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Biomedical subjects

R Antonucci

Publications and source records attributed to R Antonucci.

18 recordsLinked to original sources

Circulating haemopoietic and endothelial progenitor cells are decreased in COPD.

Circulating CD34+ cells are haemopoietic progenitors that may play a role in tissue repair. No data are available on circulating progenitors in chronic obstructive pulmonary disease (COPD). Circulating CD34+ cells were studied in 18 patients with moderate-to-severe COPD (age: mean+/-sd 68+/-8 yrs; forced expiratory volume in one second: 48+/-12% predicted) and 12 controls, at rest and after endurance exercise. Plasma concentrations of haematopoietic growth factors (FMS-like tyrosine kinase 3 (Flt3) ligand, kit ligand), markers of hypoxia (vascular endothelial growth factor (VEGF)) and stimulators of angiogenesis (VEGF, hepatocyte growth factor (HGF)) and markers of systemic inflammation (tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8) were measured. Compared with the controls, the COPD patients showed a three-fold reduction in CD34+ cell counts (3.3+/-2.5 versus 10.3+/-4.2 cells.microL-1), and a 50% decrease in AC133+ cells. In the COPD patients, progenitor-derived haemopoietic and endothelial cell colonies were reduced by 30-50%. However, four COPD patients showed progenitor counts in the normal range associated with lower TNF-alpha levels. In the entire sample, CD34+ cell counts correlated with exercise capacity and severity of airflow obstruction. After endurance exercise, progenitor counts were unchanged, while plasma Flt3 ligand and VEGF only increased in the COPD patients. Plasma HGF levels were higher in the COPD patients compared with the controls and correlated inversely with the number of progenitor-derived colonies. In conclusion, circulating CD34+ cells and endothelial progenitors were decreased in chronic obstructive pulmonary disease patients and could be correlated with disease severity.

Aged↗

Acute encephalopathy associated with respiratory syncytial virus infections in childhood. A literature review.

Respiratory syncytial virus (RSV) has been described as the single most important virus causing acute respiratory infections, especially bronchiolitis and pneumonia, in children. The most severe infections affect the youngest infants and well-defined high-risk groups, including infants with a history of premature birth, and those with chronic lung disease, congenital heart disease, cystic fibrosis and immunodeficiency. It has been reported that approximately 1/3 of high-risk children hospitalized with RSV infection are admitted to the intensive care unit, while the need for mechanical ventilation and mortality rate are increased in infants with underlying cardiac disease or chronic lung disease. The majority of infants hospitalized for RSV lower respiratory tract infection develop one complication or more, which have an impact on hospital length of stay and costs. A relatively uncommon complication consisting of seizures and other neurologic abnormalities such as lethargy, irritability and abnormal tone has been sporadically reported in infants and children with RSV respiratory infection. A recent study first focused on the association between RSV bronchiolitis and an encephalopathic process occurring in the form of a seizures disorder. This transient neurologic complication seems to be frequently associated with an abnormal EEG pattern, but no anatomic brain damages have been shown. Little is known about the long-term neurodevelopmental outcomes of children developing RSV-related encephalopathy, so a prolonged period of neurologic follow up can be recommended.

Acute Disease↗

Skeletal muscle dysfunction in chronic obstructive pulmonary disease.

During the last decade evidence has been accumulated on the role of skeletal muscle dysfunction in reducing exercise capacity and affecting the quality of life of patients with chronic obstructive pulmonary disease (COPD). An appreciable body of research has helped to identify morphological and biochemical alterations, physiological consequences, and possible therapeutic interventions. There are, however, still many areas of uncertainty. For example it is not clear how much of the alterations are within the muscle itself or the consequence of the altered environment in which the muscle works. Similarly it is not clear how much of the impairment is simply due to aging and chronic inactivity. Another key issue is the possible additive effect of drugs often used in COPD patients, such as steroids, beta 2-agonist and cyclosporin. A specific additional layer of complexity comes from nutritional considerations and in particular loss of muscle mass which not infrequently accompanies severe disease and even greater exercise intolerance. Studies on the effects of training or other therapeutic interventions have shown that muscle dysfunction is partially reversible. There is, however, a clear need for studies based on cellular and molecular methods aimed to clarify the role of factors such as oxidative stress, inflammation and nutritional deficiencies on skeletal muscle structure and function. The focus of this review is to highlight the current knowledge on skeletal muscle dysfunction in COPD and briefly summarize the possible therapeutic implications.

Humans↗

VIP-like immunoreactivity in the intestinal tract of fish with different feeding habits.

