Atmosfera de baixo oxigénio aplicada a placas autochrome em exibição

As placas autochrome foram o primeiro processo fotográfico a côr comercialmente viável. A fraca estabilidade à luz dos corantes presentes no ecrã de côr levaram a maioria das instituições culturais com este tipo de material a adoptarem uma política de não exibição de originais, recorrendo ao uso de fac-similes. A presente investigação, levada a cabo no Metropolitan Museum of Art em Nova Iorque, estudou a estabilidade à luz, sob uma atmosfera de baixo oxigénio, dos seis corantes presentes no ecrã de côr das placas autochrome – Tartrazina, Eritrosina B, Rosa Bengala, Azul Patente, Cristal Violeta, e Azul Flexo. Os corantes foram testados individualmente na primeira fase da investigação e, na segunda fase, nas combinações vermelho-laranja, verde e azul-violeta presentes no ecrã de côr das placas autochrome. Amostras produzidas seguindo as formulações históricas foram expostas a 8.29 horas megalux. Foram recolhidas leituras espectrofotométricas antes e após a exposição à luz. Um grupo de amostras foi exposto numa atmosfera de baixo oxigénio (menos de 0.1%) e um segundo grupo comparativo foi exposto à luz em condições atmosféricas de oxigénio (cerca de 21%). Os resultados indicam o benefício das condições de baixo oxigénio em retardar o grau de desvanecimento do ecrã de côr das placas autochrome expostos a elevados níveis de luz. Os resultados desta investigação permitiram o Metropolitan Museum of Art exibir placas autochrome originais pela primeira vez em mais de vinte-cinco anos, no âmbito da exposição Stieglitz, Steichen, Strand. Cinco placas autochrome da autoria de Alfred Stieglitz e Edward Steichen foram expostas em atmosfera de baixo oxigénio durante uma semana em Janeiro de 2011. Durante o restante período da exposição foram utilizados facsimiles. A terceira fase desta investigação consistiu no desenho, teste e implementação de uma embalagem selada de baixo oxigénio; na investigação de fontes de luz para exposição; no estabelecimento da metodologia de monitorização antes, durante e depois da exposição; e no desenho do método de exibição dos fac-similes

Separase prevents genomic instability by controlling replication fork speed

Proper chromosome segregation is crucial for preserving genomic integrity, and errors in this process cause chromosome mis-segregation, which may contribute to cancer development. Sister chromatid separation is triggered by Separase, an evolutionary conserved protease that cleaves the cohesin complex, allowing the dissolution of sister chromatid cohesion. Here we provide evidence that Separase participates in genomic stability maintenance by controlling replication fork speed. We found that Separase interacted with the replication licensing factors MCM2-7, and genome-wide data showed that Separase co-localized with MCM complex and cohesin. Unexpectedly, the depletion of Separase increased the fork velocity about 1.5-fold and caused a strong acetylation of cohesin's SMC3 subunit and altered checkpoint response. Notably, Separase silencing triggered genomic instability in both HeLa and human primary fibroblast cells. Our results show a novel mechanism for fork progression mediated by Separase and thus the basis for genomic instability associated with tumorigenesis

Separase prevents genomic instability by controlling replication fork speed

Proper chromosome segregation is crucial for preserving genomic integrity, and errors in this process cause chromosome mis-segregation, which may contribute to cancer development. Sister chromatid separation is triggered by Separase, an evolutionary conserved protease that cleaves the cohesin complex, allowing the dissolution of sister chromatid cohesion. Here we provide evidence that Separase participates in genomic stability maintenance by controlling replication fork speed. We found that Separase interacted with the replication licensing factors MCM2-7, and genome-wide data showed that Separase co-localized with MCM complex and cohesin. Unexpectedly, the depletion of Separase increased the fork velocity about 1.5-fold and caused a strong acetylation of cohesin's SMC3 subunit and altered checkpoint response. Notably, Separase silencing triggered genomic instability in both HeLa and human primary fibroblast cells. Our results show a novel mechanism for fork progression mediated by Separase and thus the basis for genomic instability associated with tumorigenesis

From traumatic childhood to cocaine abuse: the critical function of the immune system

Background: Experiencing traumatic childhood is a risk factor for developing substance use disorder (SUD), but the mechanisms that underlie this relationship have not been determined. Adverse childhood experiences affect the immune system and the immune system mediates the effects of psychostimulants. However, whether this system is involved in the etiology of SUD in individuals who have experience early life stress is unknown. Methods:In this study, we performed a series of ex vivo and in vivo experiments in mice and humans to define the function of the immune system in the early-life stress-induced susceptibility to the neurobehavioral effects of cocaine. Results: We provide evidence that exposure to social-stress (S-S) at an early age permanently sensitizes the peripheral (splenocytes) and brain (microglia) immune responses to cocaine in mice. In the brain, microglial activation in the ventral tegmental area (VTA) of S-S mice was associated with functional alterations in dopaminergic neurotransmission, as measured by whole-cell voltage clamp recordings in dopamine (DA) neurons. Notably, preventing immune activation during the S-S exposure reverted the effects of DA in the VTA and the cocaine-induced behavioral phenotype to control levels. In humans, cocaine modulated Toll-like receptor 4-mediated innate immunity, an effect that was enhanced in cocaine addicts who had experienced a difficult childhood. Conclusions Collectively, our findings demonstrate that sensitization to cocaine in early-life-stressed individuals involves brain and peripheral immune responses and that this mechanism is shared between mice and humans

