In Italy, a judge reduced the sentence of a defendant by 1 year in response to evidence for a genetic predisposition to violence. The best characterized of these genetic differences, those in the monoamine oxidase A (MAOA), were cited as especially relevant. Several months previously in the USA, MAOA data contributed to a jury reducing charges from 1st degree murder (a capital offence) to voluntary manslaughter. Is there a rational basis for this type of use of MAOA evidence (...) in criminal court? This paper will review in context recent work on the MAOA gene–environment interaction in predisposing individuals to violence and address the relevance of such findings to murder trials. Interestingly, the MAOA genetic variants impact future violence and aggression only when combined with the adverse environmental stimuli of childhood maltreatment. Thus nature and nurture interact to determine the individual’s risk. Based on current evidence, I argue there is a weak case for mitigation. But should future experiments confirm the hypothesis that individual differences in impulse control and response to provocation found in MAOA-L men (without abuse) are significantly magnified when combined with childhood maltreatment, the case could turn into a stronger one. (shrink)

Parkinsonism (PD) is a neurodegenerative disorder of the brain resulting in dopamine deficiency caused by the progressive death of dopaminergic neurons. PD is characterized by a combination of rigidity, poverty of movement, tremor and postural instability. Selegiline is a selective and irreversible propargylamine type B monoamine oxidase (MAO‐B) inhibitor. This drug, which inhibits dopamine metabolism, has been effectively used in the treatment of PD. However, its therapeutic effects are compromised by its many neurotoxic metabolites. To circumvent this obstacle, (...) a novel MAO‐B inhibitor, rasagiline, was developed. Paradoxically, the neuroprotective mechanism of propargylamines in different neuronal models appears to be independent of MAO‐B inhibition. Recent investigations into the neuroprotective mechanism of propargylamines indicate that glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH), MAO‐B and/or other unknown proteins may represent pivotal proteins in the survival of the injured neurons. Delineation of the mechanism(s) involved in the neuroprotective effects exerted by MAO‐B inhibitors may provide the key to preventive novel therapeutic modalities. BioEssays 26:80–90, 2004. © 2003 Wiley Periodicals, Inc. (shrink)

A comparative method of studying the biological bases of personality compares human trait dimensions with likely animal models in terms of genetic determination and common biological correlates. The approach is applied to the trait of sensation seeking, which is defined on the human level by a questionnaire, reports of experience, and observations of behavior, and on the animal level by general activity, behavior in novel situations, and certain types of naturalistic behavior in animal colonies. Moderately high genetic determination has been (...) found for human sensation seeking, and marked strain differences in rodents have been found in open-field behavior that may be related to basic differences in brain neurochemistry. Agonistic and sociable behaviors in both animals and humans and the trait measure of sensation seeking in humans have been related to certain common biological correlates such as gonadal hormones, monoamine oxidase (MAO), and augmenting of the cortical evoked potential.The monoamine systems in the rodent brain are involved in general activity, exploratory behavior, emotionality, socialization, dominance, sexual and consummately behaviors, and intracranial self-stimulation. Preliminary studies have related norepinephrine and enzymes involved in its production and degradation to human sensation seeking. A model is suggested that relates mood, behavioral activity, sociability, and clinical states to activity of the central catecholamine neurotransmitters and to neuroregulators and other transmitters that act in opposite ways on behavior or stabilize activity in the arousal systems. Stimulation and behavioral activity act on the catecholamine systems in a brain–behavior feedback loop. At optimal levels of catecholamine systems activity (CSA) mood is positive and activity and sociability are adaptive. At very low or very high levels of CSA mood is dysphoric, activity is restricted or stereotyped, and the organism is unsocial or aggressively antisocial. Novelty, in the absence of threat, may be rewarding through activation of noradrenergic neurons. (shrink)

