Digital Food Retail: Public Health Opportunities

For over two decades, digital food retail services have been emerging alongside advances in mobile technology and improved access to wi-fi. Digitalization has driven changes within the food environment, complicating an already complex system that influences food-related behaviors and eating practices. Digital food retail services support an infrastructure that enhances commercial food systems by extending access to and availability of highly processed foods, further escalating poor dietary intakes. However, digital food retail services are heterogeneous–food delivery apps, online groceries, and meal kits–and can be feasibly adapted to nutrition interventions and personalized to individual needs. Although sparse, new evidence indicates great potential for digital food retail services to address food insecurity in urban areas and to support healthy eating by making it easier to select, plan, and prepare meals. Digital food retail services are a product of the digital transformation that reflect consumers’ constant need for convenience, which must be addressed in future research and interventions. This paper will discuss public health opportunities that are emerging from the global uptake of digital food retail services, with a focus on online groceries, food delivery apps, and meal kits.     

Skin conductance fear conditioning impairments and aggression: A longitudinal study

Autonomic fear conditioning deficits have been linked to child aggression and adult criminal behavior. However, it is unknown if fear conditioning deficits are specific to certain subtypes of aggression, and longitudinal research is rare. In the current study, reactive and proactive aggression were assessed in a sample of males and females when aged 10, 12, 15, and 18 years old. Skin conductance fear conditioning data were collected when they were 18 years old. Individuals who were persistently high on proactive aggression measures had significantly poorer conditioned responses at 18 years old when compared to others. This association was not found for reactive aggression. Consistent with prior literature, findings suggest that persistent antisocial individuals have unique neurobiological characteristics and that poor autonomic fear conditioning is associated with the presence of increased instrumental aggressive behavior.     

γδ T Cells Express Activation Markers in the Central Nervous System of Mice with Chronic-relapsing Experimental Autoimmune Encephalomyelitis

In this study, we assessed the expression of activation markers on γδ T cells in central nervous system (CNS) lesions of SJL mice adoptively sensitized to develop experimental autoimmune encephalomyelitis (EAE) using myelin basic protein-reactive T cells. Although disease expression is known to be dependent upon T cells that express the αβ T cell receptor (TCR), a role for γδ T cells has been implicated in some studies but not in others. Using three-color flow cytometric analysis of both total and γδ T cells in spleen and CNS, the data showed that expression of CD69 (early activation marker), CD62L (lymphocyte homing receptor), CD25 (IL-2Rα), CD122 (IL-2Rβ) and CD95/CD95L (Fas/FasL), fluctuated on γδ T cells in EAE lesions in a disease-related fashion. Furthermore, the pattern of expression for these markers on γδ T cells was distinct from that found on the total lymphocyte population. Cytokine analysis of γδ T cells in the CNS demonstrated a bias towards a Th1-like cytokine profile. From these data, we conclude that γδ T cells in EAE lesions display an activated phenotype and form a dynamic component of the total lymphocyte population in the CNS, supporting a contributory role for these cells.     

Evoked potential models of psychopathy: a critical evaluation

Raine (1989) reviewed all evoked potential studies carried out to date and developed an information-processing model of psychopathy from the findings of these studies. Jutai (1989) and Howard (1989) have outlined conceptual and empirical criticism of this model and a reply is made to these comments. Some are found to be invalid, while acceptance of others was not found to necessitate a rejection of the model. However, caveats made in the original paper are reiterated here. The cortical immaturity model outlined by Jutai (1989) as a counter-explanation to that proposed by Raine (1989) is evaluated, and criticisms of this alternative are outlined. It is argued that further progress to a more complete understanding of of psychopathy will be achieved by empirically testing these and other models.     

Glial bridges and Schwann cell migration during chronic demyelination in the C.N.S.

Summary The formation of fibrotic bridges from subpial astrocytes into the subarachnoid space of the spinal cord and the migration of Schwann cells to the central nervous system (C.N.S.) is appraised in chronically demyelinated C.N.S. lesions. Spinal cord tissue was studied from inbred, Strain 13 guinea pigs with chronic experimental allergic encephalomyelitis (EAE). It has been found that uncommitted Schwann cells are present around remyelinated fibres in nerve root entry zones, between meningeal cells at a distance from the roots and along blood vessels within the spinal cord parenchyma. It is speculated that these cells migrate via the above route to the C.N.S. In the present model, this invasion might be aided by glial fibrosis, a process which leads to surface irregularities in the spinal cord, an extensive extracellular space and possible breaches in the glia limitans through which Schwann cells might penetrate.     

Somatic mutations of the protein kinase gene family in human lung cancer

Protein kinases are frequently mutated in human cancer and inhibitors of mutant protein kinases have proven to be effective anticancer drugs. We screened the coding sequences of 518 protein kinases (approximately 1.3 Mb of DNA per sample) for somatic mutations in 26 primary lung neoplasms and seven lung cancer cell lines. One hundred eighty-eight somatic mutations were detected in 141 genes. Of these, 35 were synonymous (silent) changes. This result indicates that most of the 188 mutations were "passenger" mutations that are not causally implicated in oncogenesis. However, an excess of approximately 40 nonsynonymous substitutions compared with that expected by chance (P = 0.07) suggests that some nonsynonymous mutations have been selected and are contributing to oncogenesis. There was considerable variation between individual lung cancers in the number of mutations observed and no mutations were found in lung carcinoids. The mutational spectra of most lung cancers were characterized by a high proportion of C:G > A:T transversions, compatible with the mutagenic effects of tobacco carcinogens. However, one neuroendocrine cancer cell line had a distinctive mutational spectrum reminiscent of UV-induced DNA damage. The results suggest that several mutated protein kinases may be contributing to lung cancer development, but that mutations in each one are infrequent.