Relazione distinta del ristretto de'processi e sentenze contro Silvestro e Giulio, padre, e figlio Legni, Bonaventura Arigoni e Bernardino Salviati, tutti quattro della Città di Velletri, e di Giovanni Vecchioli da Cisterna di detta diocesi e delle loro abiure fatte pubblicamente in Roma nella chiesa di S. Maria sopra Minerva li 25., e 26. gennajo 1719.

Mode of access: Internet.

MINERVA – the Ministerial Network for Valorising Activities in Digitisation Towards an Agreed European Platform for Digitisation of Cultural and Scientific Heritage

MINERVA is a project funded by the European Commission IST Programme within the 5th Framework Programme. It created a network of EU Ministries and other agencies in charge of cultural policies and programmes, which is open to enlargement to new countries and new sectors of the civil society. The network discusses, correlates and harmonises the activities carried out in the field of digitisation of cultural and scientific heritage, aiming at creating a common European platform made up of agreed recommendations, guidelines, standards. The network acts also to foster collaboration between European Commission and Member States, to ensure awareness of European policies at national level, to exchange good practice, to coordinate national programmes in order to embed in national digitisation activities the technical results achieved by the network. Some main outcomes of the activities are presented.

Aurora : an illustrated novella

Aurora, an illustrated novella, is a retelling of the classic fairytale Sleeping Beauty, set on the Australian coast around the grounds of the family lighthouse. Instead of following in the footsteps of tradition, this tale focuses on the long time Aurora is cursed to sleep by the malevolent Minerva; we follow Aurora as she voyages into the unconscious. Hunted by Minerva through the shifting landscape of her dreams, Aurora is dogged by a nagging pull towards the light—there is something she has left behind. Eventually, realising she must face Minerva to break the curse, they stage a battle of the minds in which Aurora triumphs, having grasped the power of her thoughts, her words. Aurora, an Australian fairytale, is a story of self-empowerment, the ability to shape destiny and the power of the mind. The exegesis examines a two-pronged question: is the illustrated book for young adults—graphic novel—relevant to a contemporary readership, and, is the graphic novel, where text and image intersect, a suitably specular genre in which to explore the unconscious? It establishes the language of the unconscious and the meaning of the term ‘graphic novel’, before investigating the place of the illustrated book for an older readership in a contemporary market, particularly exploring visual literacy and the way text and image—a hybrid narrative—work together. It then studies the aptitude of graphic literature to representing the unconscious and looks at two pioneers of the form: Audrey Niffenegger, specifically her visual novel The Three Incestuous Sisters, and Shaun Tan, and his graphic novel The Arrival. Finally, it reflects upon the creative work, Aurora, in light of three concerns: how best to develop a narrative able to relay the dreaming story; how to bestow a certain ‘Australianess’ upon the text and images; and the dilemma of designing an illustrated book for an older readership.

Narratives of the 'everyday' in Rio de Janeiro's favelas : community photographers' attempts at generating alternative news values [Narrativas do cotidiano nas favelas do Rio de Janeiro: tentativas de construção de valores-notícia alternativos pelos fotógrafos populares]

Abstract This paper presents the partial results of an ongoing research project which investigates ethnographically community (photo)journalism media initiatives, in Rio de Janeiro, Brazil. The Viva Rio and Observatorio de Favelas (NGOs) run projects that provide favela residents with skills to take, edit and print their own (photo) journalism contents that enables community-based framing and documentation of favela live, personalities and issues. Three months of fieldwork related to these projects in Rio's favelas generated remarkable theoretical issues that represent the community photographers' attempt to establish counter news values by shifting the focus from poverty, shortages, violence and criminality to images of the ordinary life which included the myriad events that occurs in the day of the favelas. Resumo Este artigo apresenta os resultados parciais de uma pesquisa em andamento que, a partir do método etnográfico, investiga os projetos de comunicação comunitária, jornalismo e fotojornalismo, no Rio de Janeiro, Brasil. As organizações não-governamentais (ONGs) Viva Rio e Observatório de Favela apoiam projetos que objetivam tornar moradores de favelas capazes de produzir, editar e publicar as suas próprias narrativas sobre personagens e questões do cotidiano de suas comunidades. O trabalho de campo sobre estes projetos, realizado durante três meses nas favelas do Rio de Janeiro, forneceu questões teóricas relevantes que representam o esforço dos fotógrafos populares para estabelecer contra valores-notícia transferindo o foco da pobreza, escassez, violência e criminalidade para imagens do cotidiano que inclui uma miríade de eventos que acontecem no dia-a-dia das favelas.

