O contributo dos trabalhos de Abel Viana e António Dias de Deus para o conhecimento do mundo funerário romano no termo sul do Alto Alentejo (Portugal) e o arqueossítio da Chaminé como caso de estudo

No presente trabalho pretende-se apresentar uma visão genérica da importância das pesquisas arqueológicas levadas a cabo por um conjunto de funcionários da antiga Colónia Correccional de Vila Fernando (Elvas, Portugal) e o arqueólogo Abel Viana (1896-1964) para o conhecimento da realidade arqueológica funerária de época romana no actual território alto alentejano. Entre meados das décadas de 30 e 50 do século XX, procedeu-se à identificação e exploração de mais de uma centena de arqueossítios, entre os quais se contabilizam, em função dos dados conhecidos, 22 espaços funerários de cronologia romana e/ou tardo-romana, correspondentes a um total de mais de 500 enterramentos. Apresenta-se o arqueossítio da Chaminé (Vila Fernando, Elvas) como exemplo paradigmático do conjunto de necrópoles exploradas, quer pelos diferentes momentos de utilização do espaço funerário, quer pela provável relação com a villa do Carrão (Vila Fernando, Elvas, Portugal).The present work intends to illustrate the importance of the archaeological works carried out by employees of the Penal Colony of Vila Fernando (Elvas) and the portuguese archaeologist Abel Viana (1896-1964) for the knowldege of roman funerary reality in Alto Alentejo (Portugal). Between the 1930s and 1950s were identified/ explored more than one hundred sites, incluinding 23 necropolis dated from roman period and/or Late Antiquity. The necropolis of Chaminé (Vila Fernando, Elvas) is presented as an example of the roman funerary reality documented in that geographic área

Role of mitochondrial dysfunction in combined bile acid-induced cytotoxicity: the switch between apoptosis and necrosis

The goal of this investigation was to determine whether chenodeoxycholic acid (CDCA)-induced apoptosis is prevented by ursodeoxycholic acid (UDCA) or tauroursodeoxycholic acid (TUDC) and to characterize the involvement of mitochondria in the process. Cultured human HepG2 cells were treated in a dose- and time-dependent protocol in order to establish a sufficiently low exposure to CDCA that causes apoptosis but not necrosis. Low-dose CDCA induced an S-phase block and G2 arrest of the cell cycle, as determined by flow cytometry. As a result, cell proliferation was inhibited. CDCA-induced apoptosis, as determined by fluorescence microscopy of Hoechst 33342-stained nuclei, was evident upon coincubation with TUDC. Additionally, after exposure to UDCA plus CDCA, the cell membrane was permeable to fluorescent dyes. Caspase-9-like activity, poly(ADP-ribose) polymerase (PARP) cleavage, and extensive DNA fragmentation were detected in CDCA-exposed cells and in cells coincubated with TUDC, but not UDCA. CDCA caused a decrease in mitochondrial membrane potential and depletion of ATP, both of which were potentiated by UDCA but not TUDC. The results suggest that UDCA potentiates CDCA cytotoxicity, probably at the level of induction of the mitochondrial permeability transition (MPT). Consequently, as suggested by the lack of the main hallmarks of the apoptotic pathway, in the presence of UDCA, CDCA-induced apoptosis is not properly executed but degenerates into necrosis

Decreased Susceptibility of Heart Mitochondria from Diabetic GK Rats to Mitochondrial Permeability Transition Induced by Calcium Phosphate

Type 2 diabetes (or non-insulin dependent diabetes mellitus, NIDDM) is a common metabolic disease in man. The Goto–Kakizaki (GK) rat has been designed as a NIDDM model. Previous studies with this strain have shown differences at the mitochondrial level. The mitochondrial permeability transition (MPT) is a widely studied phenomenon but yet poorly understood, that leads to mitochondrial dysfunction and cell death. The aim of this work was to compare the differences in susceptibility of induction of the MPT with calcium phosphate in GK and Wistar rats. Our results show that heart mitochondria from GK rats are less susceptible to the induction of MPT, and show a larger calcium accumulation before the overall loss of mitochondrial impermeability

