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Biomedical subjects

L Matturri

Publications and source records attributed to L Matturri.

At least 19 recordsLinked to original sources
PubMed2006

Hypoplasia and neuronal immaturity of the hypoglossal nucleus in sudden infant death.

OBJECTIVE: To report the case of five month old female baby with a history of episodes of gastro-oesophageal reflux and pneumonia. Her sudden death offered a unique insight into the possible role of delayed neuronal maturation and hypoplasia of the hypoglossal nucleus in representing a likely morphological substrate of sudden death. METHODS: Morphometric analysis was carried out with an Image-Pro Plus Image analyser (Media Cybernetics) on both sides of the brain stem. RESULTS: Hypoplasia and neuronal immaturity of the hypoglossal nucleus were demonstrated, accompanied by hypoplasia of the arcuate nucleus. CONCLUSIONS: Much attention should be paid to the possible role of the hypoglossal nucleus in determining a lethal outcome in infancy through impairment of deglutition and subsequent recurrent episodes of pneumonia, and as a necropsy finding.

Adult↗
PubMed2005

Sudden infant death triggered by dive reflex.

The dive reflex is the reflex mechanism most frequently considered in the aetiopathogenesis of sudden infant death syndrome (SIDS). This seems to persist in human beings as an inheritance from diver birds and amphibians. It has been reported that washing the face with cold water or plunging into cold water can provoke cardiac deceleration through the intervention of the ambiguus and the vagal dorsal nuclei. This report describes a case of SIDS that offers a unique insight into the role of the dive reflex in determining a lethal outcome. Examination of the brainstem on serial sections revealed severe bilateral hypoplasia of the arcuate nucleus and gliosis of the other cardiorespiratory medullary nuclei. The coronary and cardiac conduction arteries presented early atherosclerotic lesions. The possible role of parental cigarette smoking in the pathogenesis of arcuate nucleus hypoplasia and early coronary atherosclerotic lesions is also discussed.

Brain Stem↗
PubMed2004

Autoptic examination in sudden infant death syndrome and sudden intrauterine unexpected death: proposal of a national law.

The autoptic procedures in sudden infant death syndrome (SIDS) and sudden intrauterine unexpected death (SIUD) victims requires an in-depth examination of the autonomic nervous system, central and peripheral, as well as of the cardiac conduction system. In these pathologies, our studies have identified frequent developmental abnormalities in the brain stem, particularly hypoplasia of the arcuate nucleus, and accessory atrioventricular pathways in the cardiac conduction system. The law 'Post-mortem Investigation on the SIDS and of Unexplained Late Fetal Death' designated the Institute of Pathology of Milan University as the National Reference Center. The objectives of this law include, in article 4, widespread informative and preventive campaigns and continuous formation of programs for medical personnel.

Autopsy↗
PubMed2003

Intimal preatherosclerotic thickening of the coronary arteries in human fetuses of smoker mothers.

BACKGROUND: Many studies have described the development of preatherosclerotic coronary artery lesions in infancy. The observations reported in the literature regarding the fetal origin of coronary artery lesions are rare and controversial. OBJECTIVES: To identify the features of preatherosclerotic coronary artery lesions in late fetal stillborns and the possible atherogenic role of maternal cigarette smoking. METHODS; We examined 22 stillborns (13 males and nine females), all of whom had died sine causa after the 32nd week of gestation. All underwent autopsy. Twelve of the mothers smoked over five cigarettes per day before and during the pregnancy. The four major epicardial coronary arteries were isolated along their whole length, embedded in paraffin and serially cut for histologic examination and immunohistochemical studies, particularly searching for the proliferating cell nuclear antigen and c-Fos expression. Alterations of chromosome 7 were also investigated by the fluorescence in situ hybridization technique. RESULTS: In over 50% of the fetuses, almost all from smoker mothers, multifocal structural alterations of coronary walls were evident. The smooth muscle cells (SMCs) presented loss of polarity, forming columns perpendicular to the axis of the media and infiltrating the subendothelial connective tissue. Increased amounts of mucoid ground substance were also observed in the subendothelial connective tissue. In all the cases with coronary alterations, study of the biological markers showed intense c-Fos positivity of the SMCs. CONCLUSIONS: Preatherosclerotic intimal alterations of the coronary arteries are already detectable in the prenatal period and are significantly associated with maternal cigarette smoking.

