Geocoding health data with Geographic Information Systems: a pilot study in northeast Italy for developing a standardized data-acquiring format

Introduction. Geographic Information Systems (GIS) have become an innovative and somewhat crucial tool for analyzing relationships between public health data and environment. This study, though focusing on a Local Health Unit of northeastern Italy, could be taken as a benchmark for developing a standardized national data-acquiring format, providing a step-by-step instructions on the manipulation of address elements specific for Italian language and traditions. Methods. Geocoding analysis was carried out on a health database comprising 268,517 records of the Local Health Unit of Rovigo in the Veneto region, covering a period of 10 years, starting from 2001 up to 2010. The Map Service provided by the Environmental Research System Institute (ESRI, Redlands, CA), and ArcMap 10.0 by ESRI\uae were, respectively, the reference data and the GIS software, employed in the geocoding process. Results. The first attempt of geocoding produced a poor quality result, having about 40% of the addresses matched. A procedure of manual standardization was performed in order to enhance the quality of the results, consequently a set of guiding principle were expounded which should be pursued for geocoding health data. High-level geocoding detail will provide a more precise geographic representation of health related events. Conclusions. The main achievement of this study was to outline some of the difficulties encountered during the geocoding of health data and to put forward a set of guidelines, which could be useful to facilitate the process and enhance the quality of the results. Public health informatics represents an emerging specialty that highlights on the application of information science and technology to public health practice and research. Therefore, this study could draw the attention of the National Health Service to the underestimated problem of geocoding accuracy in health related data for environmental risk assessment

Conformational change of the catalytic subunit of glucose-6-phosphatase in rat liver during the fetal-to-neonatal transition

The glucose-6-phosphatase system was investigated in fetal rat liver microsomal vesicles. Several observations indicate that the orientation of the catalytic subunit is different in the fetal liver in comparison with the adult form: (i) the phosphohydrolase activity was not latent using glucose- 6-phosphate as substrate, and in the case of other phosphoesters it was less latent; (ii) the intravesicular accumulation of glucose upon glucose-6- phosphate hydrolysis was lower; (iii) the size of the intravesicular glucose- 6-phosphate pool was independent of the glucose-6-phosphatase activities; (iv) antibody against the loop containing the proposed catalytic site of the enzyme inhibited the phosphohydrolase activity in fetal but not in adult rat liver microsomes. Glucose-6-phosphate, phosphate, and glucose uptake could be detected by both light scattering and/or rapid filtration method in fetal liver microsomes; however, the intravesicular glucose-6-phosphate and glucose accessible spaces were proportionally smaller than in adult rat liver microsomes. These data demonstrate that the components of the glucose-6- phosphatase system are already present, although to a lower extent, in fetal liver, but they are functionally uncoupled by the extravesicular orientation of the catalytic subunit

Evidence-based considerations exploring relations between sars-cov-2 pandemic and air pollution: Involvement of pm2.5-mediated up-regulation of the viral receptor ace-2

The COVID-19/SARS-CoV-2 pandemic struck health, social and economic systems worldwide, and represents an open challenge for scientists —coping with the high inter-individual variability of COVID-19, and for policy makers —coping with the responsibility to understand environmental factors affecting its severity across different geographical areas. Air pollution has been warned of as a modifiable factor contributing to differential SARS-CoV-2 spread but the biological mechanisms underlying the phenomenon are still unknown. Air quality and COVID-19 epidemiological data from 110 Italian provinces were studied by correlation analysis, to evaluate the association between particulate matter (PM)2.5 concentrations and incidence, mortality rate and case fatality risk of COVID-19 in the period 20 February–31 March 2020. Bioinformatic analysis of the DNA sequence encoding the SARS-CoV-2 cell receptor angiotensin-converting enzyme 2 (ACE-2) was performed to identify consensus motifs for transcription factors mediating cellular response to pollutant insult. Positive correlations between PM2.5 levels and the incidence (r = 0.67, p < 0.0001), the mortality rate (r = 0.65, p < 0.0001) and the case fatality rate (r = 0.7, p < 0.0001) of COVID-19 were found. The bioinformatic analysis of the ACE-2 gene identified nine putative consensus motifs for the aryl hydrocarbon receptor (AHR). Our results confirm the supposed link between air pollution and the rate and outcome of SARS-CoV-2 infection and support the hypothesis that pollution-induced over-expression of ACE-2 on human airways may favor SARS-CoV-2 infectivity

