Preterm Birth: analysis of longitudinal Data on siblings Based on random-effects logit Models

INTRODUCTION: The literature about the determinants of a preterm birth is still controversial. We approach the analysis of these determinants distinguishing between woman’s observable characteristics, which may change over time, and unobservable woman’s characteristics, which are time invariant and explain the dependence between the typology (normal or preterm) of consecutive births. METHODS: We rely on a longitudinal dataset about 28,603 women who delivered for the first time in the period 2005–2013 in the Umbria Region (Italy). We consider singleton physiological pregnancies originating from natural conceptions with birthweight of at least 500 g and gestational age between 24 and 42 weeks; the overall number of deliveries is 34,224. The dataset is based on the Standard Certificates of Life Birth collected in the region in the same period. We estimate two types of logit model for the event that the birth is preterm. The first model is pooled and accounts for the information about possible previous preterm deliveries, including the lagged response among the covariates. The second model takes explicitly into account the longitudinal structure of data through the introduction of a random effect that summarizes all the (time invariant) unobservable characteristics of a woman affecting the probability of a preterm birth. RESULTS: The estimated models provide evidence that the probability of a preterm birth depends on certain woman’s demographic and socioeconomic characteristics, other than on the previous history in terms of miscarriages and the baby’s gender. Besides, as the random-effects model fits significantly better than the pooled model with lagged response, we conclude for a spurious state dependence between repeated preterm deliveries. CONCLUSION: The proposed analysis represents a useful tool to detect profiles of women with a high risk of preterm delivery. Such profiles are detected taking into account observable woman’s demographic and socioeconomic characteristics as well as unobservable and time-constant characteristics, possibly related to the woman’s genetic makeup. TRIAL REGISTRATION: Not applicable

Denervation does not induce muscle atrophy through oxidative stress

Denervation leads to the activation of the catabolic pathways, such as the ubiquitin-proteasome and autophagy, resulting in skeletal muscle atrophy and weakness. Furthermore, denervation induces oxidative stress in skeletal muscle, which is thought to contribute to the induction of skeletal muscle atrophy. Several muscle diseases are characterized by denervation, but the molecular pathways contributing to muscle atrophy have been only partially described. Our study delineates the kinetics of activation of oxidative stress response in skeletal muscle following denervation. Despite the denervation-dependent induction of oxidative stress in skeletal muscle, treatments with anti-oxidant drugs do not prevent the reduction of muscle mass. Our results indicate that, although oxidative stress may contribute to the activation of the response to denervation, it is not responsible by itself of oxidative damage or neurogenic muscle atrophy

Peroxynitrite activates the NLRP3 inflammasome cascade in SOD1(G93A) mouse model of amyotrophic lateral sclerosis

Neuroinflammation, characterized by the appearance of reactive microglial and astroglial cells, is one of the several pathogenic mechanisms of amyotrophic lateral sclerosis (ALS), a fast-progressing and fatal neurodegenerative disease. Cerebrospinal fluid and spinal cord of ALS patients and SOD1 mutant mice show high concentrations of IL-1β. This interleukin, expressed as an inactive precursor, undergoes a proteolytic maturation by caspase1, whose activation, in turn, depends on inflammasomes. Whether and how inflammasome is activated in ALS models is still to be clarified. The mechanism of inflammasome activation was studied in murine microglial cells overexpressing hSOD1(G93A) and verified in the spinal cord of hSOD1(G93A) mice. Murine microglial hSOD1(G93A) cells express all the inflammasome components and LPS activates caspase1 leading to an increase in the secretion of IL-1β. By activating NF-κB, LPS increases ROS and NO levels that spontaneously react to form peroxynitrite, thus leading to protein nitration. Reduction in peroxynitrite levels results in a decrease in caspase1 activity. Protein nitration and caspase1 activity are concomitantly increased in the spinal cord of pre-symptomatic SOD1(G93A) mice. Oxidative/nitrosative stress induces peroxynitrite formation that may be a key trigger of caspase1/inflammasome activation. Peroxynitrite formation may play a critical role in inflammasome activation and might be exploited as potential therapeutic target for ALS