Heterogeneity within MDD has hampered identification of biological markers (e.g., intermediate phenotypes, IPs) that might increase risk for the disorder or reflect closer links to the genes underlying the disease process. The newer characterizations of dimensions of MDD within Research Domain Criteria (RDoC) domains may align well with the goal of defining IPs. We compare a sample of 25 individuals with MDD compared to 29 age and education matched controls in multimodal assessment. The multimodal RDoC assessment included the primary IP (...) biomarker, positron emission tomography (PET) with a selective radiotracer for 5-HT1A ([11C]WAY-100635), as well as event-related functional MRI with a Go/No-go task targeting the Cognitive Control network, neuropsychological assessment of affective perception, negative memory bias and Cognitive Control domains. There was also an exploratory genetic analysis with the serotonin transporter (5-HTTLPR) and monamine oxidase A (MAO-A) genes. In regression analyses, lower 5-HT1A binding potential (BP) in the MDD group was related to diminished engagement of the Cognitive Control network, slowed resolution of interfering cognitive stimuli, one element of Cognitive Control. In contrast, higher/normative levels of 5-HT1A BP in MDD (only) was related to a substantial memory bias toward negative information, but intact resolution of interfering cognitive stimuli and greater engagement of Cognitive Control circuitry. The serotonin transporter risk allele was associated with lower 1a BP and the corresponding imaging and cognitive IPs in MDD. Lowered 5HT 1a BP was present in half of the MDD group relative to the control group. Lowered 5HT 1a BP may represent a subtype including decreased engagement of Cognitive Control network and impaired resolution of interfering cognitive stimuli. Future investigations might link lowered 1a BP to neurobiological pathways and markers, as well as probing subtype-specific treatment targets. (shrink)

Neuronal aggregates involved in conscious awareness are not evenly distributed throughout the CNS but comprise key components referred to as the neural network correlates of consciousness (NNCC). A critical node in this network is the posterior cingulate, precuneal, and retrosplenial cortices. The cytological and neurochemical composition of this region is reviewed in relation to the Brodmann map. This region has the highest level of cortical glucose metabolism and cytochrome c oxidase activity. Monkey studies suggest that the anterior thalamic projection (...) likely drives retrosplenial and posterior cingulate cortex metabolism and that the midbrain projection to the anteroventral thalamic nucleus is a key coupling site between the brainstem system for arousal and cortical systems for cognitive processing and awareness. The pivotal role of the posterior cingulate, precuneal, and retrosplenial cortices in consciousness is demonstrated with posterior cingulate epilepsy cases, midcingulate lesions that de-afferent this region and are associated with unilateral sensory neglect, observations from stroke and vegetative state patients, alterations in blood flow during sleep, and the actions of general anesthetics. Since this region is critically involved in self reflection, it is not surprising that it is similarly a site for the NNCC. Interestingly, information processing during complex cognitive tasks and during aversive sensations such as pain induces efforts to terminate self reflection and result in decreased processing in posterior cingulate and precuneal cortices. (shrink)

For the legal system to function effectively people are generally viewed as autonomous actors able to exercise choice and responsible for their actions. It is conceivable that genetic traits associated with violent and antisocial behaviour could call into question an affected individual’s responsibility for acts of criminal violence. Evidence concerning genes associated with violent and antisocial behaviour has been introduced in criminal courts in USA and Italy, either alone or with associated environmental factors. One example of a ‘genetic defence’ is (...) based on low levels of monoamine oxidase A activity, with a prevalence of around thirty percent in Caucasian males. In countries with trial by jury it is particularly relevant to consider the views of publics on criminal liability and the significance they assign to evidence citing genetic influences on behaviour. This article draws on largely qualitative research looking at participants’ explanations of, and assigning of responsibility for, violent and antisocial behaviour where environmental or genetic influences are claimed. Genetic factors were not viewed deterministically by participants but were considered by most to be irrelevant to personal responsibility. Notions of human agency, free will and choice were crucial to explanations of problem behaviours and ensured that offenders could be held responsible despite evidence on environmental and genetic factors. (shrink)

