The relationship between morphological awareness and reading comprehension in Spanish-speaking children.

In the last decades, a series of studies has explored the role of morphological awareness on reading comprehension. Path analysis studies performed in English have shown that morphological awareness benefits reading comprehension both directly and indirectly, through word decoding. This issue has seldom been explored in Spanish. The aim of this study was to replicate in Spanish the results previously found in English. We used path analysis to assess three alternative models of the relationship between morphological awareness, word decoding and reading comprehension in 4th grade Spanish-speaking children. Contrary to English, we found that morphological awareness benefits reading comprehension only directly. We conclude that in Spanish, in which accurate and fluent pronunciation of written words can be achieved through grapheme-to-phoneme conversion rules, morphological awareness does not help the correct pronunciation of words. Thus, morphological awareness is not relevant for word decoding in Spanish but is related to reading comprehension since this type of morphological knowledge provides access to the semantic and syntactic information of new words.

Morphological De-com-pos-it-ion Helps Recognize Low-er Frequency Words in Typically Developing Spanish-Speaking Children.

Several studies in Spanish and other languages have shown that, in a lexical decision task, children are more likely to accept pseudowords with a known morphological structure as words as compared to non-morphological pseudowords. Morphology also facilitates visual word recognition of actual words in children with reading difficulties. In the present study, we explored the role of morphology, frequency and reading proficiency (measured by school grade) in visual word recognition. Typically developing readers of Spanish from 2nd, 4th and 6th grades performed a lexical decision task in which the morphological complexity and the frequency of the words were factorially manipulated. Our results showed that morphology benefited the accuracy of visual word recognition for low frequency words only. We conclude that decomposition in morphemes occurs in Spanish only for less frequent words. These results in Spanish support models that posit the decomposition of morphologically complex words in the orthographic lexicon.

Development and validation of the Efficacious Self-Presentation Scale.

A new self-report measure of adolescent's self-presentation is described. The self-report scale was administered to 760 16-19-year-old subjects. Results of a factor analysis supported 6 identifiable factors reflecting different concepts, theoretically discussed, related to self-presentation: ability to regulate self-image, social sensitivity, body self-confidence, social self-confidence, social openness, and social desirability. The scale showed good convergent validity and internal consistency. Assertive tactics were predicted through ability to regulate self-image, social self-confidence, and social openness, whereas defensive tactics were predicted only through social openness and social sensitivity. The implications of the findings for future theoretical and empirical development of research in this field are discussed.

Anti-tissue transglutaminase antibodies from celiac patients are responsible for trophoblast damage via apoptosis in vitro.

OBJECTIVES: The association between maternal celiac disease (CD) and both reduced fertility and increased risk of adverse pregnancy-related events has been long documented. However, no evidences are available regarding the pathogenic mechanisms of this link. The aim of this study was to determine whether anti-tissue transglutaminase (anti-tTG) antibodies are involved in the damage of trophoblastic cells in vitro. METHODS: Human primary trophoblastic cells, isolated from term placenta, were exposed to anti-tTG immunoglobulin G (IgG) antibodies, both commercially available and separated from sera of three untreated celiac women. The ability of anti-tTG antibodies to bind to trophoblastic cells, invasiveness of placental cells through a layer of extracellular matrix, and the activity of cellular matrix metalloprotease (MMP) and cellular apoptosis were evaluated, as indicators of trophoblast damage, by TdT-mediated dUTP digoxigenin nick end labeling (TUNEL) and annexin V expression. RESULTS: Anti-tTG IgG showed a specific dose- and time-dependent binding to human trophoblast. In addition, trophoblastic cells, after being exposed to anti-tTG IgG antibodies, both commercially available and separated from sera of celiac women, showed an impaired invasiveness, a decreased activity of cellular MMP, and a greater percentage of TUNEL positivity and annexin V positivity. CONCLUSIONS: We showed that the binding of anti-tTG antibodies to trophoblast might represent a key mechanism by which the embryo implantation and pregnancy outcome are impaired in untreated celiac pregnant women. Because healthy trophoblast development is essential for placental and fetal development, these data provide a novel mechanism for CD-induced infertility, early pregnancy loss, and intrauterine growth retardation.

