Micro-EDXRF, SEM-EDS and OM characterisation of tin soldering found in handle attachments of Roman situlae from Conimbriga (Portugal)

Tin (Sn) or a Sn-rich solder applied to copper-based artefacts has been frequently used at least, since the Ancient Greece, although scarce studies have been published concerning the technology of this metallurgical joining technique. Several filler remnants were reported to be found in a Roman collection of handle attachments of situlae or cauldrons (2nd century BCE–5th century CE) from the archaeological site of Conimbriga, a Roman city from the Lusitania Province (Portugal). All these artefacts were cast in high leaded coppers and bronzes. The present study aims to contribute to the knowledge of Sn-rich soldering, an ancientmetallurgical joining technique, by the characterisation of the fusible metallic alloy present in 10 Roman artefacts by means of micro-energy dispersive X-ray fluorescence spectrometry (micro-EDXRF), scanning electron microscopy with energy dispersive X-ray (SEM-EDS) microanalysis and optical microscope (OM) observations. Results of studied solders show the presence of Cu-Sn alloys, with Sn contents ranging from δ to η phase composition (30–60wt% Sn). As the attachments were made in leaded copper alloys, it was also observed, in some cases, the melting of the interdendritic Pb-rich chains with long-range diffusion of the solder alloy into the substrate. The fillers compositions suggest that the handle attachments have been joined to a situla body by the soldering metallurgical process with Sn or a Sn-rich alloy. The studied leaded Cu-Sn attachments, probably formulated by local craftsman, were joined into the body of a situla or cauldron with a soft solder (soldering), a common metallurgical joint from Antiquity, although no relation was found between composition or typology and the Sn or Sn-rich solder

Valorisation of kraft lignin by using vanillin and lignin-based polyurethanes: Use of the biorefinery concept

In kraft pulp mills, the capacity of the recovery boiler is very often a limiting factor to the increase of the pulp production. Until several decades ago, an upgrade to boiler system for dealing with higher quantities of black liquor was the only alternative. The possibility of lignin extraction from black liquor seems to be much more attractive, either for energy production or combustion elsewhere, or to serve as feedstock for chemicals production. Since the beginning of the 90’s, associate Laboratory LSRE/LCM has been focused on overcoming expansion limitations in pulp industries and, in this work, we show an alternative to this industry segment for the utilization of lignin and producing high added value chemicals from renewable biomass materials. Based on the biorefinery concepts, an integrated process for producing vanillin from kraft lignin oxidation has been proposed and each of the needed unit operations has been investigated to provide a deeper scientific understanding on this subject.FCT - projects POCTI/EQU/33198/99, POCI/EQU/61738/2004 and Grant SFRH/BD/18415/2004. CYTED IV.17/2002-2006. Luso-French actions F13/06 and F32/08

Tin determination in fistula seals from Conimbriga and Augusta Emerita

info:eu-repo/semantics/publishedVersio

Angiotensin-converting enzyme inhibitor protects against cisplatin nephrotoxicity by modulating kinin B1 receptor expression and aminopeptidase P activity in mice

Cisplatin is a highly effective chemotherapeutic agent. However, its use is limited by nephrotoxicity. Enalapril is an angiotensin I-converting enzyme inhibitor used for the treatment of hypertension, mainly through the reduction of angiotensin II formation, but also through the increase of kinins half-life. Kinin B1 receptor is associated with inflammation and migration of immune cells into the injured tissue. We have previously shown that the deletion or blockage of kinin B1 and B2 receptors can attenuate cisplatin nephrotoxicity. In this study, we tested enalapril treatment as a tool to prevent cisplatin nephrotoxicity. Male C57Bl/6 mice were divided into 3 groups: control group; cisplatin (20 mg/kg i.p) group; and enalapril (1.5 mg;kg i.p) + cisplatin group. The animals were treated with a single dose of cisplatin and euthanized after 96 h. Enalapril was able to attenuate cisplatin-induced increase in creatinine and urea, and to reduce tubular injury and upregulation of apoptosis-related genes, as well as inflammatory cytokines in circulation and kidney. The upregulation of B1 receptor was blocked in enalapril + cisplatin group. Carboxypeptidase M expression, which generates B1 receptor agonists, is blunted by cisplatin + enalapril treatment. The activity of aminopeptidase P, a secondary key enzyme able to degrade kinins, is restored by enalapril treatment. These findings were confirmed in mouse renal epithelial tubular cells, in which enalaprilat (5 μM) was capable of decreasing tubular injury and inflammatory markers. We treated mouse renal epithelial tubular cells with cisplatin (100 μM), cisplatin+enalaprilat and cisplatin+enalaprilat+apstatin (10 μM). The results showed that cisplatin alone decreases cell viability, cisplatin plus enalaprilat is able to restore cell viability, and cisplatin plus enalaprilat and apstatin decreases cell viability. In the present study, we demonstrated that enalapril prevents cisplatin nephrotoxicity mainly by preventing the upregulation of B1 receptor and carboxypeptidase M and the increased concentrations of kinin peptides through aminopeptidase activity restoration