The moral status of babies

In their controversial paper 'After-birth abortion', Alberto Giubilini and Francesca Minerva argue that there is no rational basis for allowing abortion but prohibiting infanticide ('after-birth abortion'). We ought in all consistency either to allow both or prohibit both. This paper rejects their claim, arguing that much-neglected considerations in philosophical discussions of this issue are capable of explaining why we currently permit abortion in some cases, while prohibiting infanticide.

The court and the factory the legal construction of occupational health and safety offences in Victoria

This thesis reports on an empirically based study of the manner in which Victorian Magistrates Courts constructed occupational health and safety (OHS) issues when hearing prosecutions for offences under the Industrial Safety, Health and Welfare Act 1981 (the ISHWA) and the Occupational Health and Safety Act 1985 (OHSA) from 1983 to 1991. These statutes established OHS standards for employers and other relevant parties. The State government enforced these standards through an OHS inspectorate which had a range of enforcement powers, including prosecution. After outlining the historical development of Victoria’s OHS legislation, the magistracy’s historical role in its enforcement, and the development of an enforcement culture in which inspectors viewed prosecution as a last resort, the study shows how the key provisions of the ISHWA and OHSA required occupiers of workplaces and employers to provide and maintain safe systems of work, including the guarding of dangerous machinery. Using a wide range of empirical research methods and legal materials, it shows how the enforcement policies, procedures and practices of the inspectorate heavily slanted inspectors workplace investigations and hence prosecutions towards a restricted and often superficial, analysis of incidents (or “events”) most of which involved injuries on machinery. There was evidence, however, that after the establishment of the Central Investigation Unit in 1989 cases were more thoroughly investigated and prosecuted. From 1990 the majority of prosecutions were taken under the employer’s general duty provisions, and by 1991 there was evidence that prosecutions were focusing on matters other than machinery guarding.

No Right to Live? Malaysia’s Islam and Implications for Its Sexual Minority Storytellers

This chapter discusses the fast emerging challenges for Malay and Muslim sexual minority storytellers in the face of an aggressive state-sponsored Islamisation of a constitutionally secular Malaysia. I examine the case of Azwan Ismail, a gay Malay and Muslim Malaysian who took part in the local ‘It Gets Better’ project, and who suffered an onslaught of hostile comments from fellow Malay Muslims. Azwan’s experience makes one question how a message of discouraging suicidal tendencies among sexual minority youths can be so vehemently misperceived. Azwan’s existential challenges – stemming from the tension between his own constructions of self and those of others – (re)present a unique challenge in the long struggle for human rights. In my examination of the arising contradictions, I highlight the challenges for Azwan’s existential self – one who is deemed morally bankrupt by hostile audiences. The purist Sunni Islam agenda in a constitutionally secular Malaysia not only rejects the human rights of the sexual minorities in Malaysia but has also influenced, and is often a leading hostile voice in both regional and international blocs. This self-righteous, supremacist and authoritarian Islam discourages discourse and attacks all differing opinions. This resulting disabling environment for vulnerable, minority communities and their human rights manifests in State-endorsed discrimination, compulsory counselling, forced rehabilitation and criminalisation. It places the rights of the sexual minorities to live within such a society in doubt. In discussing the arising issues, I draw upon literature that investigates the way in which personal stories have traditionally been used to advance human rights. Included too, is the significance and implications of the work by social psychologists in explaining the loss of credibility of personal stories. I then advance an analytical framework that will allow storytelling as a very individual form of witnessing to reclaim and regain its ‘truth to power’.