Actins↗
PubMed2002

Brain stem lesions in the sudden infant death syndrome: variability in the hypoplasia of the arcuate nucleus.

In the present study we investigated quantitatively the incidence of hypoplasia of the arcuate nucleus (ARCn) of the medulla oblongata, reported earlier [Gozal D, Hathout GM, Kirlew KAT (1994) J Appl Physiol 76:207], as well as its distribution in 62 cases of sudden infant death syndrome (SIDS; mean age 14 postnatal weeks, 39 male and 23 female) and 25 controls (mean age 16 postnatal weeks, 14 male and 11 female), using detailed histopathological and morphometric analyses performed on serial sections of medulla oblongata. The SIDS cases were divided into four subtypes: SIDS A (27 cases, 43%) with histologically well-developed ARCn; SIDS B (16 cases, 26%) with severe bilateral hypoplasia along the whole length; SIDS C (11 cases, 18%) with partial bilateral hypoplasia, located mainly in the lateral portions of the caudal two thirds of the nucleus, and SIDS D (8 cases, 13%) with right monolateral hypoplasia of the ARCn. ARCn hypoplasia was detected in 56% of cases (35 cases). Three-dimensional volume reconstruction showed that in the SIDS A victims the mean volume was analogous to controls, whereas in the SIDS group with ARCn hypoplasia, severe or partial, the mean volume was significantly different from controls on both sides of the medulla oblongata (SIDS B group: P=0.003, P=0.002; SIDS C group: P=0.007, P=0.008). The mean ARCn volume in the SIDS D group was statistically significant only on the right side ( P=0.005). We also observed reduced neuron density of the ARCn, associated with a decrease in the total number of neurons over the whole length of the nucleus itself. On the basis of the morphometric results of neuronal population in the different portions of the ventrolateral medulla in SIDS cases, we hypothesized that infants without the full complement of neurons and neuropil (ARCn hypoplasia) are at risk for SIDS because they are unable to develop appropriate cardioventilatory control during this crucial developmental period.

Cell Count↗
PubMed2001

Chromosomal alterations in atherosclerotic plaques.

Alterations of chromosomes 7 and 11 have been involved in the progression of atherosclerosis. Twenty-three carotid endarterectomy specimens were studied for the presence of alterations in chromosomes 7 and 11, and fibroblastic growth factor-3 (FGF-3) gene amplification. Besides classic histological stainings, immunophenotyping of cellular and vascular components and fluorescence in situ hybridization (FISH) were performed. At the caps, unstable plaques (n=18) showed inflammatory infiltration of macrophages, smooth muscle cells, and T-lymphocytes. Specifically in these regions, the FISH showed varying percentages of trisomy (15/18) and tetrasomy (8/15) of chromosome 7. In four cases polisomy 7 was noted in some nuclei. Monosomy of chromosome 11 and gene amplification of FGF-3 gene was observed. The FISH of the five stable plaques and normal arterial walls showed no chromosome alterations; furthermore, chromosome 3, which is not involved in atherosclerotic progression, presented a normal ploidy of smooth muscle cells in stable and unstable plaques and normal arterial walls. In conclusion, chromosome 7 and 11 alterations and FGF-3 gene amplification are components of unstable plaques, and might contribute to the evolution of stable plaques into complicated plaques.

Adult↗
PubMed2001

Expression of apoptosis and proliferating cell nuclear antigen (PCNA) in the cardiac conduction system of crib death (SIDS).