Characterization of alpha thalassemic genotypes by multiplex ligation-dependent probe amplification in the Brazilian population

Alpha-thalassemia is the most common inherited disorder of hemoglobin synthesis. Genomic deletions involving the alpha-globin gene cluster on chromosome 16p13.3 are the most frequent molecular causes of the disease. Although common deletions can be detected by a single multiplex gap-PCR, the rare and novel deletions depend on more laborious techniques for their identification. The multiplex ligation-dependent probe amplification (MLPA) technique has recently been used for this purpose and was successfully used in the present study to detect the molecular alterations responsible for the alpha-thalassemic phenotypes in 8 unrelated individuals (3 males and 5 females; age, 4 months to 30 years) in whom the molecular basis of the disease could not be determined by conventional methods. A total of 44 probe pairs were used for MLPA, covering approximately 800 kb from the telomere to the MSLN gene in the 16p13.3 region. Eight deletions were detected. Four of these varied in size from 240 to 720 kb and affected a large region including the entire alpha-globin gene cluster and its upstream regulatory element (alpha-MRE), while the other four varied in size from 0.4 to 100 kb and were limited to a region containing this element. This study is the first in Brazil to use the MLPA method to determine the molecular basis of alpha-thalassemia. The variety of rearrangements identified highlights the need to investigate all cases presenting microcytosis and hypochromia, but without iron deficiency or elevated hemoglobin A2 levels and suggests that these rearrangements may be more frequent in our population than previously estimated.162

Cortisol dose-dependently impairs migration and tube-like formation in a trophoblast cell line and modulates inflammatory and angiogenic genes

Several stimuli can change maternal hormone levels during pregnancy. These changes may affect trophoblastic cells and modulate the development of the embryo and the placental tissue itself. Changes in cortisol levels are associated with impaired trophoblast implantation and function, in addition to other pregnancy complications. This study aims to analyze the effects of low and high doses of cortisol on an extravillous trophoblast cell line, and the effects of various exposures to this hormone. SGHPL-4 cells were treated with cortisol at five doses (0–1000 nM) and two exposures (continuous: 24 h/day; and intermittent: 2 h/day). In intermittent treatment, cortisol acted mainly as an anti-inflammatory hormone, repressing gene expression of kinin B1 receptors, interleukin-6, and interleukin-1β. Continuous treatment modulated inflammatory and angiogenic pathways, significantly repressing angiogenic factors and their receptors. Cortisol affected cell migration and tube-like structures formation. In conclusion, both continuous and intermittent exposure to cortisol repressed the expression of inflammatory genes, while only continuous exposure repressed the expression of angiogenic genes, suggesting that a sustained increase in the levels of this hormone is more harmful than a high short-term increase. Cortisol also impaired tube-like structures formation, and kinin receptors may be involved in this response

Kinin receptors regulate skeletal muscle regeneration: differential effects for B1 and B2 receptors

OBJECTIVE AND DESIGN: After traumatic skeletal muscle injury, muscle healing is often incomplete and produces extensive fibrosis. Bradykinin (BK) reduces fibrosis in renal and cardiac damage models through the B2 receptor. The B1 receptor expression is induced by damage, and blocking of the kallikrein-kinin system seems to affect the progression of muscular dystrophy. We hypothesized that both kinin B1 and B2 receptors could play a differential role after traumatic muscle injury, and the lack of the B1 receptor could produce more cellular and molecular substrates for myogenesis and fewer substrates for fibrosis, leading to better muscle healing. MATERIAL AND METHODS: To test this hypothesis, tibialis anterior muscles of kinin receptor knockout animals were subjected to traumatic injury. Myogenesis, angiogenesis, fibrosis, and muscle functioning were evaluated. RESULTS: Injured B1KO mice showed a faster healing progression of the injured area with a larger amount of central nucleated fiber post-injury when compared to control mice. In addition, they exhibited higher neovasculogenic capacity, maintaining optimal tissue perfusion for the post-injury phase; had higher amounts of myogenic markers with less inflammatory infiltrate and tissue destruction. This was followed by higher amounts of SMAD7 and lower amounts of p-SMAD2/3, which resulted in less fibrosis. In contrast, B2KO and B1B2KO mice showed more severe tissue destruction and excessive fibrosis. B1KO animals had better results in post-injury functional tests compared to control animals. CONCLUSIONS: We demonstrate that injured skeletal muscle tissues have a better repair capacity with less fibrosis in the presence of B2 receptor and absence of B1 receptor, including better performances in functional tests