Revelation: Overcoming Blindness to See a Common Humanity

Just over a year ago, I traveled to El Salvador and as a result of this experience, I write the following pages as a transformed person. My thinking, my longings, and my overall worldview shifted. El Salvador, the tiny Central American country, offered me a place to learn to love, [and] to be heartbroken in the words of Dean Brackley. Notoriously, El Salvador and more specifically La Casa de la Solidaridad study abroad program prove revelatory in unexpected ways. One alum of the program even stated, The Casa is a hot house for change! I often ask the question to myself, Why El Salvador? or Why did I have to travel to find myself? O\u27Connor similarly left her life in rural Georgia to find herself. She hoped to gain a broader perspective as a writer in her studies at the University of Iowa by moving beyond the familiarity of the Southern landscape where she grew up

Early Pleistocene Obliquity‐Scale pCO2 Variability at ~1.5 Million Years Ago

In the early Pleistocene, global temperature cycles predominantly varied with ~41‐kyr (obliquity‐scale) periodicity. Atmospheric greenhouse gas concentrations likely played a role in these climate cycles; marine sediments provide an indirect geochemical means to estimate early Pleistocene CO2. Here we present a boron isotope‐based record of continuous high‐resolution surface ocean pH and inferred atmospheric CO2 changes. Our results show that, within a window of time in the early Pleistocene (1.38–1.54 Ma), pCO2 varied with obliquity, confirming that, analogous to late Pleistocene conditions, the carbon cycle and climate covaried at ~1.5 Ma. Pairing the reconstructed early Pleistocene pCO2 amplitude (92 ± 13 μatm) with a comparably smaller global surface temperature glacial/interglacial amplitude (3.0 ± 0.5 K) yields a surface temperature change to CO2 radiative forcing ratio of S[CO2]~0.75 (±0.5) °C−1·W−1·m−2, as compared to the late Pleistocene S[CO2] value of ~1.75 (±0.6) °C−1·W−1·m−2. This direct comparison of pCO2 and temperature implicitly incorporates the large ice sheet forcing as an internal feedback and is not directly applicable to future warming. We evaluate this result with a simple climate model and show that the presumably thinner, though extensive, northern hemisphere ice sheets would increase surface temperature sensitivity to radiative forcing. Thus, the mechanism to dampen actual temperature variability in the early Pleistocene more likely lies with Southern Ocean circulation dynamics or antiphase hemispheric forcing. We also compile this new carbon dioxide record with published Plio‐Pleistocene δ11B records using consistent boundary conditions and explore potential reasons for the discrepancy between Pliocene pCO2 based on different planktic foraminifera.Key PointsEarly Pleistocene pCO2 roughly varied with obliquity cyclesInterglacial pCO2 was similar in the early and late Pleistocene; glacial pCO2 declined over the mid‐Pleistocene transitionDiscrepancies between δ11B values and corresponding pCO2 estimates from G. ruber and T. sacculifer are observed and may indicate evolving vital effectsPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147130/1/palo20675-sup-0004-2018PA003349-S03.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147130/2/palo20675.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147130/3/palo20675-sup-0002-2018PA003349-S01.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147130/4/palo20675_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147130/5/palo20675-sup-0005-2018PA003349-S04.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147130/6/palo20675-sup-0003-2018PA003349-S02.pd

Whole-fat or reduced-fat dairy product intake, adiposity, and cardiometabolic health in children: A systematic review

Dietary guidelines commonly recommend that children aged \u3e2 y consume reduced-fat dairy products rather than regular- or whole-fat dairy. In adults, most studies have not found the consumption of whole-fat dairy products to be associated with increased cardiometabolic or adiposity risk. Associations in children could differ due to growth and development. We systematically reviewed the literature in indexed, peer-reviewed journals to summarize pediatric studies (children aged from 2 to 18 y) assessing associations between whole- and reduced-fat dairy intake and measures of adiposity as well as biomarkers of cardiometabolic disease risk, including the serum lipid profile, blood pressure, low-grade chronic inflammation, oxidative stress, and measures of glucose homeostasis. For the purposes of this review, a “whole-fat” dairy product was defined as a product with the natural fat content, whereas a “reduced-fat” dairy product was defined as a product with some or all of the fat removed (including “low-fat” and “skim” versions). A total of 29 journal articles met our criteria for inclusion. The majority were conducted in the United States and were prospective or cross-sectional observational studies, with only 1 randomized controlled trial. Studies were consistent in reporting that whole-fat dairy products were not associated with increased measures of weight gain or adiposity. Most evidence indicated that consumption of whole-fat dairy was not associated with increased cardiometabolic risk, although a change from whole-fat to reduced-fat dairy improved outcomes for some risk factors in 1 study. Taken as a whole, the limited literature in this field is not consistent with dietary guidelines recommending that children consume preferably reduced-fat dairy products. High-quality randomized controlled trials in children that directly compare the effects of whole-fat compared with reduced-fat dairy intake on measures of adiposity or biomarkers of cardiometabolic disease risk are needed to provide better quality evidence in this area

