Biomedical subjects

A Attanasio

Publications and source records attributed to A Attanasio.

At least 19 recordsLinked to original sources

PubMed1997

Levels of leptin in maternal serum, amniotic fluid, and arterial and venous cord blood: relation to neonatal and placental weight.

The mechanisms by which maternal and fetal weight are regulated during pregnancy are poorly understood. The ob protein, termed leptin, is produced by adipocytes. It is involved in the regulation of body weight by suppressing appetite and stimulating energy expenditure both in humans and rodents. In this study we examined whether leptin concentrations in the mother and the newborn correlate with birth weight, placental weight, and maternal weight at term. Leptin concentrations were measured in amniotic fluid, venous and arterial cord blood, and maternal serum at birth (n = 27) using a specific RIA employing human recombinant leptin for tracer and standard preparation. Gestational age was 38-42 weeks, maternal age was 21-42 yr, mean maternal weight at birth was 80.0 +/- 10.8 kg, and mean body mass index before pregnancy was 23.4 +/- 2.8 kg/m2. The newborns' mean weight was 3450 +/- 580 g, and mean placental weight was 616 +/- 120 g. Serum leptin levels from nonpregnant women ranged between 1.7-18.4 ng/mL, median 5.5 ng/ml (n = 30). Mean leptin concentration in maternal serum at birth was 20.0 +/- 13.2 ng/mL and was higher (P < 0.002) than in arterial cord blood (9.7 +/- 9.4 ng/mL) and venous cord blood (8.9 +/- 8.6 ng/mL). Mean amniotic fluid leptin concentration was 3.6 +/- 2.8 ng/mL. Placental weight correlated inversely with leptin levels in maternal serum at birth (r = -0.49, P < 0.01). In addition, leptin concentrations in venous cord blood correlated significantly with the levels in arterial cord blood (r = 0.98, P < 0.0001), and leptin levels in cord blood correlated positively with birth weight (r = 0.57, P = 0.03) and placental weight (r = 0.50, P < 0.01). In contrast, there was no correlation between maternal serum leptin levels and birth weight. Thus, leptin levels are high in the fetus and in the mother at term. We hypothesize that high leptin levels could represent an important feed-back modulator of substrate supply and subsequently for adipose tissue status during late gestation.

Amniotic Fluid↗

PubMed1996

High leptin concentrations in serum of very obese children are further stimulated by dexamethasone.

Serum leptin concentrations and the levels of ob mRNA in adipocytes in obese humans are elevated. Hyperphagia and obesity are characteristics of hypercortisolism. We have therefore asked whether or not leptin levels were elevated in very obese children, and whether or not dexamethasone would increase leptin levels in obese children. A single dose dexamethasone suppression test was performed in ten obese children (5 girls, 5 boys; age 6 to 16 yrs, mean 12 +/- 1, median 12 yrs) to rule out hypercortisolism. Body mass index (BMI) in the ten children was calculated to be 27-45 kg/m2. Venous blood was sampled before dexamethasone was given in the evening and at 9.00 a.m. the following morning. Endogenous cortisol production was suppressed in all patients. Leptin levels, as measured by a newly developed specific radioimmunoassay, were 31.6 +/- 12.9 microg/l, range 19.2-59.9 microg/l before dexamethasone and 39.9 +/- 16.5 microg/l, range 26.3-80.3 microg/l after dexamethasone in the obese children (ANOVA, p = 0.01). Simple regression analysis revealed that serum levels correlated significantly with body mass index (r = 0.82, p < 0.001). Non-obese children (BMI < 27 kg/m2) had leptin levels between 0.1 and 33.3 microg/l, median 2.2 microg/l (N = 713). Girls (5.5 +/- 4.6 microg/l) (N = 401) had significantly higher leptin levels than boys (1.7 +/- 2.1 microg/l (N = 312) (p < 0.0001). We conclude that 1) high serum leptin concentrations are present in obese children. 2) A single dose of dexamethasone significantly increases the high leptin serum levels in these children. We hypothesize that glucocorticosteroids up-regulate leptin levels in the human.

Adolescent↗

PubMed1996

Paroxysmal staring and masticatory automatisms during postural hypotension in a patient with multiple system atrophy.