Characteristics of people living in Italy after a cancer diagnosis in 2010 and projections to 2020

BACKGROUND: Estimates of cancer prevalence are widely based on limited duration, often including patients living after a cancer diagnosis made in the previous 5 years and less frequently on complete prevalence (i.e., including all patients regardless of the time elapsed since diagnosis). This study aims to provide estimates of complete cancer prevalence in Italy by sex, age, and time since diagnosis for all cancers combined, and for selected cancer types. Projections were made up to 2020, overall and by time since diagnosis. METHODS: Data were from 27 Italian population-based cancer registries, covering 32% of the Italian population, able to provide at least 7 years of registration as of December 2009 and follow-up of vital status as of December 2013. The data were used to compute the limited-duration prevalence, in order to estimate the complete prevalence by means of the COMPREV software. RESULTS: In 2010, 2,637,975 persons were estimated to live in Italy after a cancer diagnosis, 1.2 million men and 1.4 million women, or 4.6% of the Italian population. A quarter of male prevalent cases had prostate cancer (n\u2009=\u2009305,044), while 42% of prevalent women had breast cancer (n\u2009=\u2009604,841). More than 1.5 million people (2.7% of Italians) were alive since 5 or more years after diagnosis and 20% since 6515 years. It is projected that, in 2020 in Italy, there will be 3.6 million prevalent cancer cases (+\u200937% vs 2010). The largest 10-year increases are foreseen for prostate (+\u200985%) and for thyroid cancers (+\u200979%), and for long-term survivors diagnosed since 20 or more years (+\u200945%). Among the population aged 6575 years, 22% will have had a previous cancer diagnosis. CONCLUSIONS: The number of persons living after a cancer diagnosis is estimated to rise of approximately 3% per year in Italy. The availability of detailed estimates and projections of the complete prevalence are intended to help the implementation of guidelines aimed to enhance the long-term follow-up of cancer survivors and to contribute their rehabilitation need

Breast cancer in young women. Case report

BACKGROUND: Breast cancer in patients under 40 years is uncommon. Surveillance, Epidemiology and End Results (SEER) program reveals that 75% of breast tumors occur in women age 50 years, only 6.5% in women age 40 years, and a mere 0.6% in women age 30 years. Breast-conserving surgery with subsequent chemo-radiotherapy has become the treatment of choice in women with breast neoplasm. CASE REPORT: Two young patients, 30 and 28 years respectively, with breast cancer. One patient with an atypical medullary breast carcinoma diagnosis, pT2 pN1 bipMx, Grade 3 Stage IIB, negative for receptors, Ki 67: 47%, cERB-2 negative; the other with an intraductal breast carcinoma, pT1c pN0 pMx, Grade 2 Stage I, negative for receptors, Ki 67: 85%, cERB-2 negative, p53 negative, Bcl-2 negative. The first patient underwent right radical mastectomy sec. Madden and axillary lymphoadenectomy in October 2001, started six cycles of adjuvant chemotherapy and radiotherapy on the right side of the chest and on axillary and supraclavicular lymph nodes area. After 2 years an ecotomography revealed small hypoechogenic nodules in the left breast. In December the patient underwent left radical mastectomy with positioning of an expander device. The histological exam revealed a not much differentiated intraductal carcinoma, pT1a N0 Mx, Stage I. After the surgical therapy, she follows another adjuvant chemotherapy. The second patient underwent left quadrantectomy with axillary limphoadenectomy in November 2004. Like the first-will follow several cycles of adjuvant chemotherapy and radiotherapy. DISCUSSION: Breast cancer in women under 40 years of age differ from breast cancer in older women in numerous clinical, pathological and biological features. The studies demonstrate that breast cancer arising in women under 40 years have a more aggressive profile than those of older patients. In both our patients family history of breast cancer was reported. That suggests a possible genetic susceptibility of these patients through BRCA1 and BRCA2 germ-line mutations. Breast conservative surgery with chemio-radiotherapy is the most commonly used treatment breast cancer, expecially in consideration of the aggressiveness of the lesions

A novel compound of triphenyltin(IV) with N-tert-butoxycarbonyl-l-ornithine causes cancer cell death by inducing a p53-dependent activation of the mitochondrial pathway of apoptosis

The triphenyltin(IV) compound with N-tert-butoxycarbonyl-L-ornithine (Boc-Orn-OH), [Ph3Sn(Boc-OrnO)], was synthesized and characterized by elemental analysis, FT-IR, solution 1 H, 13C and 119Sn NMR and ESI mass spectrometry. The organotin(IV) compound inhibited at very low micromolar concentrations the growth of human tumor cell lines HepG2 (hepatocarcinoma cells), MCF-7 (mammary cancer) and HCT116 (colorectal carcinoma) while it did not affect the viability of non-malignant human-derived hepatic cells Chang. The mechanism of the antiproliferative effect of Ph3Sn(Boc-Orn-O), investigated on human hepatoma HepG2 cells, was pro-apoptotic, being associated with externalization of plasma membrane phosphatidylserine, chromatin condensation or fragmentation and mitochondrial dysfunction as well as with increase of p53 levels