FISTOLA BRONCO-BILIARE DA ECHINOCOCCOSI EPATICA E DIAFRAMMATICA

abstract

Hypo- and hyper-virulence in apricot trees infected by European stone fruit yellows

An apricot orchard, located in an area of north eastern Italy under serious pressure from European stone fruit yellows (ESFY) infection, has been monitored since the year it was planted (1990). During this time, most of the trees displayed symptoms or were shown by PCR analyses to be infected. Two groups of apricot trees were particularly interesting: some trees were asymptomatically infected while others recovered from the symptoms but not from the pathogen. In order to isolate those strains of the phytoplasma characterised by varying virulence, each of the two groups was used as mother plants and propagated. The new trees were used to constitute experimental orchards, where they were observed for the presence of symptoms and in part were tested by PCR, starting in 2003. The results obtained confirmed the presence of strains of the pathogen characterised by varying virulence. The strains originally present in infected apricot trees which recovered from the symptoms of ESFY were seen to be hypovirulent; none of the propagated infected trees ever showed symptoms of the disease. Surprisingly, the strains present in asymptomatic apricot mother plants were hypervirulent and the propagated trees always displayed severe symptoms. In the propagated trees, the transmission of the pathogen was higher in the hypervirulent strains than in the hypovirulent ones. A graft transmission trial carried out in the greenhouse using some of the identified hypo- and hypervirulent strains, confirmed the results obtained in open field. Real time PCR analyses showed that in the trees infected by hypovirulent strains the colonisation of the pathogen was lower than in those infected by the hypervirulent strains. It is possible to affirm that the hypovirulent strains were present in those mother plants which had originally recovered. The research will continue with the aim of verifying the possibility of cross protection among the identified hypo- and hypervirulent strains.Keywords: ‘Candidatus Phytoplasma prunorum’, real-time PCR, Prunu

Pre-symptomatic modified phytohormone profile is associated with lower phytoplasma titres in an Arabidopsis seor1ko line

The proteins AtSEOR1 and AtSEOR2 occur as conjugates in the form of filaments in sieve elements of Arabidopsis thaliana. A reduced phytoplasma titre found in infected defective-mutant Atseor1ko plants in previous work raised the speculation that non-conjugated SEOR2 is involved in the phytohormone-mediated suppression of Chrysanthemum Yellows (CY)-phytoplasma infection transmitted by Euscelidius variegatus (Ev). This early and long-lasting SEOR2 impact was revealed in Atseor1ko plants by the lack of detectable phytoplasmas at an early stage of infection (symptomless plants) and a lower phytoplasma titre at a later stage (fully symptomatic plants). The high insect survival rate on Atseor1ko line and the proof of phytoplasma infection at the end of the acquisition access period confirmed the high transmission efficiency of CY-phytoplasma by the vectors. Transmission electron microscopy analysis ruled out a direct role of SE filament proteins in physical phytoplasma containment. Time-correlated HPLC\u2013MS/MS-based phytohormone analyses revealed increased jasmonate levels in midribs of Atseor1ko plants at an early stage of infection and appreciably enhanced levels of indole acetic acid and abscisic acid at the early and late stages. Effects of Ev-probing on phytohormone levels was not found. The results suggest that SEOR2 interferes with phytohormonal pathways in Arabidopsis midrib tissues in order to establish early defensive responses to phytoplasma infection

Use of agro-industrial by-products for fattening lambs: pasta factory residues. Influence on meat production and meat quality

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ACRATA: a novel electron transfer domain associated to apoptosis and cancer

BACKGROUND: Recently, several members of a vertebrate protein family containing a six trans-membrane (6TM) domain and involved in apoptosis and cancer (e.g. STEAP, STAMP1, TSAP6), have been identified in Golgi and cytoplasmic membranes. The exact function of these proteins remains unknown. METHODS: We related this 6TM domain to distant protein families using intermediate sequences and methods of iterative profile sequence similarity search. RESULTS: Here we show for the first time that this 6TM domain is homolog to the 6TM heme binding domain of both the NADPH oxidase (Nox) family and the YedZ family of bacterial oxidoreductases. CONCLUSIONS: This finding gives novel insights about the existence of a previously undetected electron transfer system involved in apoptosis and cancer, and suggests further steps in the experimental characterization of these evolutionarily related families

Aorto-bronchial and aorto-pulmonary fistulation after thoracic endovascular aortic repair: an analysis from the European Registry of Endovascular Aortic Repair Complications.

OBJECTIVES: To learn upon incidence, underlying mechanisms and effectiveness of treatment strategies in patients with central airway and pulmonary parenchymal aorto-bronchial fistulation after thoracic endovascular aortic repair (TEVAR). METHODS: Analysis of an international multicentre registry (European Registry of Endovascular Aortic Repair Complications) between 2001 and 2012 with a total caseload of 4680 TEVAR procedures (14 centres). RESULTS: Twenty-six patients with a median age of 70 years (interquartile range: 60-77) (35% female) were identified. The incidence of either central airway (aorto-bronchial) or pulmonary parenchymal (aorto-pulmonary) fistulation (ABPF) in the entire cohort after TEVAR in the study period was 0.56% (central airway 58%, peripheral parenchymal 42%). Atherosclerotic aneurysm formation was the leading indication for TEVAR in 15 patients (58%). The incidence of primary endoleaks after initial TEVAR was n = 10 (38%), of these 80% were either type I or type III endoleaks. Fourteen patients (54%) developed central left bronchial tree lesions, 11 patients (42%) pulmonary parenchymal lesions and 1 patient (4%) developed a tracheal lesion. The recognized mechanism of ABPF was external compression of the bronchial tree in 13 patients (50%), the majority being due to endoleak formation, further ischaemia due to extensive coverage of bronchial feeding arteries in 3 patients (12%). Inflammation and graft erosion accounted for 4 patients (30%) each. Cumulative survival during the entire study period was 39%. Among deaths, 71% were attributed to ABPF. There was no difference in survival in patients having either central airway or pulmonary parenchymal ABPF (33 vs 45%, log-rank P = 0.55). Survival with a radical surgical approach was significantly better when compared with any other treatment strategy in terms of overall survival (63 vs 32% and 63 vs 21% at 1 and 2 years, respectively), as well as in terms of fistula-related survival (63 vs 43% and 63 vs 43% at 1 and 2 years, respectively). CONCLUSIONS: ABPF is a rare but highly lethal complication after TEVAR. The leading mechanism behind ABPF seems to be a continuing external compression of either the bronchial tree or left upper lobe parenchyma. In this setting, persisting or newly developing endoleak formation seems to play a crucial role. Prognosis does not differ in patients with central airway or pulmonary parenchymal fistulation. Radical bronchial or pulmonary parenchymal repair in combination with stent graft removal and aortic reconstruction seems to be the most durable treatment strategy

Severe Aplastic Anemia and PNH

Severe aplastic anemia (SAA) is an autoimmune disorder (AID) due to the attack of autoreactive cytotoxic T lymphocytes to the hematopoietic component of the bone marrow