Suicidal ideation and time perspective in high school students.

OBJECTIVE: Many studies have enlightened the relevance of deepening our knowledge of suicidal ideation among adolescents. However, research has given insufficient attention to the impact of time perspective on suicidal ideation: the present study confirms this relationship in a large sample of adolescents. METHOD: A survey was conducted on a sample of 3700 Italian adolescents. We obtained data using a structured questionnaire addressing suicidal ideation, mental health status, self-esteem, individual and family characteristics, and time perspective (ZTPI) in three temporal frames: the past, present and future, and the attitude related to each one of them. Data were analyzed using bivariate and multivariate analyses. RESULTS: Overall, 9.2% of the sample reported severe suicidal ideation during the past two weeks; 7.6% reported moderate suicidal ideation. Female adolescents were more likely to report severe suicidal ideation when compared to males (chi((2))(2)=13.38, P=.001). There were no differences regarding age (chi((1))(2)=2.81, P=.245) and SES (chi((2))(2)=8.67, P=.08). The first discriminant function was mostly explained by psychopathological symptoms (General Global Index), self-esteem and two dimensions of the ZTPI (Negative Past and Fatalistic Present). CONCLUSIONS: Differences in time perspective dimensions between moderate and severe ideators suggest that these groups should be considered and analyzed as two discrete groups in further research.

Decision-making style among adolescents: relationship with sensation seeking and locus of control.

The principal aim of the study was to examine the psychometric properties and construct validity of the General Decision-Making Scale (GDMS) in a sample of 700 adolescents (aged 15-19 years). Confirmatory and exploratory factor analyses provide evidence for a solid five-dimension structure reflecting the theorized construct: rational, intuitive, dependent, avoidant and spontaneous. No differences were found with respect to gender; however older adolescents used more rational decision-making style than younger ones and had lower mean scores on intuitive, avoidant and spontaneous scales. Correlations between GDMS and both Sensation Seeking and Locus of Control scales provided substantiation for the convergent validity. Higher school achievements were positively associated with a rational decision-making style while the number of absences from school was positively related to spontaneous and avoidant styles. Data encourage the use of GDMS not only in the research of personality but for educational and counseling purposes.

Discrepancies between parents' and children's attitudes toward TV advertising.

The authors conducted a study with 500 parent-child dyads. The sample comprised 254 boys and 246 girls. The children were grouped into 5 age groups (1 group for each age from 7 to 11 years), with each group comprising 100 children. The survey regards discrepancies between children and their parents on attitudes toward TV advertising to determine how TV commercials affect children's developmental stages and, particularly, their credence, behavioral intentions, and TV enjoyment. Regarding enjoyment and purchase dimensions, the group of 7-year-old children claimed that they enjoyed and are influenced in their consumer attitude more than did the groups of 8-11-year-old children. Credence decreased significantly with age. This study showed that parents tended to undervalue TV advertising's influence on their children. Parents' conformity was a significant predictor of children's attitude toward TV advertising. Results indicated that a high level of parental conformity was linked to the number of brands children claimed to possess.

Melatonin antagonizes the intrinsic pathway of apoptosis via mitochondrial targeting of Bcl-2.