Both genetic and environmental factors have key roles in determining aggressive tendencies. In particular, reaction to stress appears to be an important factor in precipitating aggressive episodes and individuals may vary in their ability to cope with stressful environments depending on their genetic make up. Evidence from humans and primates indicates that adverse rearing conditions may interact with variants in stress and neurotransmitter pathway genes leading to antisocial and/or violent behaviour. Common alleles of some serotonin pathway genes, including those involved (...) in its degradation (monoamine oxidase A, MAOA), or its re‐uptake into pre‐synaptic neurones (serotonin transporter, SERT) have been shown to confer functional variation. Examination of the interaction between the alleles of such polymorphisms (in particular those affecting MAOA) and environmental stressors suggest that they may provide protection against, or increase sensitivity to, abusive upbringing; an observation that may explain part of the variability in developmental outcomes associated with maltreatment. BioEssays 29: 227–236, 2007. © 2007 Wiley Periodicals, Inc. (shrink)

Analysis of a diverse cross‐sample of plant‐insect interactions suggests that the abundance of vitamin C (L‐ascorbic acid, ascorbate or AsA) in plants influences their susceptibility to insect feeding. These effects may be mediated by AsAs roles as an essential dietary nutrient, as an antioxidant in the insect midgut, or as a substrate for plant‐derived ascorbate oxidase, which can lead to generation of toxic reactive oxygen species. Ascorbate can also influence the efficacy of plant defenses such as myrosinases and tannins, (...) and alter insects' susceptibility to natural enemies. Conversely, herbivores appear to influence both de novo synthesis and redox cycling of AsA in their host plants, thereby potentially altering the nutritional value of crops and their susceptibility to pests. The recent development of genetically modified crops with enhanced AsA content provides both an impetus and a tool set for further studies on the role of AsA in plant‐insect interactions. (shrink)

We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (...) (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40–85%) and sustained (30–50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory. Key Words: antidepressant drugs; brain stem lesions; dreams; functional imaging; memory consolidation; REM deprivation; REM sleep; theta rhythm. (shrink)

A variety of studies show that parental absence early in life leads to deleterious effects on the developing CNS. This is thought to be largely because evolutionary-dependent stimuli are necessary for the appropriate postnatal development of the young brain, an effect sometimes termed the “experience-expectant brain,” with parents providing the necessary input for normative synaptic connections to develop and appropriate neuronal survival to occur. Principal among CNS systems affected by parental input are the monoamine systems. In the present study,N= (...) 434 rhesus monkeys (233 males, 201 females) were reared in one of two conditions: as mother-reared controls (MR;n= 269) or without adults with 24-h access to same-aged peers (PR;n= 165). When subjects were six-months-old, they underwent a separation paradigm involving 4, sequential, four-day social separations from their mothers or peers, with each separation followed by three-day reunions with their mothers or their peers. Prior to the separation paradigm, baseline cisternal CSF samples were obtained, as well as at the end of each the four social separations, and after final separation, during a recovery period. CSF was assayed for concentrations of monoamine metabolites and a blood sample was genotyped for the serotonin transporter (5-HTT) genotype. Replicating earlier landmark findings, PR subjects with thesallele exhibited lower baseline concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA), when compared to PR subjects homozygous for theLallele. MR subjects were undifferentiated by genotype. PR subjects exhibited lower CSF 5-HIAA concentrations during baseline, but higher CSF 5-HIAA during social separations, when compared to MR subjects. There were rearing effects for the dopamine metabolite homovanillic acid (HVA) and for the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG), with PR subjects showing higher HVA and lower MHPG when compared to MR subjects. These findings indicate that there are long-term deficits in the response of monoamines following early maternal absence. The results of this study confirm and extend earlier findings that early parental absence has deleterious consequences for the development of the monoamine systems, and that these consequences are modulated by the 5-HTT genotype. (shrink)

Can there be scientific theories in psychology, medicine or psychiatry? I approach this question through an in-depth analysis of a typical experiment for clinical depression involving the monoamine hypothesis, drug action, and placebos. I begin my discussion with a reconstruction of Adolph Grünbaum's conceptual analysis of 'placebo,' and then use his notion of "intentional placebo" to discuss a typical experiment using the monoamine hypothesis, two drugs and a placebo. I focus on the theoretical aspects of the experiment, especially (...) on the notion of causal explanation. I then raise five conceptual and methodological problems for theory construction. These problems focus on questions of the causal efficacy of placebos and drugs; ad hoc versus ceteris paribus explanations in biomedicine and psychology; and the falsifiability of the monoamine hypothesis. I conclude by pointing out the need for further, rigorous philosophical analysis concerning the possibility of theory construction in psychology, medicine, or psychiatry. (shrink)

