35 research outputs found
Social Design. Design e bene comune.
No full textPer questo primo doppio numero della rivista, Social Design. Design e "bene comune", curato da Marinella Ferrara, Francesco E. Guida, Mario Piazza, Paola Proverbio e Raimonda Riccini, quasi come una sfida, si è provato a rompere l’ortodossia di un approccio lineare alla storia.
In questo orientamento, che tende a portare più vicino a noi i temi storici, il Social Design si offre in modo calzante per il suo essere questione contemporanea e complessa, ampia e ambigua financo controversa, anche solo dal punto di vista delle diverse espressioni sinonimiche con cui si presenta: design etico, design umanitario, design per la collettività, design di pubblica utilità, design per l’utenza ampliata, design per la sostenibilità, ...
Il numero ha ricevuto la Menzione d'Onore alla XXVII edizione del Compasso d'Oro (giugno 2022), ed è stato segnalato nell'ADI Design Index 2021 (promosso da ADI, Associazione per il Disegno Industriale) nella sezione "Ricerca teorica, storica, critica e progetti editoriali"
Le concept de paroimia/proverbium dans la haute et la basse antiquité
No full textLa valenza del proverbio in ambito filosofico e retoric
Transcriptional profiling of human bronchial epithelial cell BEAS-2B exposed to diesel and biomass ultrafine particles
No full textTime course transcriptomic profiling of human bronchial epithelial cell BEAS-2B exposed to a single dose of diesel and biomass ultrafine particles.
autori
Andrea Grilli, Rossella Bengalli, Eleonora Longhin, Laura Capasso, Maria Carla Proverbio, Mattia Forcato, Silvio Bicciato, Maurizio Gualtieri, Cristina Battaglia and Marina Camatini
Eccellenze Lombarde 2020-2021 conferiti da Regione Lombardia ai selezionati ADI Design Index. Progetto: AIS/Design Journal. Storia e ricerche, V. 7 N. 12-13 (2020): Social Design. Design e “bene comune”
No full textMenzione d'onore XXVII Compasso d'Oro - AIS/Design Journal. Storia e ricerche, V. 7 N. 12-13 (2020): Social Design. Design e “bene comune”
No full textLa rivista, online e open-access, l’unica rivista scientifica esclusivamente dedicata alla storia del design italiano e internazionale, ha dedicato un numero monografico a “Social Design. Design e bene comune”. Affronta dal punto di vista storico un argomento vivo nelle pratiche attuali del design e oggetto di studi e teorizzazioni, che però non è stato mai approfondito attraverso ricerche storiche puntuali. Dai saggi presentati nel numero della rivista emerge come questo ambito abbia solide radici nella seconda metà del Novecento e come il design italiano abbia dato propri e significativi contributi sia in termini di pensiero teorico, critico e metodologico, sia dal punto di vista progettuale e di buone pratiche
A novel variant in CMAH is associated with blood type AB in Ragdoll cats
No full textCitation: Gandolfi, B., Grahn, R. A., Gustafson, N. A., Proverbio, D., Spada, E., Adhikari, B., . . . Helps, C. R. (2016). A novel variant in CMAH is associated with blood type AB in Ragdoll cats. Plos One, 11(5). doi:10.1371/journal.pone.0154973The enzyme cytidine monophospho-N-acetylneuraminic acid hydroxylase is associated with the production of sialic acids on cat red blood cells. The cat has one major blood group with three serotypes; the most common blood type A being dominant to type B. A third rare blood type is known as AB and has an unclear mode of inheritance. Cat blood type antigens are defined, with N-glycolylneuraminic acid being associated with type A and N-acetylneuraminic acid with type B. Blood type AB is serologically characterized by agglutination using typing reagents directed against both A and B epitopes. While a genetic characterization of blood type B has been achieved, the rare type AB serotype remains genetically uncharacterized. A genome-wide association study in Ragdoll cats (22 cases and 15 controls) detected a significant association between blood type AB and SNPs on cat chromosome B2, with the most highly associated SNP being at position 4,487,432 near the candidate gene cytidine monophospho-N-acetylneuraminic acid hydroxylase. A novel variant, c.364C>T, was identified that is highly associated with blood type AB in Ragdoll cats and, to a lesser degree, with type AB in random bred cats. The newly identified variant is probably linked with blood type AB in Ragdoll cats, and is associated with the expression of both antigens (N-glycolylneuraminic acid and N-acetylneuraminic acid) on the red blood cell membrane. Other variants, not identified by this work, are likely to be associated with blood type AB in other breeds of cat. © 2016 Gandolfi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
The role of IL-6 released from pulmonary epithelial cells in diesel UFP-induced endothelial activation
No full textDiesel exhaust particles (DEP) and their ultrafine fraction (UFP) are known to induce cardiovascular effects in exposed subjects. The mechanisms leading to these outcomes are still under investigation, but the activation of respiratory endothelium is likely to be involved. Particles translocation through the air-blood barrier and the release of mediators from the exposed epithelium have been suggested to participate in the process. Here we used a conditioned media in vitro model to investigate the role of epithelial-released mediators in the endothelial cells activation. Diesel UFP were sampled from a Euro 4 vehicle run over a chassis dyno and lung epithelial BEAS-2B cells were exposed for 20 h (dose 5 microg/cm2). The exposure media were collected and used for endothelial HPMEC-ST1.6R cells treatment for 24 h. The processes related to oxidative stress and inflammation were investigated in the epithelial cells, accordingly to the present knowledge on DEP toxicity. The release of IL-6 and VEGF was significantly augmented in diesel exposed cells. In endothelial cells, VCAM-1 and ICAM-1 adhesion molecules levels were increased after exposure to the conditioned media. By interfering with IL-6 binding to its endothelial receptor, we demonstrate the role of this interleukin in inducing the endothelial response. DEP modulates oxidative stress, MAPK activation and IL-6 release in lung cells. Treatments with endothelial supernatants induce endothelial activation which is down-regulated by IL-6 suppression