We have recently shown that melatonin antagonizes damage-induced apoptosis by interaction with the MT-1/MT-2 plasma membrane receptors. Here, we show that melatonin interferes with the intrinsic pathway of apoptosis at the mitochondrial level. In response to an apoptogenic stimulus, melatonin allows mitochondrial translocation of the pro-apoptotic protein Bax, but it impairs its activation/dimerization The downstream apoptotic events, i.e. cytochrome c release, caspase 9 and 3 activation and nuclear vesiculation are equally impaired, indicating that melatonin interferes with Bax activation within mitochondria. Interestingly, we found that melatonin induces a strong re-localization of Bcl-2, the main Bax antagonist to mitochondria, suggesting that Bax activation may in fact be antagonized by Bcl-2 at the mitochondrial level. Indeed, we inhibit the melatonin anti-apoptotic effect (i) by silencing Bcl-2 with small interfering RNAs, or with small-molecular inhibitors targeted at the BH3 binding pocket in Bcl-2 (i.e. the one interacting with Bax); and (ii) by inhibiting melatonin-induced Bcl-2 mitochondrial re-localization with the MT1/MT2 receptor antagonist luzindole. This evidence provides a mechanism that may explain how melatonin through interaction with the MT1/MT2 receptors, elicits a pathway that interferes with the Bcl-2 family, thus modulating the cell life/death balance.

Redox modulation of the apoptogenic activity of thapsigargin.

Thapsigargin (THG), a selective inhibitor of endoplasmic reticulum (ER) Ca2+-ATPases, causes the rapid emptying of ER Ca2+; in some cell types, this is accompanied by apoptosis, whereas other cells maintain viability. In order to understand the molecular determinants of such a different behavior, we explored the role of oxygen versus nitrogen radicals, by analyzing the apoptogenic ability of THG in the presence of inhibitors of glutathione or nitric oxide (NO) synthesis, respectively. We observed that oxygen radicals play a sensitizing role whereas nitrogen radicals prevent THG-dependent apoptosis, showing that the apoptogenic effect of THG is redox sensitive.

Analysis of calcium changes in endoplasmic reticulum during apoptosis by the fluorescent indicator chlortetracycline.

Many studies suggest that endoplasmic reticulum (ER) Ca2+ pool rather than cytosolic Ca2+ may play a crucial role in triggering apoptosis. In this study, we performed an image analysis of cells loaded with the fluorescent dye chlortetracycline (CTC) to in situ analyze Ca2+ changes within the ER in apoptosing promonocytic U937 cells. The results, validated through the use of thapsigargin (THG) as ER Ca2+ depletor, confirm the findings that apoptotic cells have a Ca2+-depleted ER, in contrast with treated but still viable cells.

Non-apoptogenic Ca2+-related extrusion of mitochondria in anoxia/reoxygenation stress.

Tumor cells often develop molecular strategies for survival to anoxia/reoxygenation stress as part of tumor progression. Here we describe that the B lymphoma Epstein-Barr-positive cells E2r survive reoxygenation in spite of a very high and long-lasting increase in cytosolic Ca2+ and the loss of about half of their mitochondria due to specific extrusion of the organelles from the cells. The extrusion typically occurs 3 days after reoxygenation, and a regular mitochondrial asset is regained after further 24 h.

Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature.

There are several possible mechanisms by which antiphospholipid antibodies (aPL) may have adverse effects on placental functions. Examination of placentas and first-trimester decidua from antiphospholipid syndrome-complicated pregnancies has found little evidence of specific thrombotic placental pathology. It is now generally accepted that the clinically relevant aPL bind to proteins with affinity for phospholipids. The most important epitope for antiphospholipid syndrome-related aPL resides on beta2-glycoprotein-I (beta2GPI). aPL detected by anti-beta2GPI assays are associated with fetal loss. During differentiation to syncytium, trophoblasts express cell membrane anionic phospholipids that can bind beta2GPI. Adhered beta2GPI can be recognized by the antibodies that, once bound, interfere with trophoblast cell maturation, resulting in defective placentation. The improved outcome of pregnancies treated with heparin stimulated interest on the drug's mechanism of action. Several mechanisms could explain its beneficial effects in addition to a direct effect of heparin on the coagulation cascade. It might reduce the binding of aPL, inflammation by inhibiting complement activation, and might facilitate implantation. Further investigations are needed to better understand how aPL induce obstetric complications and to better clarify the functional role of heparin in the human placenta, leading to more successful therapeutic options.

