122,554 research outputs found
Modified carbon nanotubes: from nanomedicine to nanotoxicology
No full textNanomedicine is the science of fabricating smart devices able to diagnose and treat diseases more efficiently than conventional medicine while minimizing costs, complexity and adverse effects. Carbon nanotubes (CNTs) are receiving considerable attention for biomedical applications due to their extraordinary properties. In particular, their chemical nature and high aspect ratio (ratio between the length and the diameter) make them ideal carriers to achieve delivery of high doses of therapeutic and imaging cargo to a specific site of interest. A major obstacle to the use of pristine (unmodified) CNTs in biological systems is their complete aqueous insolubility and low biocompatibility and toxicity profiles. To endow CNTs with solubility in a biological milieu, several non-covalent and covalent modification methods have been explored. Suitably modified CNTs have shown increased solubility under physiological conditions, improved biocompatibility profiles and lack of toxicity after injection in living animals. Additionally, after being loaded with cargo (small molecules, proteins, peptides or nucleic acids) they have been successfully evaluated as pharmaceutical, therapeutic and diagnostic tools
PEG-modified carbon nanotubes in biomedicine: current status and challenges ahead
No full textSince their discovery at the end of the previous millennium, carbon nanotubes (CNTs) have been the object of thousands of papers describing their applications in fields ranging from physics to electronics, photonics, chemistry, biology, and medicine. The development of chemical approaches to modify their graphitic sidewalls enabled the generation of poly(ethylene glycol) (PEG)-modified CNTs and their exploration in multiple biomedical applications. Studies at the cellular and organism level revealed that PEG-modified CNTs have favorable pharmacokinetic and toxicology profiles. Recently, PEG-modified CNTs have been successfully tested in preclinical studies in the fields of oncology, neurology, vaccination, and imaging, suggesting that they are well suited for the generation of novel multifunctional nanodrugs. Here we will review published data about the application of PEG-modified CNTs as in vitro and in vivo therapeutic and imaging tools and describe what is known about the interaction between PEG-modified CNTs and biological systems. Although several pieces of the puzzle are still missing, we will also attempt to formulate a preliminary structure-function model for PEG-modified CNT cellular trafficking, disposition, and side effects
Role of PTPN22 in type 1 diabetes
No full textIl polimorfismo missense C1858T del gene PTPN22 e’ associato con
diverse malattie autoimmuni umane, incluso il diabete autoimmune tipo 1,
l’artrite reumatoide, il lupus eritematoso sistemico, la malattia di Graves,
l’artrite giovanile idiopatica, e la vitiligine generalizzata. Diversi studi hanno
mostrato che la associazione del polimorfismo PTPN22 C1858T con
l’autoimmunita’ e’ primaria e presente in diverse popolazioni. Il gene
PTPN22 codifica per la tirosin fosfatasi linfoide LYP, che e’ espressa solo in
cellule emopoietiche, ed e’ un importante regolatore negativo della
attivazione dei linfociti T. Il meccanismo molecolare utilizzato da LYP per
ridurre la segnazione attraverso il recettore delle cellule T (TCR) include la
formazione di un complesso fra LYP e la chinasi Csk, anche essa un
inibitore della attivazione del TCR. L’allele 1858T di PTPN22 codifica per la
variante LYP-W620 della fosfatasi, che non puo’ legare Csk. Questo studio
e’ stato condotto per elucidare il meccanismo di azione della variante LYPW620
nella trasduzione del segnale del TCR. Abbiamo trovato che cellule T
di soggetti portatori della variante LYP-W620 producono meno IL-2 dopo
stimolazione del TCR, e che la fosfatasi –W620 ha una incrementata
attivita’ enzimatica. I nostri dati suggeriscono che la variante di LYP
associata alla autoimmunita’ umana possiede incrementata funzione ed e’
un piu’ potente inibitore della attivazione dei linfociti T.A missense single-nucleotide polymorphism, C1858T in the PTPN22 gene,
is associated with several human autoimmune diseases, including type 1
diabetes, rheumatoid arthritis, systemic lupus erythematosus, Graves’
disease, juvenile idiopathic arthritis, generalized vitiligo, and others. Genetic
studies have shown that the PTPN22 C1858T polymorphism is primarily
associated with autoimmunity in different populations. The PTPN22 gene
encodes the lymphoid tyrosine phosphatase LYP, which is expressed only
in white blood cells and acts as a gatekeeper for T lymphocyte activation.
The molecular mechanism by which LYP tempers T lymphocyte activation
through the T cell receptor (TCR) involves the formation of a complex
between LYP and the negative regulatory kinase Csk. The autoimmunepredisposing
PTPN22 T1858 allele encodes the phosphatase variant LYPW620,
which cannot bind Csk. This study was undertaken in order to
elucidate the mechanism of action of LYP-W620 in TCR signaling. We
found that T cells from carriers of the predisposing allele produce less
interleukin-2 upon TCR stimulation, and the encoded phosphatase has
higher catalytic activity and is a more potent negative regulator of T
lymphocyte activation. We conclude that the autoimmune-predisposing
allele is a gain-of-function mutant
March. Ant. Bottini
No full textBotanico: Bottini, Antonio (1850-1931).