Aim of this study is to determine the expression of apoptosis and Proliferating Cell Nuclear Antigen (PCNA) in the cardiac conduction system in crib death and explained death (ED) cases. Postnatal morphogenesis of the conducting tissue is an important part of its normal development. In the atrio-ventricular node (AVN) and His bundle (HB) it consists of degeneration, cell death and replacing in an orderly programmed way. However, its nature and its relation to crib death is not yet fully explained. Apoptosis and PCNA were investigated in 8 heart conduction systems of infants dying of crib death and in 3 conduction systems of infants dying of ED as controls. The cardiac conduction system was removed in two blocks: the first included the sino-atrial node (SAN) and the crista terminalis, the second contained the atrio-ventricular node (AVN), His bundle (HB), bifurcation, and bundle branches. In the conduction systems as well as in the common myocardium the PCNA Labeling Index (PCNA-LI) was found to be negative in all cases. The apoptotic indices (AI) in SIDS and in ED were found to have no statistically significant differences (p>0.05). The SAN, in both groups, showed an AI similar to the one detected in common myocardium. In almost all cases, TUNEL labeling was detected in peripheral region of the AVN, close to the atrial myocardium. The AI was higher in the AVN, HB and the initial tract of bundle branches than in the common myocardium (p<0.05; Student's t test).

Apoptosis↗
PubMed2000

Severe hypoplasia of medullary arcuate nucleus: quantitative analysis in sudden infant death syndrome.

The human arcuate nucleus (ARCn) is postulated to be homologous to ventral medullary cells involved in chemoreception, and respiratory and blood pressure responses. Abnormalities in central respiratory control may result from dysfunction of this anatomic ventral area. We evaluated the changes of the neuronal population of the medullary ARCn in infants victims of the sudden infant death syndrome (SIDS). In this study we tested the hypothesis that anatomical deficiency of the ARCn is associated with SIDS. The volume and neuronal density of the ARCn were morphometrically quantified with an image analyzer in 36 cases of SIDS and 12 age-matched controls. We found a marked hypoplasia in the SIDS ARCn compared to controls and, particularly, in 11 SIDS cases (30%) in which the ARCn exhibited a severe hypoplasia, being almost totally absent. Three-dimensional reconstructions and morphometric measurements of ARCn confirmed this marked hypoplasia in all the serial sections examined (P = 0.0001) and the reduced neuronal density (P = 0.0025) in relation to control cases. In conclusion these abnormalities observed in the ARCn are consistent with the idea that ARCn dysfunction plays an important role among the causative factors of sudden infant death. The hypoplasia of the ARCn represents the most frequent congenital abnormality in our experience, and can be a plausible morphological substrate for a subset of SIDS.

Cell Count↗
PubMed2000

Inflammatory cells, apoptosis and Chlamydia pneumoniae infection in atherosclerosis.

Chlamydia pneumoniae (CP), chromosomal alterations and apoptosis were suggested as contributing factors in the pathogenesis of atherosclerosis. Early (EP) and unstable plaques (UP) were studied in order to assess infiltrate composition, the apoptotic index, chromosome 7 stability and to investigate the concurrent presence of CP in EP and UP. Paraffin embedded sections of three iliac arteries and four aortas from young donors (EP), and four coronaries and nine carotid arteries (UP) were used. Aside from histological techniques, immunophenotypification for macrophages, T and B cells, smooth muscle and endothelial cells; FISH and DNA nick end labeling were performed. The amplifications with PCR for CP infection were negative in all specimens. In the EP, a focal myointimal thickening with foam cells and scarce smooth muscle cells was observed. Macrophages were most frequent in the intima (10.8%) while T and B cells were found in 2.3 and 1.5%. In the UP a thin cap covering a lipid-rich core with widespread vascularization and with severe luminal obstruction was observed. Macrophages were increased (21%), and T (1.5%) and B cells (3.5%) in the caps and inner areas of the lipid cores. At these sites, the FISH showed trisomy and tetrasomy of chromosome 7 and apoptosis was very frequent (10-30%). Macrophages in intimal lesions is one of the most prominent, consistent and permanent features in EP, and an elevated apoptotic index and chromosome 7 instability might contribute to evolution from stable to complicated plaques, while CP seems to play no role. However, further studies are needed with more cases to confirm this last observation.

Adult↗
PubMed2000

[Proliferative activity and chromosomal alterations of smooth muscle cells in atherosclerosis].