The OLYMPUS Internal Hydrogen Target

An internal hydrogen target system was developed for the OLYMPUS experiment at DESY, in Hamburg, Germany. The target consisted of a long, thin-walled, tubular cell within an aluminum scattering chamber. Hydrogen entered at the center of the cell and exited through the ends, where it was removed from the beamline by a multistage pumping system. A cryogenic coldhead cooled the target cell to counteract heating from the beam and increase the density of hydrogen in the target. A fixed collimator protected the cell from synchrotron radiation and the beam halo. A series of wakefield suppressors reduced heating from beam wakefields. The target system was installed within the DORIS storage ring and was successfully operated during the course of the OLYMPUS experiment in 2012. Information on the design, fabrication, and performance of the target system is reported.Comment: 9 pages, 13 figure

Loss of Stathmin-2, a hallmark of TDP-43-associated ALS, causes motor neuropathy

TDP-43 mediates proper Stathmin-2 (STMN2) mRNA splicing, and STMN2 protein is reduced in the spinal cord of most patients with amyotrophic lateral sclerosis (ALS). To test the hypothesis that STMN2 loss contributes to ALS pathogenesis, we generated constitutive and conditional STMN2 knockout mice. Constitutive STMN2 loss results in early-onset sensory and motor neuropathy featuring impaired motor behavior and dramatic distal neuromuscular junction (NMJ) denervation of fast-fatigable motor units, which are selectively vulnerable in ALS, without axon or motoneuron degeneration. Selective excision of STMN2 in motoneurons leads to similar NMJ pathology. STMN2 knockout heterozygous mice, which better model the partial loss of STMN2 protein found in patients with ALS, display a slowly progressive, motor-selective neuropathy with functional deficits and NMJ denervation. Thus, our findings strongly support the hypothesis that STMN2 reduction owing to TDP-43 pathology contributes to ALS pathogenesis

Composition of the Survival Motor Neuron (SMN) complex in Drosophila melanogaster

Spinal Muscular Atrophy (SMA) is caused by homozygous mutations in the human survival motor neuron 1 (SMN1) gene. SMN protein has a well-characterized role in the biogenesis of small nuclear ribonucleoproteins (snRNPs), core components of the spliceosome. SMN is part of an oligomeric complex with core binding partners, collectively called Gemins. Biochemical and cell biological studies demonstrate that certain Gemins are required for proper snRNP assembly and transport. However, the precise functions of most Gemins are unknown. To gain a deeper understanding of the SMN complex in the context of metazoan evolution, we investigated its composition in Drosophila melanogaster. Using transgenic flies that exclusively express Flag-tagged SMN from its native promoter, we previously found that Gemin2, Gemin3, Gemin5, and all nine classical Sm proteins, including Lsm10 and Lsm11, co-purify with SMN. Here, we show that CG2941 is also highly enriched in the pulldown. Reciprocal co-immunoprecipitation reveals that epitope-tagged CG2941 interacts with endogenous SMN in Schneider2 cells. Bioinformatic comparisons show that CG2941 shares sequence and structural similarity with metazoan Gemin4. Additional analysis shows that three other genes (CG14164, CG31950 and CG2371) are not orthologous to Gemins 6-7-8, respectively, as previously suggested. In D.melanogaster, CG2941 is located within an evolutionarily recent genomic triplication with two other nearly identical paralogous genes (CG32783 and CG32786). RNAi-mediated knockdown of CG2941 and its two close paralogs reveals that Gemin4 is essential for organismal viability

Composition of the Survival Motor Neuron (SMN) Complex in \u3cem\u3eDrosophila melanogaster\u3c/em\u3e

Spinal Muscular Atrophy (SMA) is caused by homozygous mutations in the human survival motor neuron 1 (SMN1) gene. SMN protein has a well-characterized role in the biogenesis of small nuclear ribonucleoproteins (snRNPs), core components of the spliceosome. SMN is part of an oligomeric complex with core binding partners, collectively called Gemins. Biochemical and cell biological studies demonstrate that certain Gemins are required for proper snRNP assembly and transport. However, the precise functions of most Gemins are unknown. To gain a deeper understanding of the SMN complex in the context of metazoan evolution, we investigated its composition in Drosophila melanogaster. Using transgenic flies that exclusively express Flag-tagged SMN from its native promoter, we previously found that Gemin2, Gemin3, Gemin5, and all nine classical Sm proteins, including Lsm10 and Lsm11, co-purify with SMN. Here, we show that CG2941 is also highly enriched in the pulldown. Reciprocal co-immunoprecipitation reveals that epitope-tagged CG2941 interacts with endogenous SMN in Schneider2 cells. Bioinformatic comparisons show that CG2941 shares sequence and structural similarity with metazoan Gemin4. Additional analysis shows that three other genes (CG14164, CG31950 and CG2371) are not orthologous to Gemins 6-7-8, respectively, as previously suggested. In D.melanogaster, CG2941 is located within an evolutionarily recent genomic triplication with two other nearly identical paralogous genes (CG32783 and CG32786). RNAi-mediated knockdown of CG2941 and its two close paralogs reveals that Gemin4 is essential for organismal viability