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L Troiano

Publications and source records attributed to L Troiano.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Anthropometric skin-fold and impedance measurement assessment of the maternal nutritional status at the end of pregnancy. Comments deduced from a study of 54 cases].

BACKGROUND: It is generally accepted that an optimal maternal weight gain is indicative of a normal course of pregnancy. Nevertheless, evaluations of nutritional status should not be limited to the periodic body weight measurement alone, they should rather include the measurement of anthropoplicometric parameters more strictly associated with the variations of the different body components (fat mass, fat-free mass and body water). Therefore, it seems necessary to define standard parameters, such as to allow the attribution of a clinical value to the anthropometric variations that can be measured during pregnancy. In this study we preliminarily proposed to survey maternal nutritional status in a group of women examined in the second day after delivery. MATERIALS AND METHODS: Anthropoplicometric parameters and bioelectric impedance measurements were evaluated in order to study nutritional status of 54 puerperae within 48 hours after delivery. A linear regression analysis was carried out examining the relationship of anthropoplicometric measurements with gestational weight gain and post-partum impedance parameters. RESULTS AND CONCLUSIONS: The results of this study lead to believe that a correct examination of maternal nutritional status must necessarily include not only weight and body mass index, but also an accurate and periodic anthropoplicometric evaluation including limb circumferences and triceps plica.

Adult↗
PubMed1996

Successful immunosenescence and the remodelling of immune responses with ageing.

In recent decades, major theoretical and technological advances have been achieved in the field of immunology. These have allowed the scientific community to analyse the immune system in a much more sophisticated manner than was possible even 20 years ago. Moreover, great theoretical changes have also occurred in gerontology-in particular, the hypothesis has been put forward that ageing and diseases are two different phenomena, and that successful ageing, i.e. ageing in good psychophysical conditions, is really possible for most humans and animals. Immunosenescence was then carefully investigated, either in selected healthy people of advanced age or in the oldest old people, such as healthy centenarians. The main results showed that most immune parameters are indeed well preserved even at this far advanced age. This paper deals with some of the most important theoretical problems of immunosenescence. An immunological tenet was that the most important phenomenon of immunosenescence is the involution of the thymus. In most textbooks and papers it is taken for granted that the thymus starts its involution immediately after puberty. When people aged 60-65 were considered old, it was not difficult to think that they could live for the rest of their life with a fully involuted thymus. The findings on centenarians challenge this tenet, as they have only a small reduction of T lymphocytes, and a relatively normal number of virgin and memory T cells, together with a functional T cell repertoire. Other observations reported here on centenarians, concerning the activity of B lymphocytes and the cytokine network, as well as those on the well-preserved innate immunity and the cells' capability of undergoing proliferation after appropriate stimuli, suggest that complex immune changes occur with age, but also indicate that we have to modify our attitude, to grasp the new scenario which is emerging. Immunosenescence can no longer be considered as a unidirectional deterioration, and this complex phenomenon is much better described by terms such as 'remodelling', 'reshaping' or 'retuning'.

Aging↗
PubMed1996

[Echographic, MRI and CT features in a case of bladder endometriosis].

Endometriosis is relatively frequent in females of menstrual age and consists in the appearance of active endometrial tissue at site other than uterine cavity. Endometrial tissue has been described to colonise the urinary system, particularly the urinary bladder. The most common clinical features of vesical endometriosis are urgency and frequency, hypogastric pain and hematuria. We report on a case of vesical endometriosis whose presenting features were dysmenorrhea, stranguria and pelvic pain. MRI and CT did not provide different or more precise information than ultrasound scan: these findings were indistinguishable from an intrauterine lesion. On the contrary endovaginal sonography was more sensitivity than MRI and CT. Cystoscopy was negative. Nondiagnostic laparoscopy was performed. Patient underwent laparotomy and partial cystectomy. Histopatological findings demonstrated an endometriosis of the muscle layer of the bladder. The rarity of this condition prompted us to report on the problems encountered in making the differential diagnosis.

Adult↗
PubMed1995

Involvement of CD45 in dexamethasone- and heat shock-induced apoptosis of rat thymocytes.