Naturally occurring antibodies in cats against dog erythrocyte antigens and vice versa
No full textObjectives The aim of this study was to investigate the presence of naturally occurring antibodies against canine erythrocyte antigens in cats and vice versa. The influence of canine and feline blood type on cross-match results was also studied. Methods Blood samples from 34 cats and 42 dogs were used to perform test-tube major and minor cross-match tests and blood typing. Blood from each cat was cross-matched with blood from 2-6 dogs, for a total of 111 cross-match tests. Haemolysis, macro- and/or micro-agglutination were considered markers of a positive cross-match. Results Eighty-three overall major cross-match tests were positive at 37°C, 86 at room temperature and 90 at 4°C. The minor cross-match tests were positive in all but two cross-matches performed at 37°C, all tests performed at room temperature and all but one test performed at 4°C. No cats tested totally negative at both major and minor cross-matches performed with samples from any single dog. Prevalence of warm natural antibodies against canine erythrocyte antigens was lower in type B cats than in type A cats, regardless of the blood type of donor dogs. Conclusions and relevance This study reveals a high prevalence of naturally occurring antibodies in cats against dog erythrocyte antigens and vice versa, and suggests that transfusion of cats with canine blood is not recommended as a routine procedure owing to the potential high risk of either acute severe or milder transfusion reactions
Screening Feline Blood Donors for Bartonella henselae Infection: Comparison between Indirect Immunofluorescent Antibody Test (IFAT) and Polymerase Chain Reaction (PCR) Results
No full textIn order to minimize pathogen transmission, all blood do- nors should be appropriately screened for infectious agents. Screening for Bartonella spp. infection in feline blood donors is a recommended practice in veterinary blood banks across the world. The aim of this study was to compare results of an indirect immunofluorescence antibody test (IFAT) in identifying Bartonella henselae antibodies with the results of PCR amplification of Bartonella spp. DNA to establish the best IFAT cut off to identify non-bacteremic cats. A secondary aim of this study was to evaluate demographic and clinicopathologic factors that may be associated with Bartonella henselae infection status. From a population of stray cats in Milan city, 82 serum samples were evaluated by IFAT for Bartonella henselae antibodies and PCR was performed on 90 whole blood samples for amplification of Bartonella spp. DNA. A total of 14/82 (17.1%) samples were seropositive with an IFAT titer ≥1:64 (cut-off for infection). Bartonella spp. DNA was identified in 11/90 (12.2%) samples by PCR. Overall 20/90 (22.2%) infected cats were identified by either IFAT ≥1:64 and/or PCR-positive results. Hyperbetaglobulinemia (P=0.02) and originating from zone 2 of Milan city (P=0.03) were statistically associated with positive Bartonella infection status.
The overall IFAT sensitivity was 50.0%, specificity 87.5%, positive predictive value 35.7% and negative predictive value was 92.65%. The ROC analysis showed that the area under the curve was 0.747 (P=0.0032) and that an IFAT cut off<1:32 had the highest sensitivity in identifying Bartonella PCR-negative cats. When feline blood donors undergo serological screening for Bartonella henselae infection an IFAT cut off <1:32 has the highest sensitivity for identifying non-bacteremic cats. However some serologically negative cats could be bacteremic and therefore screening of a feline blood donor using a combination of IFAT and PCR is recommended. Protein electrophoresis should be performed in all potential donor cats
Genome-wide homozygosity mapping in Congenital Hyperinsulinism of Infancy (CHI) :a family based study
No full textCongenital hyperinsulinism of infancy (CHI) is a pathology characterized by a profound hypoglicaemia related to a disregulated insulin secretion; the frequency of the disease is 1:30000-50000 live birth world –wide, but in same isolated populations with high consanguinity like the Arabic Peninsula, frequency of 1:2500 is reported. At present it is well known that dysfunctions of pancreatic - cells K-ATP channel are a common cause of CHI. The two subunits of the channel are coded by two genes, KCNJ11 and ABCC8. Mutations in ABCC8 gene are responsible of the 50-60% of focal and diffuse CHI patients; otherwise mutations in KCNJ11 are responsible for 10-15% of cases. Other less frequent molecular mechanism responsible for CHI are glutamate dehydrogenase (GDH), glucokinase and short- chain 3 hydroxyacyl Coenzyme A dehydrogenase (SCHAD) deficiency. CHI derives from a heterogeneous genetic background and many other genes involved in the pancreatic - cells metabolism are good candidate genes for this disease. In order to identify new disease susceptibility loci in a cohort of consanguineous and not consanguineous 34 CHI Italian families, we performed genome-wide homozygosity mapping using 250K NspI Gene Chip Affymetrix SNP microarrays and to reveal the number and the nature of homozygosity trait in common between probands to underline new regions containing candidate genes involved in the ethiopathogenesis of CHI. Further screening for mutations in candidate genes was performed and biochemical pathways involved in the disease has been analyzed.