Different fates of intracellular glutathione determine different modalities of apoptotic nuclear vesiculation.

U937 monocytic cells show two main apoptotic nuclear morphologies, budding and cleavage, that are the result of two independent morphological routes, since they never interconvert one into the other, and are differently modulated by stressing or physiological apoptogenic agents [Exp Cell Res 1996; 223:340-347]. With the aim of understanding which biochemical alterations are at the basis of these alternative apoptotic morphologies, we performed an in situ analysis that showed that in U937 cells intracellular glutathione (GSH) is lost in cells undergoing apoptosis by cleavage, whereas it is maintained in apoptotic budding cells. Lymphoma cells BL41 lose GSH in apoptosis, and show the cleavage nuclear morphology; the same cells latently infected with Epstein Barr Virus (E2r line) undergo apoptosis without GSH depletion and show the budding nuclear morphology. GSH depletion is not only concomitant to, but is the determinant of the cleavage route, since the inhibition of apoptotic GSH efflux with cystathionine or methionine shifts the apoptotic morphology from cleavage to budding. Accordingly, cystathionine or methionine antagonizes apoptosis in the all-cleavage BL41, without affecting the all-budding E2r.

Molecular determinants involved in the increase of damage-induced apoptosis and delay of secondary necrosis due to inhibition of mono(ADP-ribosyl)ation.

ADP-ribosylations are reversible posttranslational modifications that regulate the activity of target proteins, catalyzed by two different classes of enzymes, namely poly(ADP-ribosyl)polymerases (PARPs) and mono(ADP-ribosyl)transferases (ADPRTs). It is now emerging that ADP-ribosylation reactions control signal transduction pathways, mostly as a response to cell damage, aimed at both cell repair and apoptosis. Inhibition of ADPRTs, but not PARPs, increases the extent of apoptosis induced by cytocidal treatments, at the same time delaying secondary necrosis, the process leading to plasma membrane collapse in apoptotic cells, and responsible for apoptosis-related inflammation in vivo. Thus, ADPRT inhibitors may be ideal as adjuvants to cytocidal therapies; to this purpose, we investigated the molecular determinant(s) for such effects by probing a set of molecules with similar structures. We found that the apoptosis-modulating effects were mimicked by those compounds possessing an amidic group in the same position as two of the most popular ADPRT inhibitors, namely, 3-aminobenzamide and nicotinamide. This study may provide useful suggestions in designing molecules with therapeutic potential to be used as adjuvant in cytocidal therapies.

Melatonin as an apoptosis antagonist.

The pineal hormone melatonin (Mel), in addition to having a well-established role as a regulator of circadian rhythms, modulates nonneural compartments by acting on specific plasma membrane receptors (MT1/MT2) present in many different cell types. Mel plays immunomodulatory roles and is an oncostatic and antiproliferative agent; this led to the widespread belief that Mel may induce or potentiate apoptosis on tumor cells, even though no clear indications have been presented so far. Here we report that Mel is not apoptogenic on U937 human monocytic cells, which are known to possess MT1 receptors at the times (up to 48 h) and doses (up to 1 mM) tested. Mel does not even potentiate apoptosis, but instead, significantly reduces apoptosis induced by both cell-damaging agents (intrinsic pathway) and physiological means (extrinsic pathway). The doses required for the antiapoptotic effect (>or=100 microM) are apparently not compatible with receptor stimulation (receptor affinity<1 nM). However, receptor involvement cannot be ruled out, because we discovered that the actual Mel concentration active on cells was lower than the nominal one because of sequestration by fetal calf serum (FCS). Accordingly, in FCS-free conditions, Mel doses required for a significant antiapoptotic effect are much lower.

Oxidative upregulation of Bcl-2 in healthy lymphocytes.