Knee alignment can help predict sedentary behaviour in children: a pilot study

AIM: The purpose of this pilot study was to introduce knee alignment as a potential predictor of sedentary activity levels in boys and girls. METHODS: Dual energy x-ray absorptiometry (DXA) and anthropometric assessment were conducted on 47 children (21 boys and 26 girls; 5-14 y) and their gender-matched parent. Body Mass Index (BMI) and abdominal-to-height ratio were calculated. Lower extremity alignment was determined by anatomic tibiofemoral angle (TFA) measurements from DXA images. Time spent in moderate-to-vigorous physical activity and sedentary activities were obtained from a parent-reported questionnaire. Stepwise multiple regression analyses identified anthropometric, musculoskeletal, and activity factors of parents and children for predicting total time spent in sedentary behaviour. RESULTS: Weight, total sedentary time of parents and TFA are moderate predictors of sedentary behaviour in children (R2=0.469). When stratifying for gender, TFA and total sedentary time of the parent, as well as waist circumference, are the most useful predictors of sedentary behaviour in boys (R2=0.648). However, weight is the only predictor of sedentary behaviour in girls (R2=0.479). CONCLUSION: Negative associations between TFA and sedentary behaviour indicate that even slight variations in musculoskeletal alignment may influence a child's motivation to be physically active. Although growth and development is complicated by many potentialities, this pilot study suggests that orthopaedic factors should also be considered when evaluating physical activity in children

Invasive and non-invasive modalities of imaging carotid stenosis

Despite recent therapeutic advances, acute ischemic complications of atherosclerosis remain the primary cause of morbidity and mortality in Western countries, with carotid atherosclerotic disease one of the major preventable causes of stroke. As the impact of this disease challenges our healthcare systems, we are becoming aware that factors influencing this disease are more complex than previously realized. In current clinical practice, risk stratification relies primarily on evaluation of the degree of luminal stenosis and patient symptomatology. Adequate investigation and optimal imaging are important factors that affect the quality of a carotid endarterectomy (CEA) service and are fundamental to patient selection. Digital subtraction angiography is still perceived as the most accurate imaging modality for carotid stenosis and historically has been the cornerstone of most of the major CEA trials but concerns regarding potential neurological complications have generated substantial interest in non-invasive modalities, such as contrast-enhanced magnetic resonance angiography. The purpose of this review is to give an overview to the vascular specialist of the current imaging modalities in clinical practice to identify patients with carotid stenosis. Advantages and disadvantages of each technique are outlined. Finally, limitations of assessing luminal stenosis in general are discussed. This article will not cover imaging of carotid atheroma morphology, function and other emerging imaging modalities of assessing plaque risk, which look beyond simple luminal measurements.

Endoplasmic reticulum stress and cell death mechanisms in the cell model of Huntington’s disease

This thesis clarifies important molecular pathways that are activated during the cell death observed in Huntington’s disease. Huntington’s disease is one of the most common inherited neurodegenerative diseases, which is primarily inherited in an autosomal dominant manner. HD is caused by an expansion of CAG repeats in the first exon of the IT15 gene. IT15 encodes the production of a Huntington’s disease protein huntingtin. Mutation of the IT15 gene results in a long stretch of polyQ residues close to the amino-terminal region of huntingtin. Huntington’s disease is a fatal autosomal neurodegenerative disorder. Despite the current knowledge of HD, the precise mechanism behind the selective neuronal death, and how the disease propagates, still remains an enigma. The studies mainly focused on the control of endoplasmic reticulum (ER) stress triggered by the mutant huntingtin proteins. The ER is a delicate organelle having essential roles in protein folding and calcium regulation. Even the slightest perturbations on ER homeostasis are effective enough to trigger ER stress and its adaptation pathways, called unfolded protein response (UPR). UPR is essential for cellular homeostasis and it adapts ER to the changing environment and decreases ER stress. If adaptation processes fail and stress is excessive and prolonged; irreversible cell death pathways are engaged. The results showed that inhibition of ER stress with chemical agents are able to decrease cell death and formation of toxic cell aggregates caused by mutant huntingtin proteins. The study concentrated also to the NF-κB (nuclear factor-kappaB) pathway, which is activated during ER stress. NF-κB pathway is capable to regulate the levels of important cellular antioxidants. Cellular antioxidants provide a first line of defence against excess reactive oxygen species. Excess accumulation of reactive oxygen species and subsequent activation of oxidative stress damages motley of vital cellular processes and induce cell degeneration. Data showed that mutant huntingtin proteins downregulate the expression levels of NF-κB and vital antioxidants, which was followed by increased oxidative stress and cell death. Treatment with antioxidants and inhibition of oxidative stress were able to counteract these adverse effects. In addition, thesis connects ER stress caused by mutant huntingtin to the cytoprotective autophagy. Autophagy sustains cellular balance by degrading potentially toxic cell proteins and components observed in Huntington’s disease. The results revealed that cytoprotective autophagy is active at the early points (24h) of ER stress after expression of mutant huntingtin proteins. GADD34 (growth arrest and DNA damage-inducible gene 34), which is previously connected to the regulation of translation during cell stress, was shown to control the stimulation of autophagy. However, GADD34 and autophagy were downregulated at later time points (48h) during mutant huntingtin proteins induced ER stress, and subsequently cell survival decreased. Overexpression GADD34 enhanced autophagy and decreased cell death, indicating that GADD34 plays a critical role in cell protection. The thesis reveales new interesting data about the neuronal cell death pathways seen in Huntington’s disease, and how cell degeneration is partly counteracted by various therapeutic agents. Expression of mutant huntingtin proteins is shown to alter signaling events that control ER stress, oxidative stress and autophagy. Despite that Huntington’s disease is mainly an untreatable disorder; these findings offer potential targets and neuroprotective strategies in designing novel therapies for Huntington’s disease.

