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The initial public health response to the breakout of COVID-19 required fundamental changes in individual behavior, such as isolation at home or wearing masks. The effectiveness of these policies hinges on generalized public obedience. Yet, people’s level of compliance may depend on their beliefs regarding the pandemic. We use original data from two waves of a survey conducted in March and April 2020 in eight Organisation for Economic Cooperation and Development countries (n = 21,649) to study gender differences in COVID-19−related beliefs and behaviors. We show that women are more likely to perceive COVID-19 as a very serious health problem, to agree with restraining public policy measures, and to comply with them. Gender differences in attitudes and behavior are sizable in all countries. They are accounted for neither by sociodemographic and employment characteristics nor by psychological and behavioral factors. They are only partially mitigated for individuals who cohabit or have direct exposure to the virus. We show that our results are not due to differential social desirability bias. This evidence has important implications for public health policies and communication on COVID-19, which may need to be gender based, and it unveils a domain of gender differences: behavioral changes in response to a new risk.

Alzheimer’s disease (AD) constitutes a major cause of dementia, affecting more women than men. It is characterized by amyloid-β (Aβ) deposition and neurofibrillary tangles (NFTs) formation, associated with a progressive cognitive decline. Evidence indicates that AD onset increases the prevalence of cerebral microinfarcts caused by vascular pathologies, which occur in approximately in half of AD patients. In this project, we postulated that multifocal cerebral microinfarcts decisively influence early AD-like pathology progression in a sex dependent manner in young APP/PS1 mice. For this purpose, we used a novel approach to model multifocal microinfarcts in APP/PS1 mice via the sporadic occlusions of the microvasculature. Our findings indicate that microinfarcts reduced Aβ deposits without affecting soluble Aβ levels in the brain of male and female APP/PS1 mice, while causing rapid and prolonged cognitive deficits in males, and a mild and transient cognitive decline in females. In male APP/PS1 mice, microinfarcts triggered an acute hypoperfusion followed by a chronic hyperperfusion. Whereas in female APP/PS1 mice, microinfarcts caused an acute hypoperfusion, which was recovered in the chronic phase. Microinfarcts triggered a robust microglial activation and recruitment of peripheral monocytes to the lesion sites and Aβ plaques more potently in female APP/PS1 mice, possibly accounting for the reduced Aβ deposition. Finally, expression of Dickkopf-1 (DKK1), which plays a key role in mediating synaptic and neuronal dysfunction in AD, was strongly induced at the lesion sites of male APP/PS1 mice, while its expression was reduced in females. Our findings suggest that multifocal microinfarcts accelerate AD pathology more potently in young males compared to young females independently upon Aβ pathology via modulation of neurovascular coupling, inflammatory response, and DKK1 expression. Our results suggest that the effects of microinfarcts should be taken into consideration in AD diagnosis, prognosis, and therapies.

A large-scale randomized experiment conducted during the 2012 French presidential and parliamentary elections shows that voter registration requirements have significant effects on turnout, resulting in unequal participation. We assigned 20,500 apartments to one control or six treatment groups that received canvassing visits providing either information about registration or help to register at home. While both types of visits increased registration, home registration visits had a higher impact than information-only visits, indicating that both information costs and administrative barriers impede registration. Home registration did not reduce turnout among those who would have registered anyway. On the contrary, citizens registered due to the visits became more interested in and knowledgeable about the elections as a result of being able to participate in them, and 93% voted at least once in 2012. The results suggest that easing registration requirements could substantially enhance political participation and interest while improving representation of all groups.

Improving patients' tuberculosis (TB) knowledge is a salient component of TB control strategies. Patient knowledge of TB may encourage infection prevention behaviors and improve treatment adherence. The purpose of this study is to examine how TB knowledge and infection prevention behaviors change over the course of treatment. A matched patient-health worker dataset (n = 6,031) of publicly treated TB patients with NGO-provided treatment support health workers was compiled in nine Indian cities from March 2013 to September 2014. At the beginning and end of TB treatment, patients were asked about their knowledge of TB symptoms, transmission, and treatment and infection prevention behaviors. Patients beginning TB treatment (n = 3,424) demonstrated moderate knowledge of TB; 52.5% (50.8%, 54.2%) knew that cough was a symptom of TB and 67.2% (65.6%, 68.7%) knew that TB was communicable. Overall patient knowledge was significantly associated with literacy, education, and income, and was higher at the end of treatment than at the beginning (3.7%, CI: 3.02%, 4.47%). Infection prevention behaviors like covering a cough (63.4%, CI: 61.2%, 65.0%) and sleeping separately (19.3%, CI: 18.0%, 20.7%) were less prevalent. The age difference between patient and health worker as well as a shared language significantly predicted patient knowledge and adherence to infection prevention behaviors. Social proximity between health worker and patients predicted greater knowledge and adherence to infection prevention behaviors but the latter rate remains undesirably low.