We used CNAG (v3.0) software to describe homozygosity traits present in 34 families with CHI affected probands. Consanguineous families bear a number of homozygous stretches much higher that not consanguineous ones and following investigations of the parental origin of homozygous stretches of more than 1 Mb in length has confirmed that they were not inherited and did not reveal any copy number loss, concluding that they were not deletions. Mendelian errors check (all below 0.1%, threshold due to genotyping errors and not transmission error) and parental haplotypes analysis has excluded uniparental disomy (UPD) and they must be considered as autozygosity traits.
To further characterize homozygosity traits in CHI probands, we used dCHIP software to underline homozygosity regions in common between at least two patients. On Chromosome 11 we found five patients sharing a common homozygous trait on cytoband 11p15, where the two major CHI candidate genes are present. In two of these probands, where mutational screening of ABCC8 and KCNJ11 genes was completed, the causative mutation was revealed. Other relevant homozigosity region in common between 4 patients are present on chromosome 6 (p21.33-p21.31) and on chromosome 10 (q26.13- q26.2), while 18 common traits between 3 patients were revealed One of the numerous traits in common between two patient on chromosome 1 showed a homozygous region in 1p31, one patient bearing a long contiguous trait of 25 Mb. This common region contains medium-chain acyl-CoA dehydrogenase (MCAD) gene, involved in organic acid metabolism deficiency, and in that proband an homozygous synonymous mutation P195P in exon 8 of MCAD gene was identified (587 T >G); her parents and brother evidenced the same heterozygous nucleotidic variation.
On chromosome 4 one probands showed the longest homozygosity stretch (from 4q13.2 to 4q31.21), which ranged 79,01 Mb and included 312 known genes in the region; this stretch contains the causative short- chain 3 hydroxyacyl Coenzyme A dehydrogenase gene (HADH). Direct sequencing of the coding region of HADH revealed a homozygous C to T transition in exon 6 causing a premature stop of the synthesized protein at codon 236 (706C>T), resulting in the nonsense mutation R236X. Mutation analysis of exon 6 of the HADH gene in the parents of the proband showed they were heterozygous carriers of the mutation. This is the fourth described mutation in HADHSC gene in a CHI patient, indicating the importance of -oxidation disregulation in this disease.
A preliminary bioinformatics pathways analysis in CHI probands underlined that more than one pathway is involved in the disease, in particular type I diabetes mellitus, glycolysis and gluconeogenesis, fatty acid metabolism and amino acids metabolism.
Homozygosity mapping in 34 CHI families has confirmed a relevant presence of autozygosity, due to presence of high inbreeding in at least 5 analysed families and to the restricted geographical provenience. Autozygosity excludes that deletions or UPD are at the molecular basis of the disease.
Even if each patient has an homozygosity profile strictly peculiar, there are common region shared between at least two probands. These regions are good candidates for the discovery of new disease associated genes/loci. The discovery that CHI probands showing homozygosity traits on chromosome 11, in particular on 11p15.1, bear a mutation in known causatives genes and the recent finding of a not jet described stop mutation in HADH gene on chromosome 4 confirm the power of SNPs genome-wide genotyping technologies to underline loci with high mutational probability and to elucidate the molecular basis of autosomic recessive diseases.
To our knowledge this is the first study in which molecular mechanism of CHI disease was investigated with genome-wide homozygosity mapping method in consanguineous and not consanguineous CHI families. Genome-wide homozygosity mapping in the present study has clearly evidenced 1p31.2-31.1, 4q27-28.1, 6p22.3-22.31, 11p15.4-15.2, and 18q12.2 chromosomal loci to be the most related to CHI disease and to better redefine that regions and to single out potential associated genes, we are planning to use SNPs genotypes calls generated from these 34 CHI family microarrays data to perform family based transmission disequilibrium analysis. On the other hand, we will increase the number of CHI families enrolled in the study in order to evidence by homozygosity mapping homozygosity traits which are strictly peculiar of the disease and not common in the normal population