GABAa Receptor Mediated Signalling in the Brain: Inhibition, Shunting and Excitation

Within central nervous system, the simple division of chemical synaptic transmission to depolarizing excitation mediated by glutamate and hyperpolarizing inhibition mediated by γ-amino butyric acid (GABA), is evidently an oversimplification. The GABAa receptor (GABAaR) mediated responses can be of opposite sign within a single resting cell, due to the compartmentalized distribution of cation chloride cotransporters (CCCs). The K+/Cl- cotransporter 2 (KCC2), member of the CCC family, promotes K+ fuelled Cl- extrusion and sets the reversal potential of GABA evoked anion currents typically slightly below the resting membrane potential. The interesting ionic plasticity property of GABAergic signalling emerges from the short-term and long-term alterations in the intraneuronal concentrations of GABAaR permeable anions (Cl- and HCO3-). The short-term effects arise rapidly (in the time scale of hundreds of milliseconds) and are due to the GABAaR activation dependent shifts in anion gradients, whereas the changes in expression, distribution and kinetic regulation of CCCs are underlying the long-term effects, which may take minutes or even hours to develop. In this Thesis, the differences in the reversal potential of GABAaR mediated responses between dopaminergic and GABAergic cell types, located in the substantia nigra, were shown to be attributable to the differences in the chloride extrusion mechanisms. The stronger inhibitory effect of GABA on GABAergic neurons was due to the cell type specific expression of KCC2 whereas the KCC2 was absent from dopaminergic neurons, leading to a less prominent inhibition brought by GABAaR activation. The levels of KCC2 protein exhibited activity dependent alterations in hippocampal pyramidal neurons. Intense neuronal activity, leading to a massive release of brain derived neurotrophic factor (BDNF) in vivo, or applications of tyrosine receptor kinase B (TrkB) agonists BDNF or neurotrophin-4 in vitro, were shown to down-regulate KCC2 protein levels which led to a reduction in the efficacy of Cl- extrusion. The GABAergic transmission is interestingly involved in an increase of extracellular K+ concentration. A substantial increase in interstitial K+ tends to depolarize the cell membrane. The effects that varying ion gradients had on the generation of biphasic GABAaR mediated responses were addressed, with particular emphasis on the novel idea that the K+/Cl- extrusion via KCC2 is accelerated in response to a rapid accumulation of intracellular Cl-. The KCC2 inhibitor furosemide produced a large reduction in the GABAaR dependent extracellular K+ transients. Thus, paradoxically, both the inefficient KCC2 activity (via increased intracellular Cl-) and efficient KCC2 activity (via increased extracellular K+) may promote excitation.