Microglia are the brain resident immune cells; they can produce a large variety of growth factors to prevent neuronal damages and recovery. In neurodegenerative diseases, microglia are both benefic and deleterious depending on different factors and diseases. In multiple sclerosis, microglia are involved in both demyelination and remyelination processes. Recent studies suggest the beneficial role of microglia in regenerative processes. These include the regenerative development of myelin after demyelination. This review gives an overlook of how microglia and growth factors can influence the remyelination properties.

This paper provides the first estimate of the effect of door-to-door canvassing on actual electoral outcomes, via a countrywide experiment embedded in François Hollande’s campaign in the 2012 French presidential election. While existing experiments randomized door-to-door visits at the individual level, the scale of this campaign (five million doors knocked) enabled randomization by precinct, the level at which vote shares are recorded administratively. Visits did not affect turnout, but increased Hollande’s vote share in the first round and accounted for one-fourth of his victory margin in the second. Visits’ impact persisted in later elections, suggesting a lasting persuasion effect.

Macrophage colony-stimulating factor (mCSF) is a cytokine known to promote the recruitment of macrophages inducing the release of CCL2, a chemokine mobilizing monocytes to sites of inflammation. Additionally, it induces microglia/macrophage proliferation and the polarization of these cells towards a M2-like phenotype, impairing their ability to release pro-inflammatory factors and toxic mediators, while favoring the release of mediators promoting tissue repair. Another important player is the mCSF receptor CSFR1, which is highly expressed in monocytes, macrophages and microglia. Here, we discuss the new interesting therapeutic avenue of the mCSF/CSFR1 axis on brain diseases. More specifically, mCSF cascade might stimulate the survival/proliferation of oligodendrocytes, enhance the immune response as well as modulate the release of growth factors and the phagocytic activity of immune cells to remove myelin debris and toxic proteins from the brain.

Conflicting results on melatonin synthesis in multiple sclerosis (MS) have been reported due to variabilities in patient lifestyles, which are not considered when supplementing melatonin. Since melatonin acts through its receptors, we identified melatonin receptors in oligodendrocytes (OLs) in the corpus callosum, where demyelination occurs; the subventricular zone, where neural stem/progenitor cells (NSPCs) are located; and the choroid plexus, which functions as a blood-cerebrospinal fluid barrier. Moreover, using chimeric mice, resident macrophages were found to express melatonin receptors, whereas bone marrow-derived macrophages lost this expression in the demyelinated brain. Next, we showed that cuprizone-fed mice, which is an MS model, tended to have increased melatonin levels. While we used different approaches to alter the circadian rhythm of melatonin and cortisol, only the constant light approach increased NSPC proliferation and differentiation to oligodendrocyte precursor cells (OPCs), OPCs maturation to OLs and recruitment to the site of demyelination, the number of patrolling monocytes, and phagocytosis. In contrast, constant darkness and exogenous melatonin exacerbated these events and amplified monocyte infiltration. Therefore, melatonin should not be considered a universal remedy, as is currently claimed. Our data emphasize the importance of monitoring melatonin/cortisol oscillations in each MS patient by considering diet and lifestyle to avoid melatonin overdose. Multiple sclerosis: Understanding the role of melatonin Regulating melatonin levels holds promise as a therapy for multiple sclerosis (MS), but treatment must be tailored to each individual. In MS, the immune system destroys the myelin sheath surrounding nerves, disturbing brain–body communication. Melatonin, a sleep-inducing hormone, is known to play a role in MS, but results so far are inconsistent. Serge Rivest at Laval University in Québec City, Canada, and coworkers investigated how melatonin affects particular brain cell types in a mouse model. They found that maintaining melatonin levels at an intermediate level, where they regulate rather than enhance immune activity, could minimize myelin destruction in MS. They conclude that melatonin should not be considered a universal remedy for MS, but that melatonin levels should be monitored for each individual patient to account for lifestyle differences.

The purinergic receptor P2Y6 is expressed in immune cells, including the microglia that are implicated in neurological disorders. Its ligand, UDP, is a signaling molecule that can serve as an “find-me” signal when released in significant quantities by damaged/dying cells. The binding of UDP by P2Y6R leads to the activation of different biochemical pathways, depending on the disease context and the pathological environment. Generally, P2Y6R stimulates phagocytosis. However, whether or not phagocytosis coincides with cell activation or the secretion of pro-inflammatory cytokines needs further investigation. The current review aims to discuss the various functions of P2Y6R in some CNS disorders. We present evidence that P2Y6R may have a detrimental or beneficial role in the nervous system, in the context of neurological pathologies, such as ischemic stroke, Alzheimer’s disease, Parkinson’s disease, radiation-induced brain injury, and neuropathic pain.

Connecting private dwellings to the water main is expensive and typically cannot be publicly financed. We show that households' willingness to pay for a private connection is high when it can be purchased on credit, not because a connection improves health but because it increases the time available for leisure and reduces inter- and intra-household conflicts on water matters, leading to sustained improvements in well-being. Our results suggest that facilitating access to credit for households to finance lump sum quality-of-life investments can significantly increase welfare, even if those investments do not result in any health or income gains.