Emergence of KPC-producing Klebsiella pneumoniae in Italy

<p>Abstract</p> <p>Background</p> <p>The emergence of KPC-producing <it>K. pneumoniae </it>has now become a global concern. KPC beta-lactamases are plasmid-borne and, like extended spectrum beta lactamases (ESBLs), can accumulate and transfer resistance determinants to other classes of antibiotics. Therefore, infection control guidelines on early identification and control of the spread of organisms carrying these resistant determinants are needed.</p> <p>Findings</p> <p><it>Klebsiella pneumoniae </it>carbapenemase (KPC) was detected in two isolates of carbapenem-resistant <it>K. pneumoniae </it>obtained from patients at an Italian teaching hospital. The first strain was isolated from a culture drawn from a central venous device (CVC) in a patient with Crohn's disease who was admitted to a gastroenterology ward. The second was isolated from a urine sample collected from an indwelling urinary catheter in an intensive care unit (ICU) patient with a subdural haematoma. The patients had not travelled abroad. Both isolates were resistant to all β-lactams and were susceptible to imipenem and meropenem but resistant to ertapenem. Isolates also showed resistance to other classes of non-β-lactam antibiotics, such as quinolones, aminoglycosides (with the exception for amikacin), trimethoprim-sulfamethoxazole (TMP-SMX) and nitrofurantoin. They were determined to contain the plasmid encoding the carbapenemase gene <it>bla-KPC </it>and were also positive in the Hodge test.</p> <p>Conclusions</p> <p>This is the second report of KPC-producing isolates in Italy, but the first concerning KPC type 2 gene, and it may have important implications for controlling the transmission of microorganisms resistant to antibiotics.</p

Influence of Classroom Acoustics on Noise Disturbance and Well-Being for First Graders

Several studies have shown so far that poor acoustics inside classrooms negatively affects the teaching and learning processes, especially at the lowest grades of education. However, the extent to which noise exposure or excessive reverberation affect well-being of children at school in their early childhood is still unanswered, as well as their awareness of noise disturbance. This work is a pilot study to investigate to which extent classroom acoustics affects the perceived well-being and noise disturbance in first graders. About 330 pupils aged from 6 to 7 years participated in the study. They belonged to 20 classes of 10 primary schools located in Torino (Italy), where room acoustic measurements were performed and where noise level was monitored during classes. The school buildings and the classrooms were balanced between socioeconomic status and acoustic conditions. Trained experimenters administered questionnaires in each class, where pupils answered all together during the last month of the school year (May). Questions included the happiness scale, subscales assessing self-esteem, emotional health, relationship at home and with friends, enjoyment of school, intensity and noise disturbance due to different sound sources, and quality of voice. The findings of the study suggest that long reverberation times, which are associated with poor classroom acoustics as they generate higher noise levels and degraded speech intelligibility, bring pupils to a reduced perception of having fun and being happy with themselves. Furthermore, bad classroom acoustics is also related to an increased perception of noise intensity and disturbance, particularly in the case of traffic noise and noise from adjacent school environments. Finally, happy pupils reported a higher perception of noise disturbance under bad classroom acoustic conditions, whereas unhappy pupils only reported complaints in bad classroom acoustics with respect to the perception of pleasances with himself or herself and of fitting in at school. Being a mother tongue speaker is a characteristic of children that brings more chances of attending classes in good acoustics, of being less disturbed, and of having more well-being, and richer districts presented better acoustic conditions, in turn resulting in richer districts also revealing a greater perception of well-being