Abstractα/β barrels have an ill‐defined origin. Evidence exists which favours their divergent evolution from a common ancestral barrel and convergent evolution to a stable fold. However, recent sequence and structural information for the flavin oxidase/dehydrogenase family of barrel enzymes indicate that sub‐families of α/β barrels have evolved divergently. The modular fusion of barrel domains with core structures from other gene families has also contributed to the evolution of related but catalytically distinct enzyme molecules within each sub‐family of the flavin (...) oxidases/dehydrogenases. An analysis of the structures and sequences of the flavin oxidases/dehydrogenases has now enabled studies focusing on the evolutionary origins and modular assembly of this important family of proteins to be initiated. (shrink)

Superoxide is produced by a NADPH oxidase of phagocytic cells and contributes to their microbicidal activities. The oxidase is activated when receptors in the neutrophil plasma membrane bind to the target microbe. These receptors recognise antibodies and complement fragments which coat the target cell. The oxidase electron transport chain, located in the plasma membrane, comprises a low potential cytochrome b heterodimer (gp 91‐phox and p22‐phox) associated with FAD. It is non‐functional until at least three proteins, p67‐phox, p47‐phox (...) and p21rac (and possibly others), move from the cytosol to dock on the cytochrome b. The docking involves the interaction of SH3 domains may become exposed follwoing phosphorylation of p47‐phox by protein kinase C or, in model systems, by addition of arachidonic acid to reconstitution mixtures. Following the docking process the electron‐transporting component is able to transfer electrons from NADPH to oxygen. This electrogenic event is charge‐compensated by the opening of a prton channel. Components of the oxidase are expressed in non‐phagocytes, where their function is uncretain but could be related to some signal function of superoxide. (shrink)

Mitochondrial respiration is the predominant source of ATP. Excessive rates of electron transport cause a higher production of harmful reactive oxygen species (ROS). There are two regulatory mechanisms known. The first, according to Mitchel, is dependent on the mitochondrial membrane potential that drives ATP synthase for ATP production, and the second, the Kadenbach mechanism, is focussed on the binding of ATP to Cytochrome c Oxidase (CytOx) at high ATP/ADP ratios, which results in an allosteric conformational change to CytOx, causing (...) inhibition. In times of stress, ATP‐dependent inhibition is switched off and the activity of CytOx is exclusively determined by the membrane potential, leading to an increase in ROS production. The second mechanism for respiratory control depends on the quantity of electron transfer to the Heme aa3 of CytOx. When ATP is bound to CytOx the enzyme is inhibited, and ROS formation is decreased, although the mitochondrial membrane potential is increased. (shrink)

Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive/behavioral developmental disorder where all clinical criteria are behavioral. Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms. The dynamic developmental behavioral theory is based on the hypothesis that altered dopaminergic function plays a pivotal role by failing to modulate nondopaminergic (primarily glutamate and GABA) signal transmission appropriately. A hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. This gives rise to delay (...) aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to “inhibit” responses (“disinhibition”). A hypofunctioning mesocortical dopamine branch will cause attention response deficiencies (deficient orienting responses, impaired saccadic eye movements, and poorer attention responses toward a target) and poor behavioral planning (poor executive functions). A hypofunctioning nigrostriatal dopamine branch will cause impaired modulation of motor functions and deficient nondeclarative habit learning and memory. These impairments will give rise to apparent developmental delay, clumsiness, neurological “soft signs,” and a “failure to inhibit” responses when quick reactions are required. Hypofunctioning dopamine branches represent the main individual predispositions in the present theory. The theory predicts that behavior and symptoms in ADHD result from the interplay between individual predispositions and the surroundings. The exact ADHD symptoms at a particular time in life will vary and be influenced by factors having positive or negative effects on symptom development. Altered or deficient learning and motor functions will produce special needs for optimal parenting and societal styles. Medication will to some degree normalize the underlying dopamine dysfunction and reduce the special needs of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can turn into relatively stable behavioral patterns. Key Words: catecholamine; clumsiness; dopamine; hyperkinesis; hyperkinetic disorder; impulsivity; monoamine; neuromodulator; overactivity; pollutants; reinforcement; reward; verbally governed behavior; soft signs; variability. (shrink)

