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"Kidd, J."
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Episodes of particle ejection from the surface of the active asteroid (101955) Bennu
Active asteroids are those that show evidence of ongoing mass loss. We report repeated instances of particle ejection from the surface of (101955) Bennu, demonstrating that it is an active asteroid. The ejection events were imaged by the OSIRIS-REx (Origins, Spectral Interpretation, Resource Identification, and Security–Regolith Explorer) spacecraft. For the three largest observed events, we estimated the ejected particle velocities and sizes, event times, source regions, and energies. We also determined the trajectories and photometric properties of several gravitationally bound particles that orbited temporarily in the Bennu environment. We consider multiple hypotheses for the mechanisms that lead to particle ejection for the largest events, including rotational disruption, electrostatic lofting, ice sublimation, phyllosilicate dehydration, meteoroid impacts, thermal stress fracturing, and secondary impacts.
Journal Article
ACE2 activation protects against cognitive decline and reduces amyloid pathology in the Tg2576 mouse model of Alzheimer’s disease
Mid-life hypertension and cerebrovascular dysfunction are associated with increased risk of later life dementia, including Alzheimer’s disease (AD). The classical renin–angiotensin system (cRAS), a physiological regulator of blood pressure, functions independently within the brain and is overactive in AD. cRAS-targeting anti-hypertensive drugs are associated with reduced incidence of AD, delayed onset of cognitive decline, and reduced levels of Aβ and tau in both animal models and human pathological studies. cRAS activity is moderated by a downstream regulatory RAS pathway (rRAS), which is underactive in AD and is strongly associated with pathological hallmarks in human AD, and cognitive decline in animal models of CNS disease. We now show that enhancement of brain ACE2 activity, a major effector of rRAS, by intraperitoneal administration of diminazene aceturate (DIZE), an established activator of ACE2, lowered hippocampal Aβ and restored cognition in mid-aged (13–14-month-old) symptomatic Tg2576 mice. We confirmed that the protective effects of DIZE were directly mediated through ACE2 and were associated with reduced hippocampal soluble Aβ
42
and IL1-β levels. DIZE restored hippocampal MasR levels in conjunction with increased NMDA NR2B and downstream ERK signalling expression in hippocampal synaptosomes from Tg2576 mice. Chronic (10 weeks) administration of DIZE to pre-symptomatic 9–10-month-old Tg2576 mice, and acute (10 days) treatment in cognitively impaired 12–13-month-old mice, prevented the development of cognitive impairment. Together these data demonstrate that ACE2 enhancement protects against and reverses amyloid-related hippocampal pathology and cognitive impairment in a preclinical model of AD.
Journal Article
Marvelocity : the Marvel Comics art of Alex Ross
\"Thirteen years after his Eisner Award-winning, nationally best-selling Mythology, here is the long-awaited Marvel Comics counterpart, a retrospective celebration of the other half of the comics galaxy that is currently ruling the world: Spider-Man, Iron Man, Captain America, Black Panther, the Avengers, the X-Men, Doctor Strange, the Guardians of the Galaxy, and the Fantastic Four. \"Alex is a legend. Even if you don't consider yourself a comics-head, you should check out his work to see what the best of the form has to offer.\" --Ta-Nehisi Coates. As he did for the DC characters in Mythology, Alex Ross now brings the heroes of the Marvel Universe into dynamic life as never before. Marvelocity includes more than 50 never-been-published sketches, working models, and other preparatory art, and a 14-panel portfolio gallery of Marvel's most beloved characters. And Ross has written a new 10-page story pitting Spider-Man against the Sinister Six--the webslinger's most popular villains--that ends with a stunning twist\"-- Provided by publisher.
Book
Microglial displacement of inhibitory synapses provides neuroprotection in the adult brain
Microglia actively survey the brain microenvironment and play essential roles in sculpting synaptic connections during brain development. While microglial functions in the adult brain are less clear, activated microglia can closely appose neuronal cell bodies and displace axosomatic presynaptic terminals. Microglia-mediated stripping of presynaptic terminals is considered neuroprotective, but the cellular and molecular mechanisms are poorly defined. Using 3D electron microscopy, we demonstrate that activated microglia displace inhibitory presynaptic terminals from cortical neurons in adult mice. Electrophysiological recordings further establish that the reduction in inhibitory GABAergic synapses increased synchronized firing of cortical neurons in γ-frequency band. Increased neuronal activity results in the calcium-mediated activation of CaM kinase IV, phosphorylation of CREB, increased expression of antiapoptotic and neurotrophic molecules and reduced apoptosis of cortical neurons following injury. These results indicate that activated microglia can protect the adult brain by migrating to inhibitory synapses and displacing them from cortical neurons.
