Perceptions of, and Obstacles to, SARS-CoV-2 Vaccination Among Adults in Lebanon: Cross-sectional Online Survey.

BACKGROUND: The COVID-19 pandemic is an additional burden on Lebanon's fragmented health care system and adds to its ongoing political, economic, and refugee crises. Vaccination is an important means of reducing the impact of the pandemic. OBJECTIVE: Our study's aims were to (1) assess the prevalences of intention to vaccinate and vaccine hesitancy in Lebanon; (2) determine how vaccine hesitancy in Lebanon varies by sociodemographic, economic, and geographic characteristics; and (3) understand individuals' motivations for vaccinating as well as concerns and obstacles to vaccination. METHODS: We performed a cross-sectional study from January 29, 2021, to March 11, 2021, using an online questionnaire of open- and closed-ended questions in Arabic via convenience "snowball" sampling to assess the perceptions of adults residing in Lebanon. RESULTS: Of the 1185 adults who participated in the survey, 46.1% (95% CI: 43.2%-49.0%) intended to receive the SARS-CoV-2 vaccine when available to them, 19.0% (95% CI 16.8%-21.4%) indicated they would not, and 34.0% (95% CI 31.3%-36.8%) were unsure (with an additional 0.9% skipping this question). The most common reasons for hesitancy were concerns about safety, limited testing, side effects, and efficacy. Top motivations for vaccinating were to protect oneself, protect one's family and the public, and end the pandemic. Despite financial hardships in Lebanon, barriers to vaccine access were not frequently described as concerns. Established health care facilities, rather than new temporary vaccination centers, were most frequently selected as preferred vaccination sites. CONCLUSIONS: Vaccine hesitancy appears to be high in Lebanon. Disseminating clear, consistent, evidence-based safety and efficacy information on vaccines may help reduce vaccine hesitancy, especially among the large proportion of adults who appear to be unsure about (rather than opposed to) vaccination.

Virtual Exchange in Global Health: an innovative educational approach to foster socially responsible overseas collaboration.

Educators who design and manage study abroad programs face a series of ethical responsibilities. Meeting these responsibilities is critical in the field of global health, where study abroad programs are often designed to provide healthcare services in under-resourced communities. Leaders in global health have thus formed working groups to study the ethical implications of overseas programming and have led the way in establishing socially responsible best practices for study abroad. Their recommendations include development of bidirectional programming that is designed for mutual and equitable benefits, focused on locally identified needs and priorities, attentive to local community costs, and structured to build local capacity to ensure sustainability. Implementation remains a key challenge, however. Sustainable, bidirectional programming is difficult and costly. In the present study, authors questioned how technology could be used to connect students of global health in distant countries to make socially responsible global health programming more accessible. Drawing on empirical research in the learning sciences and leveraging best practices in technology design, the authors developed a Virtual Exchange in Global Health to connect university students in the U.S. with counterparts in Lebanon, who worked in teams to address humanitarian problems in Syrian refugee camps. Early results demonstrate the value of this approach. At dramatically lower cost than traditional study abroad-and with essentially no carbon footprint-students recognized complementary strengths in each other through bidirectional programming, learned about local needs and priorities through Virtual Reality, and built sustaining relationships while addressing a difficult real-world problem. The authors learned that technology could effectively facilitate socially responsible global health programming and do so at low cost. The program has important implications for teaching and learning during the COVID-19 crisis and beyond.

The first life skills intervention to enhance well-being amongst university students in the Arab world: 'Khotwa' pilot study.

Although Life Skills programs showed to improve the psychological and physical wellbeing of individuals, little attention has been paid, worldwide and in the Arab countries in specific to implementing life skills intervention for university students. In this study, we tested the effectiveness of a life skills based health promotion intervention KHOTWA (STEP) in enhancing the wellbeing of university students in Lebanon, a country that faces economic and political instability. This is a quasi-experimental study, with pre and post-test, intervention-control design. Each group was formed of 78 participants studying in a private university in Lebanon. Mixed design was used to address the process and outcomes objectives of the intervention. The program was carried online due to COVID-19 pandemic. Significant differences were observed between the intervention and the control groups for life skills, dietary habits and mental health scores at the 3-month follow-up. For the intervention group, a significant increase was observed in the mean score of each of the following Life Skills subscales: self-care (p = 0.001), work and study (p = 0.013), career and education planning (p = 0.011) and looking forward/goal settings (p < 0.001). Students also achieved a healthier eating habit compared to those in the control group by decreasing their consumption of processed food. There was no significant effect in terms of body mass index (p = 0.827). Also, there was a significant change in the mental health status (p = 0.012) only in the intervention group as its mean score decreased after 3 months of the intervention implementation. This intervention enhances the mental health and promotes healthy habits leading consequently to a better quality of life and more productivity amongst university students. Therefore, such interventions should be replicated in other similar context to improve university students' well-being.

