Urban Refugee Education: Strengthening Policies and Practices for Access, Quality, and Inclusion

The number of forcibly displaced people across the globe has increased dramatically in the past two decades, exceeding 65 million in 2016--a level not seen since the period directly following World War II. The image of refugees living together in camps is no longer the norm. Sixty percent of today’s refugees live scattered and embedded across large urban areas. The urbanization of refugees is creating new obstacles for refugee children who find it difficult or impossible to attend school, even though they are entitled by international law to do so. According to the United Nations High Commissioner for Refugees, half the world’s displaced people are children under 18. Half of refugee children are enrolled in primary school, 22 percent in secondary school and only one percent in higher education. Adding to the complications of urbanization, longer conflicts have increased the average worldwide duration of refugee status to 20 years. Millions of refugee children are spending their entire childhoods in exile without ever attending school, despite their right to obtain an education. Despite much public discussion of the global refugee crisis in wealthy, westernized nations, 86 percent of all displaced people reside in the “Global South,” in poor, developing countries, often in countries adjacent to their homelands. That is where we focused our study. This report presents findings of our survey of 190 professionals involved in the delivery of educational services to refugees in 16 countries, including an in-depth studies of refugee education in three cities--Beirut, Lebanon; Nairobi, Kenya; and Quito, Ecuador. The report includes policy recommendations based on our findings

HIV-1 Subtype C Mother-to-Child Transmission: Genetic and Immunologic Correlates

Mother-to-child transmission (MTCT) of human immunodeficiency virus-1 (HIV-1) infects over 300,000 infants each year. This transmission can occur in utero (IU), intrapartum (IP), or post-partum through breastfeeding (PP). One feature of transmission from mother to child is a reduction (or 'bottleneck') in viral genetic diversity, particularly within the envelope (env) gene. A heteroduplex tracking assay was used to examine env diversity in women whose infants remained uninfected at least through 6 weeks, and in mother-infant IU and IP transmission pairs. Maternal diversity was similar regardless of transmission status. We confirmed a bottleneck in subtype C IU and IP transmission. We further found that infants infected IU had fewer variants than those infected IP, and that these variants transmitted IU were major variants in the maternal populations more often than variants transmitted IP. Also, minor maternal variants were transmitted with a frequency that demonstrates neither IU nor IP transmission is stochastic. Shorter env sequences and fewer glycosylation sites, ie more 'compact' viruses, have been associated with greater neutralization sensitivity, and compact subtype C viruses are often transmitted through horizontal infection. env genes from a subset of IU and IP transmission pairs were sequenced and showed that compact maternal variants were transmitted IP, but not IU. env sequences from 3 mother-infant pairs where transmission occurred through breastfeeding were also analyzed and we found reductions in genetic diversity, sequence length, and glycosylation. These results demonstrate selection occurs in MTCT, and mechanisms may vary with the timing of transmission. High titers of neutralizing antibodies (NAB) have been correlated with lower rates of horizontal and vertical transmission in animal models, and in some small studies of human transmission. Because we identified selection had occurred in these transmission pairs, we next tested sera from non-transmitting, IU-, and IP-transmitting women for neutralizing activity against virus pseudotyped with heterologous subtype B and C Env proteins. Though non-transmitting women more often had NAB titers against multiple Envs, NAB titer to any one Env did not correlate to transmission status. Thus, we cannot attribute vertical transmission or a lack of transmission to different levels of neutralizing antibodies in the context of subtype C HIV-1 transmission events

A Bibliometric Study of Authorship and Collaboration Trends Over the Past 30 Years in Four Major Musculoskeletal Science Journals