CD45 is a transmembrane tyrosine-specific phosphatase which participates in lymphoid cell signal transduction during T cell activation, as well as in intrathymic negative and positive selection. In mammals, this molecule exhibits a variety of isoforms of different molecular weight, whose roles have still to be fully elucidated. We report here that apoptosis of rat thymocytes after in vitro dexamethasone and heat shock treatment was accompanied by an early significative increase of cells expressing CD45RC, the high molecular weight isoform of CD45 molecule. The same phenomenon was observed in thymocytes derived from in vivo dexamethasone-treated rats. However, the increase of CD45RC+ cells was not apparently characteristic of cells undergoing apoptosis, as the same phenomenon was also observed in rat thymocytes induced to proliferate by Concanavalin A. On the whole, these results suggest that CD45 modulation can be added to the list of early molecular events, such as the increased expression of genes (ornithine decarboxylase), proto-oncogenes (c-fos, c-jun, c-myc) and activation of transcription factors (AP-1, NFkB), we previously demonstrated in the same experimental model to occur and to be shared by these two apparently opposite biological processes, i.e., cell proliferation and apoptosis, both likely depending on a complex balance of protein phosphorylation and dephosphorylation.

Animals↗
PubMed1995

Sendai virus and herpes virus type 1 induce apoptosis in human peripheral blood mononuclear cells.

Recent reports suggest that several viruses, besides human immunodeficiency virus, induce apoptosis in infected cells. We report here that Sendai virus or Herpes simplex virus type 1 (HSV-1), two potent inducers of interferon-alpha, caused cell death in a consistent number of human peripheral blood mononuclear cells. A careful analysis of infected cells by different techniques, such as optical and electron microscopy, DNA agarose gel electrophoresis, and cytofluorimetric analysis of DNA content, showed that cell death was of apoptotic type. Sendai virus was more apoptogenic than HSV-1, and it was further studied to understand the mechanism(s) by which it induced apoptosis. Physical (uv and heat) and chemical (beta-propiolactone) inactivation reduced or abolished the apoptogenic power of Sendai virus. The use of a novel technique, which allows the study of mitochondrial membrane potential (MMP) in intact cells by flow cytometry, showed that a decrease of MMP is concomitant with the appearance of the hypodiploid peak. These results suggest that Sendai virus and HSV-1 can be added to the list of viruses causing apoptosis, which appears to be a general mechanism occurring during viral infection.

Apoptosis↗
PubMed1994

Apoptosis and spermatogenesis: evidence from an in vivo model of testosterone withdrawal in the adult rat.

The seminiferous epithelium is a highly proliferating tissue in which germ cell "degeneration" is a constant feature. Recent data based on morphological analysis have shown that spontaneously dying germ cells display some characteristics of apoptosis. In order to evaluate the molecular signals controlling the phenomenon, adult male rats were studied after in vivo treatment with ethane dimethane sulphonate, an agent which leads to testosterone withdrawal by a selective destruction of Leydig cells. DNA fragmentation by agarose gel electrophoresis and cell DNA content by flow cytometry after propidium iodide staining were used to evaluate and quantify apoptosis in the testis. Despite the simultaneous presence of cells with different ploidies, the present data suggest that testosterone withdrawal induces death by apoptosis and that this phenomenon is particularly evident in haploid germ cells. Thus, this study support the involvement of testosterone in regulating programmed cell death, beside cell proliferation and differentiation, during spermatogenesis.

Animals↗
PubMed1994

Mitochondrial modifications during rat thymocyte apoptosis: a study at the single cell level.

Apoptosis is an active type of cell death, occurring under several physiological and pathological conditions. The role of cellular organelles such as mitochondria in this process is still an open question. We recently described a new method to measure mitochondrial membrane potential in intact cells using flow cytometry. Using this method we studied alterations of mitochondrial membrane potential in a classical model of apoptosis, i.e., dexamethasone-treated rat thymocytes. Moreover, apoptosis induced by heat shock was also studied in the same cells. Mitochondria are functionally intact during the early phases of apoptosis, when DNA fragmentation occurs, whereas early alteration in their potential and mass takes place after DNA damage. According to flow-cytometric analysis, the presence of a hypodiploid peak, an index of nuclear DNA loss, predates depolarization of mitochondrial membrane and decrease of mitochondrial mass. Loss of plasma membrane integrity, which indicates cell death and is revealed by the permeability to propidium iodide, eventually follows. All these phenomena are more evident in dexamethasone-treated cells than in heat-shocked cells. Thus, in these types of apoptosis the involvement of mitochondria is apparently not a primary event.

