«Enemies of human beings» : Josep Ferrater Mora on blood fiestas

Ferrater Mora maintained that «an enemy of animals is another way of being an enemy of human beings», and similarly many famous thinkers from Aquinas to Kant have held that cruelty to animals leads to cruelty to humans. But how precisely are we to understand this connection? This paper reviews the work of Brian Klug, Thomas I. White, Jonathan Edwards, and James Gustafson, and suggests that cruelty to animals should be rightly characterised as a «degradation» arising from multidimensional deficiency: (i) a failure of perception, resulting in (ii) an enfeebled intellect, and (iii) a contracted, shrivelled sensitivity. If true, animal abuse should be taken with greater seriousness by moralists, if only because there is an ineradicable human interest in curbing our degradation of animals. Indeed, there is now mounting medical, psychological, and statistical evidence of the link between animal cruelty and human anti-social behaviour.Ferrater Mora afirmava que ser «un enemic dels animals és una altra manera de ser un enemic dels éssers humans», així com molts pensadors il·lustres des de Tomàs d'Aquino fins a Kant han sostingut que la crueltat envers els animals condueix a la crueltat envers els humans. Però, com hem d'entendre exactament aquesta connexió? Aquest article examina l'obra de Brian Klug, Thomas I. White, Jonathan Edwards i James Gustafson, i suggereix que la crueltat envers els animals s'hauria de caracteritzar pròpiament com una «degradació » que emergeix d'una deficiència multidimensional: (i) un error de percepció, que produeix (ii) un intel·lecte feble, i (iii) una sensibilitat reduïda i esmorteïda. Si això fos cert, el maltractament dels animals hauria de ser considerat amb molta serietat pels moralistes, encara que només fos perquè hi ha un interès humà irrenunciable a posar fi a la nostra degradació dels animals. De fet, hi ha actualment una enorme evidència mèdica, psicològica i estadística del vincle entre la crueltat cap als animals i un comportament humà antisocial

‘The Powers That Be’: Mechanisms that Prevent us Recognising Animal Sentience

I propose to identify and illustrate what might be described as ‘the powers that be’ – four mechanisms that prevent us from recognising sentience in animals, and to indicate the challenges that should follow for future work in this field

The Theological and Ethical Grounds against Keeping Elephants Captive

As set forth below, animal theology experts Dr. Andrew Linzey and Dr. Clair Linzey of the Oxford Centre for Animal Ethics believe that Petitioner Nonhuman Rights Project, Inc. (“NhRP”) has made a prima facie case that the elephants confined at Fresno Chaffee Zoo in Fresno, CA—Nolwazi, Amahle, and Mabu—are entitled to habeas corpus relief. Accordingly, we respectfully urge the Supreme Court of California to issue an order to show cause in this matter

The Theological and Ethical Grounds against Keeping Elephants Captive

As set forth below, animal theology experts Dr. Andrew Linzey and Dr. Clair Linzey of the Oxford Centre for Animal Ethics believe that Petitioner Nonhuman Rights Project, Inc. (“NhRP”) has made a prima facie case that the elephants confined at Fresno Chaffee Zoo in Fresno, CA—Nolwazi, Amahle, and Mabu—are entitled to habeas corpus relief. Accordingly, we respectfully urge the Supreme Court of California to issue an order to show cause in this matter

Divergent complement system activation in two clinically distinct murine models of multiple sclerosis

Multiple sclerosis (MS) is a neurological disease featuring neuroinflammation and neurodegeneration in young adults. So far, most research has focused on the peripheral immune system, which appears to be the driver of acute relapses. Concurrently, the mechanisms underlying neurodegeneration in the progressive forms of the disease remain unclear. The complement system, a molecular component of the innate immunity, has been recently implicated in several neurological disorders, including MS. However, it is still unknown if the complement proteins detected in the central nervous system (CNS) are actively involved in perpetuating chronic inflammation and neurodegeneration. To address this knowledge gap, we compared two clinically distinct mouse models of MS: 1) proteolipid protein (PLP)-induced experimental autoimmune encephalomyelitis (rEAE) resembling a relapsing-remitting disease course, and 2) Theiler’s murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) resembling a progressive disease. Real-time PCR was performed in the spinal cord of rEAE mice, TMEV-IDD mice and age-matched sham controls to quantify gene expression for a broad range of complement components. In both experimental models, we found significantly increased expression of complement factors, such as C1q, C3, CfB, and C3aR. We showed that the complement system, specifically the classical complement pathway, was associated with TMEV-IDD pathogenesis, as the expression of C1q, C3 and C3aR1 were all significantly correlated to a worse disease outcome (all P≤0.0168). In line with this finding, C1q and C3 deposition was observed in the spinal cord of TMEV-IDD mice. Furthermore, C1q deposition was detected in spinal cord regions characterized by inflammation, demyelination, and axonal damage. Conversely, activation of the classical complement cascade seemed to result in protection from rEAE (C1q: P=0.0307). Interestingly, the alternative pathway related to a worse disease outcome in rEAE (CFb: P=0.0006). Overall, these results indicate potential divergent roles for the complement system in MS. The chronic-progressive disease form is more reliant on the activation of the classic complement pathway, while protecting from acute relapses. Conversely, relapsing MS appears more likely affected by the alternative pathway. Understanding the functions of the complement system in MS is critical and can lead to better, more targeted therapies in the future