Ethylene (C2H4) is a gaseous plant hormone produced by higher and lower (green) plants and, when grown on appropriate substrates, also by fungi, yeasts and bacteria. Ethylene is involved in many developmental processes in plants and is biologically active in trace amounts (10 – 100 nl/I of air) that may be present in the outside air due to industrial air pollution(1). Fruit ripening and flower senescence especially, in a variety of commercially important crops, are dramatically stimulated by ethylene. Following characterization (...) of the genes coding for the key enzymes in ethylene biosynthesis, i.e. ACC synthase and ACC oxidase, it has become clear that their expression is regulated in a complex manner involving developmental, hormonal and tissue‐specific factors. This was recently very elegantly demonstrated for the expression of ACC oxidase genes in developing petunia flowers by Tang et al.(2). The spatial and temporal expression patterns, especially in the reproductive organs, suggest a hitherto unknown role for ethylene in reproductive processes such as the self‐incompatible response and the secretion of cellular exudate by the stigma and nectary. (shrink)

The Problem of Perception offers two arguments against direct realism--one concerning illusion, and one concerning hallucination--that no current theory of ...

In this paper I examine Grace A. de Laguna’s theory of universals in its historical context and in relation to contemporary debates in analytic metaphysics. I explain the central features of her theory, arguing that her theory should be classified as a form of immanent realism and as a powers ontology. I then show in what ways her theory affords a theory of modality in terms of potentialities and discuss some of its consequences along the way.

A. H. Louie's More Than Life Itself is an exploratory journey in relational biology, a study of life in terms of the organization of entailment relations in living systems. This book represents a synergy of the mathematical theories of categories, lattices, and modelling, and the result is a synthetic biology that provides a characterization of life. Biology extends physics. Life is not a specialization of mechanism, but an expansive generalization of it. Organisms and machines share some common features, but organisms (...) are not machines. Life is defined by a relational closure that places it beyond the reach of physicochemical and mechanistic dogma, outside the reductionistic universe, and into the realm of impredicativity. Function dictates structure. Complexity brings forth living beings. (shrink)

This companion is a cutting-edge primer to critical forms of the posthumanities and the feminist posthumanities, aimed at students and researchers who want to catch up with the recent theoretical developments in various fields in the humanities, such as new media studies, gender studies, cultural studies, science and technology studies, human animal studies, postcolonial critique, philosophy and environmental humanities. It contains a collection of nineteen new and original short chapters introducing influential concepts, ideas and approaches that have shaped and developed (...) new materialism, inhuman theory, critical posthumanism, feminist materialism, and posthuman philosophy. A resource for students and teachers, this comprehensive volume brings together established international scholars and emerging theorists, for timely and astute definitions of a moving target – posthuman humanities and feminist posthumanities. (shrink)

Inspired by Castañeda (1966, 1968), Perry (1979) and Lewis (1979) showed that a specific variety of singular thoughts, thoughts about oneself “as oneself” – de se thoughts, as Lewis called them – raise special issues, and they advanced rival accounts. Their suggestive examples raise the problem of de se thought – to wit, how to characterize it so as to give an accurate account of the data, tracing its relations to singular thoughts in general. After rehearsing the main tenets of (...) two contrasting accounts – a Lewisian one and a Perrian one – in the first section of this paper, in the second I will present a proposal of my own, which is a specific elaboration of the Perrian account. In the first section I will indicate some weaknesses of Perry’s presentation of his view; the proposal I will articulate in the second overcomes them. I will conclude with a brief discussion of reasons for preferring one or another account, in particular regarding the issue of the communication of de se thoughts. (shrink)

Trope theory is a leading metaphysical theory in analytic ontology. One of its classic statements is found in the work of Donald C. Williams who argued that tropes qua abstract particulars are the very alphabet of being. The concept of an abstract particular has been repeatedly attacked in the literature. Opponents and proponents of trope theory alike have levelled their criticisms at the abstractness of tropes and the associated act of abstraction. In this paper I defend the concept of a (...) trope qua abstract particular by rejecting arguments that purport to show that tropes should not be understood as abstract and by arguing that the abstractness of tropes plays an indispensable role in one of our more promising trope-theoretic analyses of universals and of concrete objects. (shrink)