We studied the distribution of vasoactive intestinal polypeptide immunoreactive (VIP-ir) cells and fibres in the intestine of three fish species with different feeding habits: the silver carp (Hypophthalmichthys molitrix), the goldfish (Carassius auratus), and the pumpkinseed sunfish (Lepomis gibbosus). Each species was divided into two groups: (1) fish fed once a day up until sacrifice and (2) fish fed once a day and then fasted three days before sacrifice. Immunoreactive endocrine cells and fibres were present in all three fish species. The immunoreactive cells were distributed along the entire intestinal mucosa of the carp and goldfish but were found only in the anterior intestine of the sunfish. The immunoreactive fibres were present along the entire intestinal wall, in the myenteric plexus, in the circular muscular layer, and in the connective tissue of the mucosa in all three fish species. No differences were found between the cells and fibres of normally-fed animals and the cells and fibres of fasted animals. The authors hypothesize that the different distributions of VIP-ir cells and fibres are related to the different contents of hard and indigestible matter of the fish food.

Animals↗

A water-vapour giga-maser in the active galaxy TXFS2226-184.

Active galactic nuclei are thought to be powered by gas falling into a massive black hole; the different types of active galaxy may arise because we view them through a thick torus of molecular gas at varying angles of inclination. One way to determine whether the black hole is surrounded by a torus, which would obscure the accretion disk around the black hole along certain lines of sight, is to search for water masers, as these exist only in regions with plentiful molecular gas. Since the first detection of an extra-galactic water maser in 1979, they have come to be associated primarily with active galaxies, and have even been used to probe the mass of the central engine. Here we report the detection of a water giga-maser in the radio galaxy TXFS2226-184. The strength of the emission supports a recently proposed theory of maser pumping that allows for even more powerful masers, which might be detectable at cosmological distances. Water masers may accordingly provide a way to determine distances to galaxies outside the usual distance ladder, providing an independent calibration of the Hubble constant.

Astronomical Phenomena↗

[The effect of cadmium on the intestine of Carassius auratus].

The paper deals with the cadmium effects on the intestinal mucosa of adult Carassius auratus after 7, 14 and 40 days of exposure. After 7 days the mucosa becomes oedematous; the mucous cells show intensive secretion. The cells showing immunoreactivity for the Met- and Leu-enkephalin miss this feature. After 14 days these modifications diminish and after 40 days disappear completely and the mucosa gains its normal characteristics.

Animals↗

Serum lipoprotein pattern as modified in G6PD-deficient children during haemolytic anaemia induced by fava bean ingestion.

In the present study, plasma lipid concentrations were determined at different times after admission in sera from G6PD-deficient children during haemolytic crisis induced by fava bean ingestion. Reductions in total, LDL and HDL cholesterol were found in association with the maximum of bone marrow hyperplasia. A return towards normal values occurred with regression of the disease. No changes in other lipid parameters were observed. These data suggest that alterations of lipoprotein pattern, other than in experimental animals, are also present in humans with non-malignant proliferative processes. These changes appear to be a consequence of the disease, probably due to an increased utilization of cholesterol by proliferating cells.

Anemia, Hemolytic↗

[Immunohistochemical and ultrastructural study of endocrine cells from the pyloric region of the European mole (Talpa europaea)].

The distribution and the morphology of some endocrine cells (gastrin, somatostatin and 5-HT immunoreactive) in the pyloric region were studied in the Talpa europaea, an insectivore representing one of the most primitive living Eutherians. The immunohistochemical studies enabled us to identify and calculate the percentage of each cell type: the most numerous endocrine cells were gastrin immunoreactive; fairly numerous appeared somatostatin immunopositive; less numerous were 5-HT immunoreactive cells. While the ultrastructural observations let us describe four endocrine cell types: G cells producing gastrin, D cells containing somatostatin, EC cells of the gastric type producing 5-HT and D1 cells whose content is still unknown.

Animals↗

Enhancement of sickle erythrocyte adherence to endothelium by autologous platelets.

The increased adhesiveness of sickle erythrocytes (SS RBC) to endothelial cells has been confirmed in a static system utilizing fresh umbilical vein endothelium. Adherence of SS RBC to the endothelium was as great in the presence of calcium-containing buffer as when incubated in plasma. SS RBC suspended in autologous platelet-rich plasma adhered to a greater extent than when suspended in autologous platelet poor plasma. Prostacyclin, thromboxane B2, and an inhibitor of collagen- and epinephrine-induced platelet aggregation (B13.177) did not affect SS RBC adherence to endothelium. Aspirin in a concentration of 5 micrograms/ml slightly decreased SS RBC adherence to endothelium in the presence of platelets. Platelets may play a significant role in the increased adhesiveness of SS RBC to endothelium. To the extent that increased SS RBC adhesiveness contributes to the genesis of painful crises and to the extent platelets augment this adhesiveness, agents affecting platelet function may prove useful in preventing painful crises.

Anemia, Sickle Cell↗

Immunohistochemical localization of some endocrine cells in the gastroenteropancreatic system of Erinaceus europaeus.