Anabolic effects and inhibition of interleukin 6 production induced by neridronate on human osteoblasts

Bisphosphonates (BPs) are pharmacological compounds widely used in the treatment of a variety of bone-related diseases, particularly where the bone-turnover is skewed in favour of osteolysis. The mechanisms by which BPs reduce bone-resorption directly acting on osteoclasts (OCs) are now largely clarified even at molecular level. The researches concerning the BPs effects on osteoblasts (OBs) have instead shown variable results. Objectives: We have investigated the efficacy of neridronate (NER), an amino-BP, as anabolic agent on human OBs. Moreover, we have tried to verify if NER is able to negatively modulate the production of IL-6 on OBs stimulated or not by the pro-inflammatory cytokine Il-1b. Methods: We have tested if different concentrations of NER (from 10-11M to 10-3M), added to primary human OB cultures, could affect the cells number, the endogenous cellular alkaline phosphatase (ALP) activity, the collagen I (COLI) synthesis, the formation of mineralized nodules and the IL-6 production. Our experimental approach was performed testing a wide range of NER concentrations because, under physiological conditions, OBs seems to be exposed to variable and transient levels of the drug. Results: Our results show that NER doesn't negatively affect in vitro the viability, proliferation and cellular activity of human OBs, even after 20 days of exposure to concentrations ²10-5 M (therapeutic dose). In addition, NER seems to enhance the differentiation of cultured OBs in mature bone-forming cells. A maximum increase of COL-I synthesis (+25% after 4 days; p<0.05), ALP activity (+50% after 10 days; p<0.01) and mineralized nodules (+48% after 20 days; p<0.05) was observed in cultures treated with NER 10-8M. A maximal reduction of IL-6 secretion (-24% on IL-1b stimulated cultures and -29% on unstimulated cultures) was observed for NER 10-9 M. Conclusions: These results encourage the use of neridronate in therapy of demineralizing metabolic bone disorders

Lissencephaly-pachygyria and cerebellar hypoplasia in a calf.

ABSTRACT: A case of lissencephaly-pachygyria and cerebellar hypoplasia diagnosed in a Charolais x Tabapuã calf is described. The calf presented since birth, clinical signs characterized by apathy, prolonged recumbency, tremors of the head and neck, ataxia, hypermetria, difficulty walking, blindness and swelling of the joints of the four limbs. Due to the unfavorable prognosis, the animal was euthanized and necropsied at 34 days of age. At necropsy, a rudimentary development of the brain folds (gyri) and grooves (sulci) was observed, and the cerebellum was hypoplastic. The cut surface of the brain exhibited thickening of the gray matter (pachygyria) in the frontal, parietal, temporal and occipital cortices and narrowing of the white matter. In the organs of the thoracic and abdominal cavities, no significant lesions were observed. Histologically, cerebral cortex was thick and exhibited neuronal disorganization of the gray matter. The cerebellum had a thin molecular layer, and neuronal disorganization with ectopia of the Purkinje neurons in the region of the granular and molecular layers. There were no bacterial growths in cultures of joint swabs. This was the only case on the property, which suggests that this malformation, which has not previously been described in cattle, was a sporadic case, and it was not possible to determine its cause. Neurological lesions and clinical sings presented here should be considered in the differential diagnosis of congenital diseases of the central nervous systems of cattle

Study of radiation effects on bipolar transistors

Abstract In this paper it was shown that the irradiation with neutrons and carbon ions leads to gain degradation in bipolar transistors due to generation of defects. The density of these generated defects is independent of the type of irradiation (neutrons or carbon ions). Thus, it is possible to evaluate Δ(1/β), once the expected Frenkel pair density is known. The dependence of the damage constant on collector current is a power law function, with the exception of the lateral pnp transistors, that shows a higher sensitivity to radiation and a different behaviour. Neutrons give a smaller density of Frenkel pairs (CF) than the two sorts of carbon ions of high energy (CHE) and medium energy (CME). It was found that CME causes a higher concentration of CF. The calculated ratio R=CF/Φ, where CF is the Frenkel pair density and Φ fluence does not depend on Φ, for a given type of radiation. However, it depends on the incoming particle type. Its smallest calculated value was obtained for neutrons (R=6.1×10), which increases to 1.25×103 for CHE and to 1.1×104 for CME