I. Ókor -- II. A középkor és a reneszánsz -- III. Az újkor.

The book questions two key dichotomies: that of the apparent and real, and that of the internal and external. This leads to revised notions of the structure of experience and the object of knowledge. Our world is experienced as possibilities of action, and to know is to know what to do. A further consequence is that the mind is best considered as a property of organisms' interactions with their environment. The unit of analysis is the loop of action and perception, (...) and the central concept is the notion of habit of action, which provides the embodied basis of cognition as the anticipation of action. This holds for non-linguistic tacit meanings as well as for linguistic meanings. Habit of action is a teleological notion and thus opens a possibility for defining intentionality and normativity in terms of the soft naturalism adopted in the book. The mind is embodied, and this embodiment determines our physical perspective on the world. Our sensory organs and other instruments give us instrumental access to the world, and this access is epistemic in character. The distinction between the physical and conceptual viewpoint allows us to define truth as the correspondence with operational fit. This embodied epistemic truth is however not a sign of antirealism, as the instrumentally accessed theoretical objects are precisely those objects that experimental science deals with.. (shrink)

In many vertebrates, the enzymatic oxidation of dietary yellow carotenoids generates red keto‐carotenoids giving color to ornaments. The oxidase CYP2J19 is here a key effector. Its purported intracellular location suggests a shared biochemical pathway between trait expression and cell functioning. This might guarantee the reliability of red colorations as individual quality signals independent of production costs. We hypothesize that the ornament type (feathers vs. bare parts) and production costs (probably CYP2J19 activity compromising vital functions) could have promoted tissue‐specific gene (...) relocation. We review current avian tissue‐specific CYP2J19 expression data. Among the ten red‐billed species showing CYP2J19 bill expression, only one showed strong hepatic expression. Moreover, a phylogenetically‐controlled analysis of 25 red‐colored species shows that those producing red bare parts are less likely to have strong hepatic CYP2J19 expression than species with only red plumages. Thus, both production costs and shared pathways might have contributed to the evolution of red signals. (shrink)

La admirable riqueza cultural y artística del Renacimiento esconde una desoladora miseria y aquella "edad de la abundancia" contrasta con una inmensa pobreza. Lejos de ser una broma o una pesadilla, la celebrada Utopía de Tomás Moro fue antes que nada un desafío insoslayable, pues proponía que ninguna sociedad merece tal nombre si tolera la miseria de un solo pobre. Rico y pobre explora la cuestión en ese libro de 1516 y en otros del escritor londinense para concluir con un (...) esbozo de su vida a la luz de la pobreza como virtud indispensable y libertadora. He aquí un hombre afortunado que no fue indiferente ante el infortunio de tantos y que vio en la humanitas la virtud por excelencia que lleva a una constante atención y cuidado del prójimo. Inspirado por un cambio de actitud en su época, así como por su fe cristiana y la mejor tradición estoica, mostró una robusta preocupación sobre el tema subrayando el valor social que debe tener toda riqueza, tanto a nivel estatal como individual, destacando la grave obligación cívica de los ricos y la necesidad que tienen todos, ricos y pobres, de empeñarse en la práctica de cierto desprendimiento y generosidad si no quieren mermar su propia humanidad y fallecer en su avaricia. La percepción de la miseria había cambiado de tal manera que su remedio ya no podía estar en una u otra limosna en plazas e iglesias, sino en la acción bien pensada y perentoria de todo gobierno que se tenga por justo. Sir Tomás Moro, privilegiado desde la cuna y seguro en su trabajo profesional, vio la pobreza de tantos como un desastre social, pero uno que, al mismo tiempo, debería llevar a todo ser humano a ver en el desprendimiento y generosidad una excelencia o virtud que alumbra la "otra" libertad, y tan íntima y valiosa que en su caso brilló aun en la prisión y ante el horror de una muerte injusta y atroz." -- Page 4 of cover. (shrink)