PURPOSE: We studied a 51-year-old man with multiple system atrophy and autonomic insufficiency. He had repeated episodes of loss of contact, staring, and masticatory automatisms. METHODS: Blood pressure during these events documented a systolic pressure of 60 mm Hg. Cardiovascular reflex tests provided evidence of autonomic failure. Head computed tomography (CT) revealed moderate, diffuse cortical and cerebellar atrophy. RESULTS: These events were strictly related to blood pressure decreases and could be reproduced consistently by having the patient sit up after a meal. Ictal polygraphic recordings showed EEG changes consistent with anoxia, preceded by sudden hypotension with fixed heart rate. CONCLUSIONS: Cerebral anoxia during a syncopal attack may therefore precipitate transient, sudden neurologic dysfunction that closely mimics complex partial seizures. Masticatory automatisms may represent a release phenomenon resulting from inactivation of neocortical structures by cerebral anoxia or reticular disconnection.

Automatism↗

PubMed1996

[Daily survey of procedures as markers of resources utilization].

OBJECTIVE: To assess and to follow along the time-span of ICU stay the process of resources allocation and utilization. DESIGN: Prospective study. PATIENTS: A cohort of 778 patients consecutively admitted to 7 multipurpose general ICU in the Milano area were enrolled in a survey of the daily performed interventions/procedures. MEASUREMENTS AND MAIN RESULTS: The majority of diagnostic procedure/interventions were performed during the first two days. The number and quality of interventions were transferred into points obtaining a score system in non-monetary units. The resource allocation process shows a regular trend in the sub-intensive patients who were only monitorized. On the contrary the 258 patients who were intensively treated and survived show a phase of high resource-consumption (about 30 daily points: roughly twice the score of monitorized patients) then followed by a post-intensive phase with a resource consumption resulting in a daily score absolutely equal to the sub-intensive patients. The intensive patients who die show a significantly higher score than survived patients. Both daily and cumulative scores do not show differences among different type of patients. CONCLUSION: The evaluation of the process of resources allocation, even if in non-monetary units enables the knowledge of the trend of ICU costs and allows the elaboration of the appropriate budget mechanism.

Cohort Studies↗

PubMed1995

Detection of apoptosis in weaver cerebellum by electron microscopic in situ end-labeling of fragmented DNA.

Massive degeneration of granule cell precursors occurs perinatally in the cerebellum of weaver mutant mice. We have studied the electron microscopic (EM) features of granule cell death in weaver and control mice, using an in situ end-labeling (ISEL) technique for detecting DNA fragmentation, a hallmark of apoptosis. In all animals, EM-ISEL revealed the pattern of apoptosis, with an enhanced expression in weaver mice. The weaver gene appears to accelerate the death program, most likely through potassium channel-mediated signals.

Aging↗

PubMed1995

Apoptosis and cell proliferation in human neuroepithelial tumors.

Apoptosis and cell proliferation were studied in 180 human neuroepithelial tumors (30 medulloblastomas, 30 intracranial ependymomas, 30 oligodendrogliomas and 90 astrocytic tumors, including 30 astrocytomas, 30 anaplastic astrocytomas and 30 glioblastomas). Apoptotic nuclei were detected by morphology and in situ end-labeling (ISEL) of DNA breaks. The frequency of apoptotic nuclei varied from oncotype to oncotype and their distribution in each oncotype was uneven. An apoptotic index (AI) was calculated; this was high in malignant tumors and in tumors of embryonal origin and lower in tumors of the glial series. The AI/mitotic index (MI) ratio was lower in malignant tumors and higher in benign tumors, suggesting a relationship between apoptosis and cell proliferation. There was no significant correlation of either AI or AI/MI ratio with either labeling index (LI) of Ki-67 clone MIB-1 or with survival. A trends towards low AI/MI ratio in tumors with high LI and short survival was observed. Apoptosis expresses cell loss in tumors, but it did not appear to be a prognostic factor.

Apoptosis↗

PubMed1995

Ultrastructural detection of DNA strand breaks in apoptotic neural cells by in situ end-labelling techniques.

