectin was elevated. In 51/60 (85%) cases (p < 0.001) presenting advanced or complicated atherosclerotic lesions, the characteristic distribution of fibronectin in continuous fibrils was interrupted, fibronectin strands were fragmented and in regions where the sclerotic process was complete, fibronectin seemed to be almost absent. These findings reveal that fibronectin during atherosclerosis plays a role similar to that reported during the wound healing process and demonstrate a close relationship between quantity and topographical distribution of fibronectin and evolution of atherosclerosis. Further studies are required to determine whether fibronectin could be used as a marker for evaluation of the severity of atherosclerotic lesions.

Adult↗