Myosin Va increases the efficiency of neurofilament transport by decreasing the duration of long-term pauses.

We investigated the axonal transport of neurofilaments in cultured neurons from two different strains of dilute lethal mice, which lack myosin Va. To analyze the motile behavior, we tracked the movement of green fluorescent protein (GFP)-tagged neurofilaments through naturally occurring gaps in the axonal neurofilament array of cultured superior cervical ganglion neurons from DLS/LeJ dilute lethal mice. Compared with wild-type controls, we observed no statistically significant difference in velocity or frequency of movement. To analyze the pausing behavior, we used a fluorescence photoactivation pulse-escape technique to measure the rate of departure of PAGFP (photoactivatable GFP)-tagged neurofilaments from photoactivated axonal segments in cultured dorsal root ganglion neurons from DLS/LeJ and dl20J dilute lethal mice. Compared with wild-type controls, we observed a 48% increase in the mean time for neurofilaments to depart the activated regions in neurons from DLS/LeJ mice (p < 0.001) and a 169% increase in neurons from dl20J mice (p < 0.0001). These data indicate that neurofilaments pause for more prolonged periods in the absence of myosin Va. We hypothesize that myosin Va is a short-range motor for neurofilaments and that it can function to enhance the efficiency of neurofilament transport in axons by delivering neurofilaments to their microtubule tracks, thereby reducing the duration of prolonged off-track pauses.

Axonal transport of TDP-43 mRNA granules is impaired by ALS-causing mutations.

The RNA-binding protein TDP-43 regulates RNA metabolism at multiple levels, including transcription, RNA splicing, and mRNA stability. TDP-43 is a major component of the cytoplasmic inclusions characteristic of amyotrophic lateral sclerosis and some types of frontotemporal lobar degeneration. The importance of TDP-43 in disease is underscored by the fact that dominant missense mutations are sufficient to cause disease, although the role of TDP-43 in pathogenesis is unknown. Here we show that TDP-43 forms cytoplasmic mRNP granules that undergo bidirectional, microtubule-dependent transport in neurons in vitro and in vivo and facilitate delivery of target mRNA to distal neuronal compartments. TDP-43 mutations impair this mRNA transport function in vivo and in vitro, including in stem cell-derived motor neurons from ALS patients bearing any one of three different TDP-43 ALS-causing mutations. Thus, TDP-43 mutations that cause ALS lead to partial loss of a novel cytoplasmic function of TDP-43.

VCP is essential for mitochondrial quality control by PINK1/Parkin and this function is impaired by VCP mutations.

Mutations in VCP cause multisystem degeneration impacting the nervous system, muscle, and/or bone. Patients may present with ALS, Parkinsonism, frontotemporal dementia, myopathy, Paget's disease, or a combination of these. The disease mechanism is unknown. We developed a Drosophila model of VCP mutation-dependent degeneration. The phenotype is reminiscent of PINK1 and parkin mutants, including a pronounced mitochondrial defect. Indeed, VCP interacts genetically with the PINK1/parkin pathway in vivo. Paradoxically, VCP complements PINK1 deficiency but not parkin deficiency. The basis of this paradox is resolved by mechanistic studies in vitro showing that VCP recruitment to damaged mitochondria requires Parkin-mediated ubiquitination of mitochondrial targets. VCP recruitment coincides temporally with mitochondrial fission, and VCP is required for proteasome-dependent degradation of Mitofusins in vitro and in vivo. Further, VCP and its adaptor Npl4/Ufd1 are required for clearance of damaged mitochondria via the PINK1/Parkin pathway, and this is impaired by pathogenic mutations in VCP.

Tight functional coupling of kinesin-1A and dynein motors in the bidirectional transport of neurofilaments.

We have tested the hypothesis that kinesin-1A (formerly KIF5A) is an anterograde motor for axonal neurofilaments. In cultured sympathetic neurons from kinesin-1A knockout mice, we observed a 75% reduction in the frequency of both anterograde and retrograde neurofilament movement. This transport defect could be rescued by kinesin-1A, and with successively decreasing efficacy by kinesin-1B and kinesin-1C. In wild-type neurons, headless mutants of kinesin-1A and kinesin-1C inhibited both anterograde and retrograde movement in a dominant-negative manner. Because dynein is thought to be the retrograde motor for axonal neurofilaments, we investigated the effect of dynein inhibition on anterograde and retrograde neurofilament transport. Disruption of dynein function by using RNA interference, dominant-negative approaches, or a function-blocking antibody also inhibited both anterograde and retrograde neurofilament movement. These data suggest that kinesin-1A is the principal but not exclusive anterograde motor for neurofilaments in these neurons, that there may be some functional redundancy among the kinesin-1 isoforms with respect to neurofilament transport, and that the activities of the anterograde and retrograde neurofilament motors are tightly coordinated.