Differences in birth-weight outcomes: A longitudinal study based on siblings

Objectives We investigate about the differences in birthweight between firstand second-borns, evaluating the impact of changes in pregnancy (e.g., gestational age), demographic (e.g., age), and social (e.g., education level, marital status) maternal characteristics. Data and Methods All analyses are performed on data collected in Umbria (Italy) taking into account a set of 792 women who delivered twice from 2005 to 2008. Firstly, we use a univariate paired t-test for the comparison between weights of first- and second-borns. Secondly, we use linear and nonlinear regression approaches in order to: (i) evaluate the effect of demographic and social maternal characteristics and (ii) predict the odds-ratio of low and high birthweight infants, respectively. Results We find that the birthweight of second-borns is significantly higher than that of first-borns. Statistically significant effects are related with a longer gestational age, an increased number of visits during the pregnancy, and the gender of infants. On the other hand, we do not observe any significant effect related with mother’s age and with other characteristics of interest

Evidence of an interaction between FXR1 and GSK3β polymorphisms on levels of Negative Symptoms of Schizophrenia and their response to antipsychotics

Introduction: Genome Wide Association Studies (GWAS) have identified several genes associated with schizophrenia (SCZ) and exponentially increased knowledge on the genetic basis of the disease. Additionally, products of GWAS genes interact with neuronal factors coded by genes lacking association, such that this interaction may confer risk for specific phenotypes of this brain disorder. In this regard, FXR1 (Fragile-X mental-retardation-syndrome-related 1) gene has been GWAS associated with SCZ. FXR1 protein is regulated by Glycogen Synthase Kinase-3 (GSK3), which has been implicated in pathophysiology of SCZ and response to Antipsychotics (APs). rs496250 and rs12630592, two eQTLs of FXR1 and GSK3 respectively, interact on emotion stability and amygdala/PFC activity during emotion processing. These two phenotypes are associated with Negative Symptoms (NS) of SCZ suggesting that the interaction between these SNPs may also affect NS severity and responsiveness to medication. Methods: To test this hypothesis, in two independent samples of patients with SCZ, we investigated rs496250 by rs12630592 interaction on NS severity and response to APs. We also tested a putative link between APs administration and fxr1 expression, as already reported for GSK3 expression. Results: We found that rs496250 and rs12630592 interact on NS severity. We also found evidence suggesting interaction of these polymorphisms also on response to APs. This interaction was not present when looking at positive and general psychopathology scores. Furthermore, chronic olanzapine administration led to a reduction of FXR1 expression in mouse frontal cortex. Discussion: Our findings suggest that, like GSK3 , FXR1 is affected by APs while shedding new light on the role of the FXR1/GSK3 pathway for NS of SCZ

Acinetobacter baumannii in intensive care unit: A novel system to study clonal relationship among the isolates

<p>Abstract</p> <p>Background</p> <p>The nosocomial infections surveillance system must be strongly effective especially in highly critic areas, such as Intensive Care Units (ICU). These areas are frequently an epidemiological epicentre for transmission of multi-resistant pathogens, like <it>Acinetobacter baumannii</it>. As an epidemic outbreak occurs it is very important to confirm or exclude the genetic relationship among the isolates in a short time. There are several molecular typing systems used with this aim. The Repetitive sequence-based PCR (REP-PCR) has been recognized as an effective method and it was recently adapted to an automated format known as the DiversiLab system.</p> <p>Methods</p> <p>In the present study we have evaluated the combination of a newly introduced software package for the control of hospital infection (VIGI@ct) with the DiversiLab system. In order to evaluate the reliability of the DiversiLab its results were also compared with those obtained using f-AFLP.</p> <p>Results</p> <p>The combination of VIGI@ct and DiversiLab enabled an earlier identification of an <it>A. baumannii </it>epidemic cluster, through the confirmation of the genetic relationship among the isolates. This cluster regards 56 multi-drug-resistant <it>A. baumannii </it>isolates from several specimens collected from 13 different patients admitted to the ICU in a ten month period. The <it>A. baumannii </it>isolates were clonally related being their similarity included between 97 and 100%. The results of the DiversiLab were confirmed by f-AFLP analysis.</p> <p>Conclusion</p> <p>The early identification of the outbreak has led to the prompt application of operative procedures and precautions to avoid the spread of pathogen. To date, 6 months after the last <it>A. baumannii </it>isolate, no other related case has been identified.</p