This study explored changes in bibliometric variables over the last 30 years for four major musculoskeletal science journals (BONE®), Calcified Tissue International® (CTI®), Journal of Bone and Mineral Research® (JBMR®), and Journal of Orthopaedic Research® (JOR®), with a specific focus on author gender. Bibliometric data were collected for all manuscripts in 1985 (BONE®, CTI®, JOR®), 1986 (JBMR®), 1995, 2005, and 2015; 2776 manuscripts met inclusion criteria. Manuscripts from Europe were more often published in BONE® or CTI®, while those from North America in JBMR® or JOR®. All journals demonstrated an increase over time in the number of authors (3.67–7.3), number of countries (1.1–1.4), number of institutions (1.4–3.1), and number of references (25.1–45.4). The number of manuscript pages increased (6.6–8.9) except for JOR® which showed a decline. CTI® had the lowest number of authors (4.9 vs. 5.6–6.8). There was a change in the corresponding author position from first to last for all journals; this change was highest for CTI® (35%) and lowest for BONE® (14.0%). All journals demonstrated an increase over time in female authors; however, CTI® was the highest amongst these four journals. The percentage of female first authors rose from 24.6 to 44.3% (CTI® 29.1–52.3%). The percentage of corresponding female authors rose from 17.5 to 33.6% (CTI® 22.9–40.0%). The proportion of female authors is increasing, likely reflecting the increasing number of women obtaining doctorates in science, medicine, and engineering

Opioids depress cortical centers responsible for the volitional control of respiration

Respiratory depression limits provision of safe opioid analgesia and is the main cause of death in drug addicts. Although opioids are known to inhibit brainstem respiratory activity, their effects on cortical areas that mediate respiration are less well understood. Here, functional magnetic resonance imaging was used to examine how brainstem and cortical activity related to a short breath hold is modulated by the opioid remifentanil. We hypothesized that remifentanil would differentially depress brain areas that mediate sensory-affective components of respiration over those that mediate volitional motor control. Quantitative measures of cerebral blood flow were used to control for hypercapnia-induced changes in blood oxygen level-dependent (BOLD) signal. Awareness of respiration, reflected by an urge-to-breathe score, was profoundly reduced with remifentanil. Urge to breathe was associated with activity in the bilateral insula, frontal operculum, and secondary somatosensory cortex. Localized remifentanil-induced decreases in breath hold-related activity were observed in the left anterior insula and operculum. We also observed remifentanil-induced decreases in the BOLD response to breath holding in the left dorsolateral prefrontal cortex, anterior cingulate, the cerebellum, and periaqueductal gray, brain areas that mediate task performance. Activity in areas mediating motor control (putamen, motor cortex) and sensory-motor integration (supramarginal gyrus) were unaffected by remifentanil. Breath hold-related activity was observed in the medulla. These findings highlight the importance of higher cortical centers in providing contextual awareness of respiration that leads to appropriate modulation of respiratory control. Opioids have profound effects on the cortical centers that control breathing, which potentiates their actions in the brainstem

Relating multi-sequence longitudinal intensity profiles and clinical covariates in new multiple sclerosis lesions

Structural magnetic resonance imaging (MRI) can be used to detect lesions in the brains of multiple sclerosis (MS) patients. The formation of these lesions is a complex process involving inflammation, tissue damage, and tissue repair, all of which are visible on MRI. Here we characterize the lesion formation process on longitudinal, multi-sequence structural MRI from 34 MS patients and relate the longitudinal changes we observe within lesions to therapeutic interventions. In this article, we first outline a pipeline to extract voxel level, multi-sequence longitudinal profiles from four MRI sequences within lesion tissue. We then propose two models to relate clinical covariates to the longitudinal profiles. The first model is a principal component analysis (PCA) regression model, which collapses the information from all four profiles into a scalar value. We find that the score on the first PC identifies areas of slow, long-term intensity changes within the lesion at a voxel level, as validated by two experienced clinicians, a neuroradiologist and a neurologist. On a quality scale of 1 to 4 (4 being the highest) the neuroradiologist gave the score on the first PC a median rating of 4 (95% CI: [4,4]), and the neurologist gave it a median rating of 3 (95% CI: [3,3]). In the PCA regression model, we find that treatment with disease modifying therapies (p-value < 0.01), steroids (p-value < 0.01), and being closer to the boundary of abnormal signal intensity (p-value < 0.01) are associated with a return of a voxel to intensity values closer to that of normal-appearing tissue. The second model is a function-on-scalar regression, which allows for assessment of the individual time points at which the covariates are associated with the profiles. In the function-on-scalar regression both age and distance to the boundary were found to have a statistically significant association with the profiles

Conservation of a crystallographic interface suggests a role for β-sheet augmentation in influenza virus NS1 multifunctionality