The distribution of chromogranin A and neuron specific enolase (NSE) in the neuroendocrine gut system and the morphology and distribution of cells containing gastrin, somatostatin, neurotensin and VIP in the gastroenteropacreatic (GEP) apparatus of Erinaceus europaeus were investigated by immunohistochemical methods. Chromogranin A and somatostatin immunoreactive cells were present throughout the gastrointestinal mucosa, with the exception of the oesophagus and in the pancreas. Gastrin cells were peculiar of the pyloric glands and duodenal mucosa and neurotensin cells of the small intestine. No VIP immunoreactive endocrine cells were noticed in the GEP system. VIP and NSE immunoreactivities were detected both in nerve cell bodies and terminals of the wall of the GEP apparatus. NSE immunoreactivity was found in the endocrine cells of the fundic and pyloric mucosa.

Animals↗

Water and sodium imbalance in COPD patients.

Water retention and hyponatraemia are typically observed in the final stages of Chronic Obstructive Pulmonary Disease (COPD) and the onset of edema is a poor prognostic factor. For several years the pathogenesis of edema in COPD patients was attributed to heart impairment because of pulmonary hypertension, but the evidence that cardiac output is often adequate for the metabolic demands has suggested, since 1960, that the pathogenesis of edema in these patients would be correlated with gas exchange impairment and in particular with carbon dioxide (CO2) retention. The gas exchange impairment induces, in these patients several hormonal abnormalities: renin (Rn), angiotensin II (AnII), aldosterone (Ald), atrial natriuretic peptide (ANP), vasopressin (ADH) and endothelial factors are some of the factors involved. The systemic response to hypercapnia has the effect of reducing the renal blood flow and, as a result, increasing water and sodium retention with the final effect of edema and hyponatraemia. The aim of this brief review is to highlight the current knowledge on renal/hormonal abnormalities in COPD and their therapeutic implications.

Atrial Natriuretic Factor↗

Exercise physiology in COPD.

Multiple mechanisms contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). The ability to increase ventilation during exercise is reduced; the more advanced the disease, the more impaired the exercise tolerance is. However, factors other than ventilatory limitation play an important role in reducing the exercise capacity in COPD. Data implicating peripheral muscle atrophy and muscle weakness as cofactors have been reported in individuals with advanced disease. At this stage daily activities are curtailed to avoid exertional respiratory discomfort. Recent studies have demonstrated that the muscle aerobic capacity of stable hypoxemic COPD patients is impaired; oxygen uptake (V'O2) kinetics and 31P magnetic resonance spectroscopy studies have shown that these patients rely heavily on non-aerobic energy sources even during moderate, sustained workloads. Finally, early occurrence of metabolic acidosis has been demonstrated in patients with mild to severe COPD during exercise. Inadequate tissue oxygenation appears to result from a defect in peripheral oxygen utilization rather than from a reduction in O2 bulk flow. Peripheral factors may include: a) impaired diffusive conductance for O2 between red cells and mitochondria; b) heterogeneous distribution of O2 bulk flow within the exercising muscle fibers; c) inertia of the oxidative processes at the cellular level; d) changes in distribution of muscle fibers, e) reduction in muscle aerobic enzymes; and f) poor nutritional status. Since muscle dysfunction has an important role in the development of exercise intolerance, physical rehabilitation is more and more used as part of the treatment of COPD. The aim of this review is to briefly discuss current views on the mechanisms responsible for the reduced ability to exercise and the rationale for exercise rehabilitation in COPD patients.

Exercise↗

[Duodenal ulcer in 2 dizygotic twins].

We report two cases of duodenal ulcer (DU) identified at endoscopy in a pair of dizygotic twins; their outstanding clinically recognizable features were a very early onset, a great familiar occurrence, a lack of triggering conditions (drugs, burns, stress, sepsis, respiratory distress), normal serum levels of gastrin and pepsinogen I, inadequate response to medical treatment with H2-receptor antagonists, but satisfactory response to associated therapy with H2-receptor antagonists and sucralfate. Results of this study show that examined twins were affected by a form of early-onset primary DU, probably inherited like an autosomal dominant disorder with high degree of penetrance, associated with normal serum pepsinogen I and gastrin; in this form of Du a decreased tissue resistance of duodenal mucosa is likely more important, pathogenically, than an increased peptic secretion. At present long-term prognosis of our patients is unknown.

Diseases in Twins↗

[Wiedemann-Beckwith syndrome in childhood].

A follow up examination was carried out in a 10 year old child who had been diagnosed as having Wiedemann-Beckwith syndrome soon after birth. Macrosomy was seen to persist and body asymmetry and some dysmorphic aspects had become more pronounced over the years. The presence of moderate mental deficiency had led to difficulty in social relationships. In the prepuberty phase, the reappearance of hypoglycemia crises, which were also noted in the neonatal age, was of particular interest.

Beckwith-Wiedemann Syndrome↗