In many cell systems, pharmacological glutathione (GSH) depletion with the GSH neosynthesis inhibitor buthionine sulfoximine (BSO) leads to cell death and highly sensitizes tumor cells to apoptosis induced by standard chemotherapeutic agents. However, some tumor cells upregulate Bcl-2 in response to BSO, thus surviving the treatment and failing to be chemosensitized. Cell lines of monocytic and lymphocytic origins respond to BSO treatment in an opposite way, lymphocytes being chemosensitized and unable to transactivate Bcl-2. In this article we investigate the response to BSO of lymphocytes freshly isolated from peripheral blood of healthy donors. After ensuring that standard separation procedures do not alter per se lymphocytes redox equilibrium nor Bcl-2 levels in the first 24 h of culture, we show that BSO treatment promotes the upregulation of Bcl-2, with a mechanism involving the increased radical production consequent to GSH depletion. Thus, BSO treatment may increase the differential cytocidal effect of cytotoxic drugs in tumor versus normal lymphocytes.

Intracellular pro-oxidant activity of melatonin deprives U937 cells of reduced glutathione without affecting glutathione peroxidase activity.

It was long believed that melatonin might counteract intracellular oxidative stress because it was shown to potentiate antioxidant endogenous defences, and to increase the activity of many antioxidant enzymes. However, it is now becoming evident that when radicals are measured within cells, melatonin increases, rather than decreasing, radical production. Herein we demonstrate a pro-oxidant effect of melatonin in U937 cells by showing an increase of intracellular oxidative species and a depletion of glutathione (GSH). The activity of glutathione peroxidase is not modified by melatonin treatment as it does occur in other experimental models.

The problem of binge drinking among Italian university students: a preliminary investigation.

Although binge drinking and excessive alcohol consumption are relevant public health problems in Italy, no research has been carried out on those topics for years. In the first months of the year 2005, 1000 undergraduates in a number of Italian universities were administered a survey regarding their attitudes in alcohol consumption. Participants were to complete a questionnaire including demographic and alcohol variables, the Sensation-Seeking Scale (SSSV) and the Positive Drinking Expectancy Scale (PDMS). According to previous research, students were categorized in non-drinkers, social, binge, and heavy drinkers. Results showed that the estimated percentage of binge drinking among university students is 32.9%. The survey revealed-by means of univariate and multivariate analysis-that social, binge, and heavy drinkers differ in terms of some drinking variables, in their expectancies about alcohol and in sensation-seeking dimensions. Implications for the prevention of binge drinking in young adults are currently under discussion even if further investigation into the Italian context is urgently needed.

Glutathione depletion up-regulates Bcl-2 in BSO-resistant cells.

Glutathione depletion by inhibition of its synthesis with buthionine sulfoximine (BSO) is a focus of the current research in antitumor therapy, BSO being used as chemosensitizer. We had previously shown that two human tumor cell lines (U937 and HepG2) survive to treatment with BSO: BSO can elicit an apoptotic response, but the apoptotic process is aborted after cytochrome c release and before caspase activation, suggesting the development of an adaptive response (FASEB J., 1999, 13, 2031-2036). Here, we investigate the mechanisms of such an adaptation. We found that following BSO, U937 up-regulate Bcl-2 mRNA and protein levels, by a mechanism possibly involving NF-kappaB transcription factor; the increase in protein level is limited by a rapid decay of Bcl-2 in BSO-treated cells, suggesting that redox imbalance speeds up Bcl-2 turnover. BSO-dependent Bcl-2 up-regulation is associated with the ability to survive to BSO. Indeed, 1) its abrogation by CAPE or protein synthesis inhibition sensitizes U937 to BSO; 2) in a panel of four tumor lines, BSO-resistant (U937, HepG2, and HGB1) but not BSO-sensitive (BL41) cells can up-regulate Bcl-2 following GSH depletion; remarkably, only the latter are chemosensitized by BSO.