Recently developed techniques based on 'in situ end-labelling' (ISEL) of DNA strand breaks may help to identify apoptotic cells in tissue sections. We have applied ISEL techniques at the electron microscopic (EM) level, in order to verify if ultrastructural features of apoptosis are indeed associated with evidence of DNA fragmentation, and whether cells committed to, but which have not yet entered the stage of cell death are also labelled. Terminal transferase and DNA polymerase assays were applied to thin sections of Araldite and LR Gold-embedded medulloblastomas and embryonic mouse dorsal root ganglia. Digoxigenin-labelled nucleotides were used; incorporation was demonstrated by immunogold staining. Apoptotic cells in various stages of the death process were easily labelled in both tissues. In addition, DNA fragmentation was demonstrated in cells with initial chromatin condensation, but otherwise indistinguishable from adjacent unstained cells. Our results show that EM-ISEL techniques effectively demonstrate the occurrence of DNA strand breaks in apoptotic and possibly 'pre-apoptotic' cells in neural tissues. Since the labelling is easily obtained on tissue that is routinely processed for electron microscopy, this technique may allow retrospective studies on archival material.

Animals↗

PubMed1995

Primary diffuse leptomeningeal gliomatosis with anaplastic features.

A case of primary diffuse leptomeningeal gliomatosis with anaplastic features, diagnosed during life and confirmed at autopsy, is presented. The clinical, radiological and pathological features are compared with those of the very few cases reported in the literature. Early papilloedema and hydrocephalus were followed by spinal and cranial nerve palsies. The NMR images and the tissue biopsy turned out to be useful for reaching an in vivo diagnosis. While in the previously reported cases the glial proliferation was microscopically a slow growing astrocytoma, the present case was histologically malignant and had a high labelling index (LIs) for proliferation markers (PCNA and KI-67). The high growth rate and the wide diffusion of the tumour at presentation may account for the poor prognosis of diffuse leptomeningeal gliomatosis and the inefficacy of radiotherapy and chemotherapy. The presence of basal lamina arount tumour cells and the immunohistochemical distribution of the proliferation markers are consistent with the origin of primary leptomeningeal gliomatosis from ectopic glia.

Biomarkers, Tumor↗

PubMed1995

Synaptic vesicle proteins, synaptophysin and chromogranin A in amyotrophic lateral sclerosis.

In amyotrophic lateral sclerosis (ALS) it is not known which motoneuron is affected first. The study of synaptic proteins may contribute to the clarification of the problem. Fifteen cases of ALS and five control cases were studied with the immunohistochemical demonstration of synaptophysin (Sy) and chromogranin A (CgA). Sy is a typical membrane protein of small synaptic vesicles (SSV), whereas CgA is found in large dense core vesicles (LDCV) and in neurosecretory granules. In controls, Sy is distributed as dots on the neuronal surface, on proximal dendrites and in neuropil, whereas CgA is found in perikarya and dendrites and as puncta in the neuropil. In ALS there is a marked decrease of Sy-positive dots. In chromatolytic neurons and spheroids a diffuse reaction may occur. CgA-positive dots disappear in ALS, sometimes replaced by a dust-like positivity. CgA is produced by Golgi apparatus and its reduction in ALS corresponds to the fragmentation of the Golgi complex, described in the literature. The findings are interpreted as secondary to the lower motoneuron degeneration and discussed in relation to our knowledge on vesicle production and migration in the neuron and on synapses in the anterior horns of spinal cord.

Adult↗

PubMed1995

Final height after long-term growth hormone treatment in Turner syndrome. European Study Group.