A low-noise CMOS front-end for TOF-PET

An analogue CMOS front-end for triggering and amplification of signals produced by a silicon photomultiplier (SiPM) coupled to a LYSO scintillator is proposed. The solution is intended for time-of-flight measurement in compact Positron Emission Tomography (TOF-PET) medical imaging equipments where excellent timing resolution is required (approximate to 100 ps). A CMOS 0.13 mu m technology was used to implement such front end, and the design includes preamplification, shaping, baseline holder and biasing circuitry, for a total silicon area of 500x90 mu m. Waveform sampling and time-over-threshold (ToT) techniques are under study and the front-end provides fast and shaped outputs for time and energy measurements. Post layout simulation results show that, for the trigger of a single photoelectron, the time jitter due to the pre-amplifier noise can be as low as 15 ps (FWHM), for a photodetector with a total capacitance of 70 pF. The very low input impedance of the pre-amplifier (approximate to 5 Omega) allows 1.8 ns of peaking time, at the cost of 10 mW of power consumption

Evidence for the evolutionary steps leading to mecA-mediated ß-lactam resistance in staphylococci

The epidemiologically most important mechanism of antibiotic resistance in Staphylococcus aureus is associated with mecA–an acquired gene encoding an extra penicillin-binding protein (PBP2a) with low affinity to virtually all β-lactams. The introduction of mecA into the S. aureus chromosome has led to the emergence of methicillin-resistant S. aureus (MRSA) pandemics, responsible for high rates of mortality worldwide. Nonetheless, little is known regarding the origin and evolution of mecA. Different mecA homologues have been identified in species belonging to the Staphylococcus sciuri group representing the most primitive staphylococci. In this study we aimed to identify evolutionary steps linking these mecA precursors to the β-lactam resistance gene mecA and the resistance phenotype. We sequenced genomes of 106 S. sciuri, S. vitulinus and S. fleurettii strains and determined their oxacillin susceptibility profiles. Single-nucleotide polymorphism (SNP) analysis of the core genome was performed to assess the genetic relatedness of the isolates. Phylogenetic analysis of the mecA gene homologues and promoters was achieved through nucleotide/amino acid sequence alignments and mutation rates were estimated using a Bayesian analysis. Furthermore, the predicted structure of mecA homologue-encoded PBPs of oxacillin-susceptible and -resistant strains were compared. We showed for the first time that oxacillin resistance in the S. sciuri group has emerged multiple times and by a variety of different mechanisms. Development of resistance occurred through several steps including structural diversification of the non-binding domain of native PBPs; changes in the promoters of mecA homologues; acquisition of SCCmec and adaptation of the bacterial genetic background. Moreover, our results suggest that it was exposure to β-lactams in human-created environments that has driven evolution of native PBPs towards a resistance determinant. The evolution of β-lactam resistance in staphylococci highlights the numerous resources available to bacteria to adapt to the selective pressure of antibiotics

Inhibitory effect of carvedilol in the high-conductance state of the mitochondrial permeability transition pore

The mitochondrial permeability transition is a widely studied, but poorly understood, phenomenon in mitochondrial bioenergetics. It has been recognised that this phenomenon is related to the opening of a protein pore in the inner mitochondrial membrane, and that opening of this pore is the cause of some forms of mitochondrial dysfunction. In this work, we propose that carvedilol, a multi-role cardioprotective compound, may act as an inhibitor of the high-conductance state of the mitochondrial permeability transition pore, a conclusion supported by the finding that carvedilol provides differential protection against mitochondrial swelling in sucrose and KCl-based media, and that it is unable to protect against calcium-induced depolarisation of the mitochondrial membrane. We also show that carvedilol inhibits the oxidation of mitochondrial thiol groups and that, beyond causing a slight depression of the membrane potential, it has no inhibitory effect on mitochondrial calcium uptake.http://www.sciencedirect.com/science/article/B6T1J-4292HK0-5/1/3f9b42626ac2f0c2ab80880219b5d9c

A low-noise CMOS front-end for TOF-PET

An analogue CMOS front-end for triggering and amplification of signals produced by a silicon photomultiplier (SiPM) coupled to a LYSO scintillator is proposed. The solution is intended for time-of-flight measurement in compact Positron Emission Tomography (TOF-PET) medical imaging equipments where excellent timing resolution is required (approximate to 100 ps). A CMOS 0.13 mu m technology was used to implement such front end, and the design includes preamplification, shaping, baseline holder and biasing circuitry, for a total silicon area of 500x90 mu m. Waveform sampling and time-over-threshold (ToT) techniques are under study and the front-end provides fast and shaped outputs for time and energy measurements. Post layout simulation results show that, for the trigger of a single photoelectron, the time jitter due to the pre-amplifier noise can be as low as 15 ps (FWHM), for a photodetector with a total capacitance of 70 pF. The very low input impedance of the pre-amplifier (approximate to 5 Omega) allows 1.8 ns of peaking time, at the cost of 10 mW of power consumption