The TRAM flap for breast reconstruction : Studies on perioperative cutaneous blood flow, vasoconstriction, and indices of obesity

Breast reconstruction is performed for 10-15 % of women operated on for breast cancer. A popular method is the TRAM (transverse rectus abdominis musculocutaneous) flap formed of the patient’s own abdominal tissue, a part of one of the rectus abdominis muscles and a transverse skin-subcutis area over it. The flap can be raised as a pedicled or a free flap. The pedicled TRAM flap, based on its nondominant pedicle superior epigastric artery (SEA), is rotated to the chest so that blood flow through SEA continues. The free TRAM flap, based on its dominant pedicle deep inferior epigastric artery (DIEA), is detached from the abdomen, transferred to the chest, and DIEA and vein are anastomosed to vessels on the chest. Cutaneous necrosis is seen in 5–60 % of pedicled TRAM flaps and in 0–15 % of free TRAM flaps. This study was the first one to show with blood flow measurements that the cutaneous blood flow is more generous in free than in pedicled TRAM flaps. After this study the free TRAM flap has exceeded the pedicled flap in popularity as a breast reconstruction method, although the free flap it is technically a more demanding procedure than the pedicled TRAM flap. In pedicled flaps, a decrease in cutaneous blood flow was observed when DIEA was ligated. It seems that SEA cannot provide sufficient blood flow on the first postoperative days. The postoperative cutaneous blood flow in free TRAM flaps was more stable than in pedicled flaps. Development of cutaneous necrosis of pedicled TRAM flaps could be predicted based on intraoperative laser Doppler flowmetry (LDF) measurements. The LDF value on the contralateral skin of the flap decreased to 43 ± 7 % of the initial value after ligation of the DIEA in flaps developing cutaneous necrosis during the next week. Endothelin-1 (ET-1) is a powerful vasoconstrictory peptide secreted by vascular endothelial cells. A correlation was found between plasma ET-1 concentrations and peripheral vasoconstriction developing during and after breast reconstructions with a pedicled TRAM flap. ET-1 was not associated with the development of cutaneous necrosis. Felodipine, a vasodilating calcium channel antagonist, had no effect on plasma ET-1 concentrations, peripheral vasoconstriction or development of cutaneous necrosis in free TRAM flaps. Body mass index and thickness of abdominal were not associated with cutaneous necrosis in pedicled TRAM flaps.

Adipose tissue inflammation, liver fat and insulin resistance in humans

BACKGROUND: Obesity is closely associated with insulin resistance, which is a pathophysiologic condition contributing to the important co-morbidities of obesity, such as the metabolic syndrome and type 2 diabetes mellitus. In obese subjects, adipose tissue is characterized by inflammation (macrophage infiltration, increased expression insulin resistance genes and decreased expression of insulin sensitivity genes). Increased liver fat, without excessive alcohol consumption, is defined as non-alcoholic fatty liver disease (NAFLD) and also associated with obesity and insulin resistance. It is unknown whether and how insulin resistance is associated with altered expression of adipocytokines (adipose tissue-derived signaling molecules), and whether adipose tissue inflammation and NAFLD coexist independent of obesity. Genetic factors could explain variation in liver fat independent of obesity but the heritability of NAFLD is unknown. AIMS: To determine whether acute regulation of adipocytokine expression by insulin in adipose tissue is altered in obesity. To investigate the relationship between adipose tissue inflammation and liver fat content independent of obesity. To assess the heritability of serum alanine aminotransferase (ALT) activity, a surrogate marker of liver fat. METHODS: 55 healthy normal-weight and obese volunteers were recruited. Subcutaneous adipose tissue biopsies were obtained for measurement of gene expression before and during 6 hours of euglycemic hyperinsulinemia. Liver fat content was measured by proton magnetic resonance spectroscopy, and adipose tissue inflammation was assessed by gene expression, immunohistochemistry and lipidomics analysis. Genetic factors contributing to serum ALT activity were determined in 313 twins by statistical heritability modeling. RESULTS: During insulin infusion the expression of insulin sensitivity genes remains unchanged, while the expression of insulin resistance genes increases in obese/insulin-resistant subjects compared to insulin-sensitive subjects. Adipose tissue inflammation is associated with liver fat content independent of obesity. Adipose tissue of subjects with high liver fat content is characterized infiltrated macrophages and increased expression of inflammatory genes, as well as by increased concentrations of ceramides compared to equally obese subjects with normal liver fat. A significant heritability for serum ALT activity was verified. CONCLUSIONS: Effects of insulin infusion on adipose tissue gene expression in obese/insulin-resistant subjects are not only characterized by hyporesponse of insulin sensitivity genes but also by hyperresponse of insulin resistance and inflammatory genes. This suggests that in obesity, the impaired insulin action contributes or self-perpetuates alterations in adipocytokine expression in adipose tissue. Adipose tissue inflammation is increased in subjects with high liver fat compared to equally obese subjects with normal liver fat content. Concentrations of ceramides, the putative mediators of insulin resistance, are increased in adipose tissue in subjects with high liver fat. Genetic factors contribute significantly to variation in serum ALT activity, a surrogate marker of liver fat. These data imply that adipose tissue inflammation and increased liver fat content are closely interrelated, and determine insulin resistance even independent of obesity.