OBJECTIVES: To study final height after long-term growth hormone (GH) treatment in girls with Turner syndrome (TS). PATIENTS: One hundred fifty three patients with TS, participating in five European trials, were included. They started GH treatment in 1987-1989 at an age of 10 years or older. Mean age at start of treatment ranged between 11.7 and 14.6 years among countries and mean bone age between 9.4 and 11.8 years. Fourteen girls were lost to follow-up, leaving 139 for analysis. Most girls have now attained final height (FH), defined as a linear growth velocity (GV) of 4 mm/yr or less, measured over at least 6 months (group 1, n = 56), or near-FH, defined as a GV of 5 to 9 mm/yr (group 2, n = 22). Sixty-one girls were still growing 10 mm/yr or more. METHODS AND MAIN RESULTS: At the last measurement, mean (SD) height was 150.7 (4.9) cm in group 1 and 148.5 (5.1) cm in group 2. The differences between FH and projected final height based on extrapolation of the initial height-standard deviation score on Turner syndrome reference values, were 2.9 (3.8) and 3.0 (3.3) cm, respectively. The mean gain over the Bayley-Pinneau prediction of FH was 3.3 (3.9) cm in both groups. No significant differences between countries were found. The range of gains over projected height (-4.7 to 12.1 cm) was large, and 25% of gains were 5 cm or more. Gain over initial projection was strongly related to initial growth delay and to growth response during the first 2 years of treatment. A logistic regression model is presented that predicts gain of more than 5 cm with a positive predictive value of 62% and a negative predictive value of 84%. CONCLUSIONS: Long-term GH treatment in girls with TS, starting treatment at a relatively advanced age ( > 10 years) resulted in a modest mean gain in FH of 3 cm, with wide interindividual variation.

Adolescent↗

PubMed1995

Final height and long-term outcome after growth hormone therapy in Turner syndrome: results of a German multicentre trial.

Final height was investigated in 85 patients from a German multicentre trial of human growth hormone (GH) therapy in Turner syndrome. Six patients (mean age, 15.4 +/- 1.0 years; mean duration of therapy, 4.4 +/- 1.0 years) fulfilled the criteria for having reached final height (i.e. a height velocity < 0.5 cm/year). Four subjects had stopped therapy and two were still receiving GH. The mean final height of patients was 150.9 +/- 4.7 cm (range, 143.3-154.9 cm). In 3 subjects, projected final height was exceeded by 1.4, 6.5 and 10.8 cm, 1 patient just failed to reach projected final height by -1.7 cm and the 2 remaining patients did not attain projected final height by -3.2 and -12.1 cm. In the latter case, lack of height gain was associated with early onset and rapid progress of spontaneous puberty. The changes in height SDS were analysed in the other patients still receiving GH therapy over a period of 6 years, and it appeared that 2 IU/m2/day was less effective than 3 or 4 IU/m2/day, but that 4 IU/m2/day was no more effective than 3 IU/m2/day. These limited, non-controlled results indicate that GH therapy may be effective in increasing final height in Turner syndrome, though some patients may not benefit.

Adolescent↗

PubMed1994

Ubiquitinated dystrophic neurites suggest corticospinal derangement in patients with amyotrophic lateral sclerosis.

Pathologic changes affecting the upper motoneuron (UMN) were studied in 37 cases of amyotrophic lateral sclerosis (ALS) by histology and immunohistochemistry and by electron and immunoelectron microscopy. The most striking finding was represented by ubiquitin-positive dot-like structures related to (1) glial lipofuscin granules, (2) small polyglucosan bodies and (3) dystrophic neurites. Their distribution areas did not overlap. In ALS cases, ubiquitinated dystrophic neurites were twice as frequent as in controls in the arcuate region of motor cortex; moreover, in ALS cases they were twice as frequent in the spinal cord at the end of corticospinal tracts, compared with the motor cortex. These findings may indicate the presence in ALS of a 'dying-back' of the corticospinal motoneuron, independently of its primary or secondary involvement.

Adult↗

PubMed1994

Abortion in Italy.

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Abortion, Legal↗

PubMed1994

Colocalization of cytokeratin 18 and villin in type III alveolar cells (brush cells) of the rat lung.

Alveoli of the rat lung are lined by three different cell types, the flat type I cells and the cuboidal type II and type III cells. Type III cells differ from type II cells by the presence of an apical tuft of microvilli and the absence of lamellar type secretory granules. In the present study we show by double immunolabelling that type III cells of the rat lung can be identified at the light- and electron microscope level by antibodies against both cytokeratin 18 and the actin-crosslinking protein villin. At the ultrastructural level, microvilli and their rootlets in the apical cytoplasm were labelled by the anti-villin antibodies, whereas a monoclonal antibody against cytokeratin 18 (Ks18.04) labelled bundles of intermediate filaments. In conclusion, antibodies against villin and certain monoclonal antibodies specific for cytokeratin 18 can be used as tools for selective visualization of type III cells in the rat lung.