Age is not the only risk factor in COVID-19: the role of comorbidities and of long staying in residential care homes

Background: The actual SARS-CoV-2 outbreak caused a highly transmissible disease with a tremendous impact on elderly people. So far, few studies focused on very elderly patients (over 80 years old). In this study we examined the clinical presentation and the outcome of the disease in this group of patients, admitted to our Hospital in Rome. Methods: This is a single-center, retrospective study performed in the Sant’Andrea University Hospital of Rome. We included patients older than 65 years of age with a diagnosis of COVID-19, from March 2020 to May 2020, divided in two groups according to their age (Elderly: 65–80 years old; Very Elderly &gt; 80 years old). Data extracted from the each patient record included age, sex, comorbidities, symptoms at onset, the Pneumonia Severity Index (PSI), the ratio of the partial pressure of oxygen in arterial blood (PaO2) to the inspired oxygen fraction (FiO2) (P/F) on admission, laboratory tests, radiological findings on computer tomography (CT), length of hospital stay (LOS), mortality rate and the viral shedding. The differences between the two groups were analyzed by the Fisher’s exact test or the Wilcoxon signed-rank test for categorical variables and the Mann-Whitney U test for continuous variables. To assess significance among multiple groups of factors, we used the Bonferroni correction. The survival time was estimated by Kaplan-Meier method and Log Rank Test. Univariate and Multivariate logistic regression were performed to estimate associations between age, comorbidities, provenance from long-stay residential care homes (LSRCH) s and clinical outcomes. Results: We found that Very Elderly patients had an increased mortality rate, also due to the frequent occurrence of multiple comorbidities. Moreover, we found that patients coming from LSRCHs appeared to be highly susceptible and vulnerable to develop severe manifestations of the disease. Conclusion: We demonstrate that there were considerable differences between Elderly and Very Elderly patients in terms of inflammatory activity, severity of disease, adverse clinical outcomes. To establish a correct risk stratification, comorbidities and information about provenience from LSRCHs should be considered

Evidence from Family Studies for Autoimmunity in Arrhythmogenic Right Ventricular Cardiomyopathy: Associations of Circulating Anti-Heart and Anti-Intercalated Disk Autoantibodies with Disease Severity and Family History

Background: Serum anti-heart autoantibodies (AHA) and anti-intercalated disk autoantibodies (AIDA) are autoimmune markers in myocarditis. In arrhythmogenic right ventricular cardiomyopathy (ARVC) myocarditis has been reported. To provide evidence for autoimmunity, we searched for AHA and AIDA in ARVC. Methods: We studied: 42 ARVC probands, 23 male, aged 42, interquartile range (IQR) 33;49, 20 from familial and 22 non-familial pedigrees; 37 clinically affected relatives (AR), 24 male aged 35, IQR 18;46; 96 healthy relatives (HR), 49 male, aged 27, IQR 17;45. Serum AHA and AIDA were tested by indirect immunofluorescence on human myocardium and skeletal muscle in 171 of the 175 ARVC individuals and in controls with: non-inflammatory cardiac disease (NICD) (n=160), ischemic heart failure (IHF) (n=141), normal blood donors (NBD) (n=270). Screening of five desmosomal genes was performed in probands; when a sequence variant was identified, cascade family screening followed, blind to immunological results. Results: AHA frequency was higher (36.8%) in probands, AR (37.8%) and HR (25%) than in NICD (1%), IHF (1%) or NBD (2.5%) (p=0.0001). AIDA frequency was higher in probands (8%, p=0.006), in AR (21.6%, p=0.00001) and in HR (14.6% p=0.00001) than in NICD (3.75%), IHF (2%) or NBD (0.3%). AHA positive status was associated with higher frequency of palpitation (p=0.004), ICD implantation (p=0.021), lower left ventricular ejection fraction (LVEF) (p=0.004), AIDA positive status with both lower RV and LVEF (p=0.027 and p=0.027 respectively). AHA and/or AIDA positive status in the proband and/or at least one of the respective relatives was more common in familial (17/20, 85%) than in sporadic (10/22, 45%) pedigrees (p=0.007). Conclusions: Presence of AHA and AIDA provides evidence of autoimmunity in the majority of familial and in almost half of sporadic ARVC. In probands and in AR these antibodies were associated with disease severity features; longitudinal studies are needed to clarify whether they may predict ARVC development in HR or if they be a result of manifest ARVC