Atherosclerosis is the most frequent cause of death in industrialized countries. Lesions are characterized by lipid deposits, focal thickening of the arterial wall with proliferation of smooth muscle cells (SMC), mononuclear infiltrates and neoformed vessels. In this paper, we studied the proliferative characteristics and cytogenetic alterations of SMC. These cells, expressing specific muscular actin, were diploid with an increased proliferative index for PCNA. A high percentage of SMC showed intense expression of p53. There were signs of chromosomal instability, being the most frequent findings chromosome 7 trisomy and chromosome 11 monosomy. Additionally, the gene for FGF-3 showed a marked amplification. These findings strongly suggest that SMC proliferation is active, and is related to the accumulation or mutation of the p53 oncoprotein. It also presents specific chromosomal alterations in close relation with growth factors. According to these findings SMC hyperplasia in the atherosclerosis plaque may be considered as a cellular clonal expansion.

Arteriosclerosis↗
PubMed1999

The prognostic value of cell proliferation in colorectal adenomas assessed with tritiated thymidine and anti-proliferating cell nuclear antigen.

We analyze the cell kinetics of colorectal adenomas by tritiated thymidine (3HTdR) autoradiographic method and anti-proliferating cell nuclear antigen (PCNA) antibodies. A total of 46 patients who underwent prior endoscopic polypectomy for colorectal adenomas were reevaluated by colonoscopy for 4 years. Thymidine labeling index (T-LI) in index adenomas ranged from 1.40 to 38.0% (median value: 10. 75%); PCNA labeling index (PCNA-LI) in index adenomas ranged from 0 to 27.0% (median value: 1.95%). Among the 46 patients studied, 16 developed recurrent adenomas (Group A) and 30 were free of recurrent adenomas (Group B). The T-LI and PCNA-LI comparisons between Groups A and B were statistically significant (p < 0.0001, chi2 test). These results demonstrate that T-LI and PCNA-LI in colorectal adenomas might be helpful to predict the development of metachronous adenomas and hence to plan the follow-up of patients with adenomatous polyps after polypectomy.

Adenomatous Polyps↗
PubMed1999

Proliferating cell nuclear antigen (PCNA) and apoptosis in hyperacute and acute myocardial infarction.

The aim of this study was to determine whether cell proliferation and/or apoptotic cell death occur in hyperacute and acute infarction. Proliferating cell nuclear antigen (PCNA) and apoptosis were investigated in ten autoptic hearts within a few hours of infarction and in three normal hearts as controls. The PCNA Labeling Index (PCNA-LI) ranged from 0 to 3.1 in hyperacute infarction (mean 1.38), from 0.3 to 4 in acute infarction (mean 2.04) and from 0 to 1.2 in controls (mean 0.7). Although the results were not statistically significant, PCNA-LI was higher in acute than in hyperacute myocardial infarctions; and it was higher in hyperacute infarctions than in controls. Regarding apoptosis, the Apoptotic Index (AI) in hyperacute infarctions ranged from 0.7 to 3 (mean 1.78), in acute infarctions from 0.9 to 5 (mean 3.24) and in controls from 0 to 0.4 (mean 0.1). The AI was significantly higher in hyperacute and acute infarctions than in controls (p < 0.05).

Aged↗
PubMed1999

Evidence for apoptosis in non-small cell lung carcinoma. Relationship with cell kinetics and prognosis.

OBJECTIVE: To investigate cell death via apoptosis in non-small cell lung carcinoma (NSCLC) and its correlation with proliferative indices and follow-up. STUDY DESIGN: In 38 cases of NSCLC (21 squamous cell carcinomas and 17 adenocarcinomas) we analyzed apoptosis by nuclear morphology and in situ DNA fragmentation end labeling and the cell kinetics by an autoradiographic method with tritiated thymidine and by immunohistochemistry with anti-proliferating cell nuclear antigen (anti-PCNA) antibodies. We also evaluated mitotic frequency. Apoptotic index (AI) was correlated with the thymidine and PCNA labeling indices (T-LI and PCNA-LI, respectively) and with the mitotic index. RESULTS: The percentage of proliferating cells (T-LI range, 0.1-20.1%; PCNA-LI range, 0-14.7%) was generally considerably higher than that of apoptotic cells (range, 0-8%) and of mitotic cells (range, 0.1-1%). Survival at six years was significantly higher in patients with high levels of apoptosis and low T-LI values. CONCLUSION: AI and T-LI are independent and very useful prognostic factors in NSCLC. A high percentage of proliferating cells in terms of T-LI correlates with poor prognosis, whereas a high AI indicates a favorable outcome.