The structure of a monomeric effector domain from influenza A virus NS1 is presented from diffraction data extending to 1.8 Å resolution. Comparison of this and other NS1 effector-domain structures shows conformational changes at a strand–strand packing interface, hinting at a role for β-strand augmentation in NS1 function

Complementâ induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction

Polymicrobial sepsis in mice causes myocardial dysfunction after generation of the complement anaphylatoxin, complement component 5a (C5a). C5a interacts with its receptors on cardiomyocytes (CMs), resulting in redox imbalance and cardiac dysfunction that can be functionally measured and quantitated using Doppler echocardiography. In this report we have evaluated activation of MAPKs and Akt in CMs exposed to C5a in vitro and after cecal ligation and puncture (CLP) in vivo. In both cases, C5a in vitro caused activation (phosphorylation) of MAPKs and Akt in CMs, which required availability of both C5a receptors. Using immunofluorescence technology, activation of MAPKs and Akt occurred in left ventricular (LV) CMs, requiring both C5a receptors, C5aR1 and â 2. Use of a waterâ soluble p38 inhibitor curtailed activation in vivo of MAPKs and Akt in LV CMs as well as the appearance of cytokines and histones in plasma from CLP mice. When mouse macrophages were exposed in vitro to LPS, activation of MAPKs and Akt also occurred. The copresence of the p38 inhibitor blocked these activation responses. Finally, the presence of the p38 inhibitor in CLP mice reduced the development of cardiac dysfunction. These data suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activation of MAPKs and Akt in heart.â Fattahi, F., Kalbitz, M., Malan, E. A., Abe, E., Jajou, L., Huberâ Lang, M. S., Bosmann, M., Russell, M. W., Zetoune, F. S., Ward, P. A. Complementâ induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction. FASEB J. 31, 4129â 4139 (2017). www.fasebj.orgâ Fattahi, Fatemeh, Kalbitz, Miriam, Malan, Elizabeth A., Abe, Elizabeth, Jajou, Lawrence, Huberâ Lang, Markus S., Bosmann, Markus, Russell, Mark W., Zetoune, Firas S., Ward, Peter A., Complementâ induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction. FASEB J. 31, 4129â 4139 (2017)Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154261/1/fsb2fj201700140r.pd

The Beacon Community Centers Middle School Initiative: Report on Implementation and Youth Experience in the Initiative's Second Year

Evaluates the second year of an initiative to offer fifth-to-eighth graders structured out-of-school-time programs. Looks at implementation, such as engagement, staffing, and activities; youths' social and educational development; and underlying factors

Complementâ induced activation of the cardiac NLRP3 inflammasome in sepsis

Cardiac dysfunction develops during sepsis in humans and rodents. In the model of polymicrobial sepsis induced by cecal ligation and puncture (CLP), we investigated the role of the NLRP3 inflammasome in the heart. Mouse heart homogenates from shamâ procedure mice contained high mRNA levels of NLRP3 and ILâ 1β. Usingthe inflamm a some protocol, exposure of cardiomyocytes (CMs) to LPS followed by ATP or nigericin caused release of mature ILâ 1β. Immuno staining of left ventricular frozen sections before and 8 h after CLP revealed the presence of NLRP3 and ILâ 1β proteins inCMs. CLP caused substantial increases in mRNAs for ILâ 1β and NLRP3 in CMs which are reduced in the absence of either C5aR1 or C5aR2. After CLP, NLRP32/2 mice showed reduced plasma levels of ILâ 1βand ILâ 6. In vitro exposure of wildâ type CMs to recombinant C5a (rC5a) cause delevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5aâ receptor dependent. Use of a selective NOX2 inhibitor prevented increased cytosolic and nuclear/mitochondrial ROS levels and release of ILâ 1β. Finally, NLRP32/2 mice had reduced defects in echo/Doppler parameters in heart afterCLP. These studies establish that the NLRP3 inflammasome contributes to the cardiomyopathy of polymicrobial sepsis.â Kalbitz, M., Fattahi, F., Grailer, J. J., Jajou, L., Malan, E. A., Zetoune, F. S., Huberâ Lang, M., Russell, M. W., Ward, P. A. Complementâ induced activation of the cardiac NLRP3 inflammasome in sepsis. FASEB J. 30, 3997â 4006 (2016). www.fasebj.orgPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154362/1/fsb2fasebj30120728r.pd