Animals↗

PubMed1994

Ubiquitin and neurofilament expression in anterior horn cells in amyotrophic lateral sclerosis: possible clues to the pathogenesis.

Cytoskeletal abnormalities are a prominent pathological feature of anterior horn cells in amyotrophic lateral sclerosis (ALS), and are thought to be involved in the process of motor neuron death. Skein-like filamentous inclusions have been detected by immunocytochemical staining for ubiquitin, a stress protein involved in targeting abnormal proteins for proteolysis. So far, identification of the target protein has been elusive. We have studied the ultrastructural localization of ubiquitin and neurofilaments by post-embedding immunogold staining. In skein-like arrays, strong ubiquitin labelling was concentrated on abnormally formed 15-20 nm filaments; neurofilament labelling was localized on 10 nm filaments adjacent or in continuity with the abnormal filaments. In addition, Bunina bodies were a major site of ubiquitin accumulation. Our results suggest that ubiquitinated filaments in skein-like inclusions might originate from abnormally aggregated neurofilament proteins, which are no longer recognized by antibodies to neurofilament epitopes. Furthermore, the presence of ubiquitin in Bunina bodies suggests that, in addition to its protective role, ubiquitin might be directly implicated in the mechanism of programmed neuronal death in ALS.

Amyotrophic Lateral Sclerosis↗

PubMed1994

Reactive cell proliferation and microglia following injury to the rat brain.

The non-astrocytic cells which proliferate in the rat brain after the induction of an area of necrosis have been characterized and counted by means of combined in vivo bromodeoxyuridine (BrdU) administration and immunohistochemical demonstration of glial fibrillary acid protein (GFAP), vimentin, Ricinus communis agglutinin 120 (RCA-1), Griffonia simplicifolia B4 isolectin (GSI-B4), keratan sulphate (KS), carbonic anhydrase C (CA.C), transferrin (TF) and ferritin. Two days after the injury, 7.5% of the proliferating cells were GFAP-positive reactive astrocytes, 5.7% were RCA-1-positive cells and 17.4% were GSI-B4-positive cells. Lectin-binding cells had the microscopic and ultrastructural aspects of microglia; they proliferated around the needle track and in the corpus callosum. Microglia represented a large fraction of the proliferating cells. Evidence is presented for the origin of at least a proportion of perilesional astrocytes and microglia from the periventricular matrix, and of microglia from blood precursors. Other non-proliferating microglia cells transiently appeared in the normal brain around the wound, in agreement with the existence of two different microglia cell populations reacting with different modalities to an area of necrosis.

Animals↗

PubMed1994

Atrial natriuretic factor antagonises angiotensin II--induced vasopressin release in rat subfornical organ.

The coexistence of Atrial Natriuretic Factor (ANF) and Angiotensin II (Ang II) receptors in the subfornical organ suggested that ANF may influence the action of Ang II at this level. To test this hypothesis the effect of ANF pre injected into subfornical organ (SFO) on Ang II-induced vasopressin release was investigated in rats. ANF blunted vasopressin release elicited by circulating Ang II. This study indicates SFO as one of the main sites at which ANF-Ang II interactions occur.

Angiotensin II↗

PubMed1993

Immunohistochemistry of glial reaction after injury in the rat: double stainings and markers of cell proliferation.

The astrocytic reaction in the rat after brain injury has been studied immunohistochemically for intermediate filaments (GFAP and vimentin), also with double staining procedures, and for markers of proliferation (BrdU and PCNA). GFAP-positive reactive astrocytes appeared around the lesion, where they were vimentin-positive and at a distance. BrdU and PCNA showed a high labelling index around the wound at day 2 and scattered positive nuclei were also found at a distance in the ipsilateral side. BrdU-positive astrocytes represented a minor fraction of GFAP- and vimentin-positive astrocytes. The expression of vimentin persisted at least 15 days after the lesion. Our results could suggest that distant reactive astrocytes originate through hypertrophy while those close to lesion arise by hyperplasia from mature or immature glial cells. The hypothesis is formulated that cells of the periventricular matrix contribute to the post-traumatic proliferative activity.

Animals↗