Adenocarcinoma↗
PubMed1999

p53 over-expression and its correlation with PCNA index in nasal polyps.

Our knowledge about the etiopathogenesis of nasal polyps (Nps) is still limited. In this study, in order to define the biological features of these neoformations, we investigated with immunohistochemistry the p53 over-expression and the proliferating cell nuclear antigen (PCNA) in 32 cases of Nps and in normal mucosa of 11 control cases. The evaluation of PCNA showed a wide range of indices (0.5-18.2%) with a mean value (6.8%) significantly higher than in normal mucosa (2.9%). Over-expression of the p53 oncoprotein, observed in 50% of Nps, was statistically related to a high PCNA-index (> 6.8%). Our results suggest that Nps can behave, in a high percentage of cases, like tumours.

Female↗
PubMed1998

Cardiac involvement in acquired immunodeficiency syndrome--a review to push action. The Committee for the Study of Cardiac Involvement in AIDS.

As more effective therapies have produced longer survival times for human immunodeficiency virus (HIV)-infected patients, new complications of late-stage HIV infection including HIV-related heart disease have emerged. Almost any agent that can cause disseminated infection in patients with acquired immunodeficiency syndrome (AIDS) may involve myocardium, but clinical evidence of cardiac disease is usually overshadowed by manifestations in other organs, primarily the brain and lungs. Cardiac abnormalities are found at autopsy in two-thirds of patients with AIDS, and more than 150 reports of cardiac complications have been published. Cardiac involvement in HIV disease includes pericardial effusion, myocarditis, dilated cardiomyopathy, and/or endocardial involvement at any stage of the disease. This review deals with all the cardiac manifestations of AIDS and serves to highlight two problems and one indication. First of all, there are very few clinical studies. Current knowledge is based almost exclusively on echocardiography and autopsy studies. Observational or clinical trials would be useful. Second, there exists very poor information on the impact of treatment; and epidemiologic and clinicopathologic studies are mandatory for obtaining detailed data concerning the mechanisms of myocardial damage in AIDS. Finally, because cardiac complications are often clinically inapparent or subtle in the initial stages, periodic screening of HIV-positive patients by electrocardiogram and echocardiogram is probably indicated. In addition, AIDS may also provide the opportunity to gain insights into the pathogenesis of little understood cardiac diseases such as lymphocytic myocarditis and dilated cardiomyopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Carotid rupture and intraplaque hemorrhage: immunophenotype and role of cells involved.

BACKGROUND: A complete immunohistochemical characterization in complicated carotid plaques is still lacking. The cellular components of 165 carotid endarterectomy specimens were analyzed to assess their role in the pathogenesis of plaque rupture and intraplaque hemorrhage without rupture. METHODS AND RESULTS: The fibrous caps at the sites of plaque rupture showed CD68+ macrophages, T-lymphocytes, and scarce B-lymphocytes. Ruptured plaques showed mononuclear infiltrates in the caps, shoulders, and bases of the plaques in 85% of the cases. Only 46% of nonruptured plaques showed such infiltrates (P <.0001). Two types of lipid cores were recognized: avascular or mildly vascularized and highly vascularized. The vessels of the latter type reacted with CD31 and CD34. In 57.5% of the cases, the base and the shoulders of the plaques showed neoformed, CD34+ vessels, often surrounded by mononuclear infiltrates. Intraplaque hemorrhage without rupture had highly vascularized lipid cores in all cases. T-lymphocytes and macrophages were in close contact with neoformed vessels. CONCLUSIONS: Plaque rupture is characterized by mononuclear cell infiltration of the caps, whereas intraplaque hemorrhage without rupture is characterized by extensive vascularization of the plaque.

Adult↗