Animals↗
PubMed1993

Studies of the relationship between cell proliferation and cell death. III. AP-1 DNA-binding activity during concanavalin A-induced proliferation or dexamethasone-induced apoptosis of rat thymocytes.

In previous papers we started to investigate the possible relationship existing between cell proliferation and cell death. We reported that in rat thymocytes, undergoing cell proliferation upon stimulation with Concanavalin A or cell death following dexamethasone treatment, an induction of c-fos and c-jun occurs with different but partially overlapping kinetics (Grassilli et al., BBRC, 1992, 188, 1261-1266). To test the hypothesis that, in both processes, the early induction of these nuclear oncogenes is necessary to allow the induction of later-expressed genes regulated at the transcriptional level by AP-1 complex, AP-1 DNA-binding activity was investigated in the aforementioned model. Indeed, we found that AP-1 is activated not only in proliferating but also in apoptotic cells, with a kinetics in accord with our data about c-fos and c-jun mRNA accumulation in the same experimental model. Moreover, our findings suggest that an interaction between AP-1 and glucocorticoid receptor also occurs in our model of dexamethasone-mediated apoptosis.

Animals↗
PubMed1992

Studies of the relationship between cell proliferation and cell death. II. Early gene expression during concanavalin A-induced proliferation or dexamethasone-induced apoptosis of rat thymocytes.

Several data in the literature suggest that an intriguing relationship exists between cell proliferation and cell death. Accordingly, we studied the early expression of different genes in the same cells, i.e. rat thymocytes, undergoing cell proliferation upon stimulation with Concanavalin A or cell death following dexamethasone treatment. We showed that an early accumulation of c-fos, c-jun and c-myc mRNA occurred in both phenomena but with different kinetics. It can be speculated that the early induction of nuclear oncogenes is necessary to allow the later induction of other genes probably regulated at the transcriptional level by the AP-1 complex and/or by Myc protein. The accumulation of the transcript for another gene, i.e. poly(ADP-ribose)polymerase, an enzyme responsible for posttranslational modifications of several nuclear proteins, could instead be related to chromatin modifications occurring in both processes.

Animals↗
PubMed1992

Inhibition of apoptosis by zinc: a reappraisal.

Apoptosis--or programmed cell death--is an active type of cell death, occurring in several pathophysiological conditions. One of the most important characteristics of apoptosis is that cell death is preceded by DNA fragmentation, consequent to the activation of nuclear calcium- and magnesium-dependent endonuclease(s). DNA fragmentation can be inhibited by zinc ions. By using several techniques, such as DNA agarose gel electrophoresis, cytofluorimetric analysis of DNA content and of cell cycle, 3H-thymidine incorporation and trypan blue dye exclusion test, we show that zinc, despite completely inhibiting DNA fragmentation and the consequent loss of nuclear DNA content, does not protect rat thymocytes from spontaneous or dexamethasone-induced death. Our data also suggest that DNA fragmentation, although characteristic, is not a critical event for thymocyte death of apoptotic type.

Animals↗
PubMed1992

Apoptosis--programmed cell death: a role in the aging process?

Cells continuously exposed to genotoxic agents, such as oxygen free radicals (OFRs), deeply involved in the aging process use a variety of cellular defense mechanisms. These defense mechanisms include DNA repair enzymes, antioxidants, poly(ADP-ribosyl)polymerase (pADPRP), and stress proteins and they constitute an integrated network. An age-related failure of the efficiency of this network can affect cell proliferation and cell death, two phenomena tightly linked and regulated. Recent data from our laboratory on the role of DNA damage and pADPRP activation and on the type of cell death induced by OFRs in human lymphocytes are reviewed. In vitro and in vivo data on possible strategies to reduce oxidative stress in lymphocytes from normal and Down syndrome subjects, by using natural compounds and trace elements, are presented. They indicate that nicotinamide and L-carnitine protect human cells from OFR-induced damage and suggest that they are possible candidates as antiaging substances.

Aging↗