Dottore in Scienze naturali, docente di botanica e aiuto all\u27Orto botanico dell\u27università di Pisa.
Titolo manoscritto sul recto, dove compaiono anche le note: autograf.; Racc. [raccolta] Levier, 1912; f. 1885; n. 1850.
Nota manoscritta sul verso: Antonio Bottini nato a Lucca in Decembre 1850, fotografato in novembre 1885.
Montata su cartoncino 110 x 68 mm.
1 fotografia : albumina ; 93 x 60 mm.
Vai alla scheda bibliografica: https://galileodiscovery.unipd.it/discovery/fulldisplay?context=L&vid=39UPD_INST:VU1&search_scope=MyInst_and_CI&tab=Everything&docid=alma99001500720020604
Atopic and non atopic asthma in children
No full textIn 155 asthmatic children we have studied the relationship between prick test positivity and a set of genetic factors previously found to be associated with bronchial asthma. Among these factors, MN system (p = 0.009) and age at onset of symptoms (p = 0.05) are the most important variables separating prick test negative from prick test positive children. MN and age at onset influence independently prick test positivity pointing to an additive effect of the two variables. M phenotype appears correlated positively with an increased susceptibility to nonallergic asthma in all age groups, whereas N phenotype appears correlated positively with age at onset but in allergic asthma only. The MN system codifies for glycophorin A, a sialoglycoprotein that represents a major ligand for several bacteria and viruses that recognize the N-acetylneuraminic acid present in this protein. The present data suggest that genetic variability in this system might influence bacterial and viral competition and mucosal damage influencing susceptibility to asthmatic reactions in absence of IgE hyperproduction
Acid phosphatase locus 1 (ACP1): Possible relationship of allelic variation to body size and human population adaptation to thermal stress - A theoretical perspective
No full textThe acid phosphatase locus 1 (ACP1) codes for a low molecular weight phosphotyrosine protein phosphatase that has the important action of dephosphorylating tyrosine phosphorylated proteins and peptides and a second important role in modulating flavin cofactor levels and the activity of flavo-enzymes. These functions significantly influence cell division, differentiation, and growth. Two alleles (ACP1*A and ACP1*B) reach polymorphic frequencies at the ACP1 locus in all human populations, while the ACP1*C and ACP1*R alleles reach polymorphic frequencies in restricted geographical regions. The worldwide distribution of these alleles, and data from several clinical studies, strongly suggest that the ACP1 locus functions to modulate growth and that selection at this locus is a component of the selective processes influencing body mass and human population adaptation to thermal stress. The ACP1*A allele reaches highest frequencies at extreme latitudes and appears to be associated with maximizing body mass and adaptation to cold stress, whereas the ACP1*B allele reaches highest frequencies in tropical and subtropical environments and appears to be associated with minimizing body mass and adaptation to heat stress. The high frequency of the ACP1*C allele at northern latitudes, where ACP1*A allele frequencies are elevated, may be a mechanism for limiting fetal and maternal complications associated with fetal macrosomia and adult obesity in populations where protein and calorie intake are relatively hig
Does the interaction between services and manufacturing explain the recent trends in export specialization? A look at the evidence from the EU
No full textDiabetic complications and the genetics of signal transduction. A study of retinopathy in NIDDM
No full textCytosolic low molecular weight acid phosphatase (ACP1) is a high polymorphic phosphotyrosine-protein-phosphatase involved in signal transduction. In NIDDM subjects we have found that ACP1 genotype is a highly significant predictor of retinopathy, suggesting that genetic variability of signal transduction may have an important role in the susceptibility to this complication. Adenosine deaminase, ABO blood groups and several clinical variables have been also considered. The results point out the importance of interactions between genetic systems. Among non-genetic variables dislipidemia and treatment with insulin are significantly associated with retinopathy
Phosphotyrosine-protein-phosphatase and diabetic disorders. Further studies on the relationship between low molecular weight acid phosphatase genotype and degree of glycemic control
No full textWe have studied a new sample of 276 NIDDM patients from the population of Penne (Italy). Comparison of the new data with those of 214 diabetic pregnant women from the population of Rome reported in a previous paper has shown that the pattern of association between low molecular weight acid phosphatase genotype and degree of glycemic control is similar in the two classes of diabetic patients. Among nonobese subjects the proportion of ACP1*A (the allele showing the lowest enzymatic activity) is lower in diabetic patients with high glycemic levels (mean value greater than 8.9 mmol/l) than in diabetic patients with a low glycemic level (mean value less than 8.9 mmol/l). Among obese subjects no significant association is observed between glycemic levels and ACP1. Among nonobese subjects the concentration of f isoform of ACP1 is higher in patients showing a high glycemic level than in patients showing a low glycemic level. No significant difference is observed for s isoform
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