Heme oxygenase-1 in cardiovascular diseases

Myocardial infarction (MI) and heart failure are major causes of morbidity and mortality worldwide. Treatment of MI involves early restoration of blood flow to limit infarct size and preserve cardiac function. MI leads to left ventricular remodeling, which may eventually progress to heart failure, despite the established pharmacological treatment of the disease. To improve outcome of MI, new strategies for protecting the myocardium against ischemic injury and enhancing the recovery and repair of the infarcted heart are needed. Heme oxygenase-1 (HO-1) is a stress-responsive and cytoprotective enzyme catalyzing the degradation of heme into the biologically active reaction products biliverdin/bilirubin, carbon monoxide (CO) and free iron. HO-1 plays a key role in maintaining cellular homeostasis by its antiapoptotic, anti-inflammatory, antioxidative and proangiogenic properties. The present study aimed, first, at evaluating the role of HO-1 as a cardioprotective and prohealing enzyme in experimental rat models and at investigating the potential mechanisms mediating the beneficial effects of HO-1 in the heart. The second aim was to evaluate the role of HO-1 in 231 critically ill intensive care unit (ICU) patients by investigating the association of HO-1 polymorphisms and HO-1 plasma concentrations with illness severity, organ dysfunction and mortality throughout the study population and in the subgroup of cardiac patients. We observed in an experimental rat MI model, that HO-1 expression was induced in the infarcted rat hearts, especially in the infarct and infarct border areas. In addition, pre-emptive HO-1 induction and CO donor pretreatment promoted recovery and repair of the infarcted hearts by differential mechanisms. CO promoted vasculogenesis and formation of new cardiomyocytes by activating c-kit+ stem/progenitor cells via hypoxia-inducible factor 1 alpha, stromal cell-derived factor 1 alpha (SDF-1a) and vascular endothelial growth factor B, whereas HO-1 promoted angiogenesis possibly via SDF-1a. Furthermore, HO-1 protected the heart in the early phase of infarct healing by increasing survival and proliferation of cardiomyocytes. The antiapoptotic effect of HO-1 persisted in the late phases of infarct healing. HO-1 also modulated the production of extracellular matrix components and reduced perivascular fibrosis. Some of these beneficial effects of HO-1 were mediated by CO, e.g. the antiapoptotic effect. However, CO may also have adverse effects on the heart, since it increased the expression of extracellular matrix components. In isolated perfused rat hearts, HO-1 induction improved the recovery of postischemic cardiac function and abrogated reperfusion-induced ventricular fibrillation, possibly in part via connexin 43. We found that HO-1 plasma levels were increased in all critically ill patients, including cardiac patients, and were associated with the degree of organ dysfunction and disease severity. HO-1 plasma concentrations were also higher in ICU and hospital nonsurvivors than in survivors, and the maximum HO-1 concentration was an independent predictor of hospital mortality. Patients with the HO-1 -413T/GT(L)/+99C haplotype had lower HO-1 plasma concentrations and lower incidence of multiple organ dysfunction. However, HO-1 polymorphisms were not associated with ICU or hospital mortality. The present study shows that HO-1 is induced in response to stress in both experimental animal models and severely ill patients. HO-1 played an important role in the recovery and repair of infarcted rat hearts. HO-1 induction and CO donor pretreatment enhanced cardiac regeneration after MI, and HO-1 may protect against pathological left ventricular remodeling. Furthermore, HO-1 induction potentially may protect against I/R injury and cardiac dysfunction in isolated rat hearts. In critically ill ICU patients, HO-1 plasma levels correlate with the degree of organ dysfunction, disease severity, and mortality, suggesting that HO-1 may be useful as a marker of disease severity and in the assessment of outcome of critically ill patients.