The nature of blindsight: implications for current theories of consciousness.

Blindsight regroups the different manifestations of preserved discriminatory visual capacities following the damage to the primary visual cortex. Blindsight types differentially impact objective and subjective perception, patients can report having no visual awareness whilst their behaviour suggests visual processing still occurs at some cortical level. This phenomenon hence presents a unique opportunity to study consciousness and perceptual consciousness, and for this reason, it has had an historical importance for the development of this field of research. From these studies, two main opposing models of the underlying mechanisms have been established: (a) blindsight is perception without consciousness or (b) blindsight is in fact degraded vision, two views that mirror more general theoretical options about whether unconscious cognition truly exists or whether it is only a degraded form of conscious processing. In this article, we want to re-examine this debate in the light of recent advances in the characterization of blindsight and associated phenomena. We first provide an in-depth definition of blindsight and its subtypes, mainly blindsight type I, blindsight type II and the more recently described blindsense. We emphasize the necessity of sensitive and robust methodology to uncover the dissociations between perception and awareness that can be observed in brain-damaged patients with visual field defects at different cognitive levels. We discuss these different profiles of dissociation in the light of both contending models. We propose that the different types of dissociations reveal a pattern of relationship between perception, awareness and metacognition that is actually richer than what is proposed by either of the existing models. Finally, we consider this in the framework of current theories of consciousness and touch on the implications the findings of blindsight have on these.

Multifaceted modes of action of the anticancer probiotic Enterococcus hirae.

A deviated repertoire of the gut microbiome predicts resistance to cancer immunotherapy. Enterococcus hirae compensated cancer-associated dysbiosis in various tumor models. However, the mechanisms by which E. hirae restored the efficacy of cyclophosphamide administered with concomitant antibiotics remain ill defined. Here, we analyzed the multifaceted modes of action of this anticancer probiotic. Firstly, E. hirae elicited emigration of thymocytes and triggered systemic and intratumoral IFNγ-producing and CD137-expressing effector memory T cell responses. Secondly, E. hirae activated the autophagy machinery in enterocytes and mediated ATG4B-dependent anticancer effects, likely as a consequence of its ability to increase local delivery of polyamines. Thirdly, E. hirae shifted the host microbiome toward a Bifidobacteria-enriched ecosystem. In contrast to the live bacterium, its pasteurized cells or membrane vesicles were devoid of anticancer properties. These pleiotropic functions allow the design of optimal immunotherapies combining E. hirae with CD137 agonistic antibodies, spermidine, or Bifidobacterium animalis. We surmise that immunological, metabolic, epithelial, and microbial modes of action of the live E. hirae cooperate to circumvent primary resistance to therapy.

The Stage-Specific Plasticity of Descending Modulatory Controls in a Rodent Model of Cancer-Induced Bone Pain.

Pain resulting from metastatic bone disease is a major unmet clinical need. Studying spinal processing in rodent models of cancer pain is desirable since the percept of pain is influenced in part by modulation at the level of the transmission system in the dorsal horn of the spinal cord. Here, a rodent model of cancer-induced bone pain (CIBP) was generated following syngeneic rat mammary gland adenocarcinoma cell injection in the tibia of male Sprague Dawley rats. Disease progression was classified as "early" or "late" stage according to bone destruction. Even though wakeful CIBP rats showed progressive mechanical hypersensitivity, subsequent in vivo electrophysiological measurement of mechanically evoked deep dorsal horn spinal neuronal responses revealed no change. Rather, a dynamic reorganization of spinal neuronal modulation by descending controls was observed, and this was maladaptive only in the early stage of CIBP. Interestingly, this latter observation corresponded with the degree of damage to the primary afferents innervating the cancerous tissue. Plasticity in the modulation of spinal neuronal activity by descending control pathways reveals a novel opportunity for targeting CIBP in a stage-specific manner. Finally, the data herein have translational potential since the descending control pathways measured are present also in humans.