Microglia play essential roles in sculpting synaptic connections during brain development but their role in the adult brain is less clear. Here the authors show that activated microglia can prophylactically protect the adult rodent brain from injury by migrating to and displacing inhibitory synapses from cortical neurons.
Journal Article
Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone
Emergence of epidemic clones and antibiotic resistance development compromises the management of
Pseudomonas aeruginosa
cystic fibrosis (CF) chronic respiratory infections. Whole genome sequencing (WGS) was used to decipher the phylogeny, interpatient dissemination, WGS mutator genotypes (mutome) and resistome of a widespread clone (CC274), in isolates from two highly-distant countries, Australia and Spain, covering an 18-year period. The coexistence of two divergent CC274 clonal lineages was revealed, but without evident geographical barrier; phylogenetic reconstructions and mutational resistome demonstrated the interpatient transmission of mutators. The extraordinary capacity of
P
.
aeruginosa
to develop resistance was evidenced by the emergence of mutations in >100 genes related to antibiotic resistance during the evolution of CC274, catalyzed by mutator phenotypes. While the presence of classical mutational resistance mechanisms was confirmed and correlated with resistance phenotypes, results also showed a major role of unexpected mutations. Among them, PBP3 mutations, shaping up β-lactam resistance, were noteworthy. A high selective pressure for
mexZ
mutations was evidenced, but we showed for the first time that high-level aminoglycoside resistance in CF is likely driven by mutations in
fusA1
/
fusA2
, coding for elongation factor G. Altogether, our results provide valuable information for understanding the evolution of the mutational resistome of CF
P
.
aeruginosa
.
Journal Article
Positive Psychology Interventions in Practice
\"This book presents recent advancements in positive psychology, specifically its application across broad areas of current interest. Chapters include submissions from various international authors in the field and cover discussion and presentation of relevant research, theories, and applications. The volume covers topics such as CBT, Psychotherapy, Coaching, Workplaces, Aging, Education, Leadership, Emotion, Interventions, Measurement, Technology, Design, Health, Relationships, Experiences, Communities. With the growing interest in the applications of positive psychology across diverse fields within psychology and beyond, this book will make a worthwhile contribution to the field. It will also fill the current need for a volume that highlights specifically the various recent advancements in positive psychology into diverse fields and as such will be of benefit to a wide range of professionals, including psychologists, educators, clinicians, therapists, and many others.\" -- Publisher's website.
Book
A Klebsiella pneumoniae antibiotic resistance mechanism that subdues host defences and promotes virulence
Klebsiella pneumoniae
is an important cause of multidrug‐resistant infections worldwide. Recent studies highlight the emergence of multidrug‐resistant
K. pneumoniae
strains which show resistance to colistin, a last‐line antibiotic, arising from mutational inactivation of the
mgrB
regulatory gene. However, the precise molecular resistance mechanisms of
mgrB
‐associated colistin resistance and its impact on virulence remain unclear. Here, we constructed an
mgrB
gene
K. pneumoniae
mutant and performed characterisation of its lipid A structure, polymyxin and antimicrobial peptide resistance, virulence and inflammatory responses upon infection. Our data reveal that
mgrB
mutation induces PhoPQ‐governed lipid A remodelling which confers not only resistance to polymyxins, but also enhances
K. pneumoniae
virulence by decreasing antimicrobial peptide susceptibility and attenuating early host defence response activation. Overall, our findings have important implications for patient management and antimicrobial stewardship, while also stressing antibiotic resistance development is not inexorably linked with subdued bacterial fitness and virulence.
Synopsis
The emergence of multidrug‐resistant (MDR)
Klebsiella pneumoniae
that develop colistin resistance, often associated with inactivation of
mgrB
, is a health challenge worldwide. Here, inactivation of
mgrB
is shown to confer colistin resistance and to enhance virulence.
mgrB
inactivation triggers extensive remodelling of the lipopolysaccharide (LPS) lipid A section.
mgrB
‐induced lipid A remodelling mediates resistance to colistin but also to human antimicrobial peptides.
mgrB
inactivation is associated with a hypervirulence phenotype in the worm
Galleria mellonella
infection model.
mgrB
inactivation does not affect
Klebsiella
fitness in the pneumonia mouse model.
mgrB
inactivation limits the activation of inflammatory responses which are crucial to clear
Klebsiella
infections.
Graphical Abstract
The emergence of multidrug‐resistant (MDR)
Klebsiella pneumoniae
that develop colistin resistance, often associated with inactivation of
mgrB
, is a health challenge worldwide. Here, inactivation of
mgrB
is shown to confer colistin resistance and to enhance virulence.
Journal Article