Expanding the Capability of Satellite Operations using a Global Federated Ground Station Network

Small-scale spaceflight programs such as those found at universities and start-up companies may operate satellites from a single ground station. This station’s location may not be optimal for radio communications, and a single station limits the contact time available to conduct operations. The idea of a global federated ground station network (FGN) has been theorized in the past, and with today’s wide-spread internet connectivity it is now possible for such a network to exist. One example of an FGN that is functioning today is an open-source project called SatNOGS. The Michigan eXploration Laboratory (MXL) at the University of Michigan has applied the benefits of this network to enhance operations of their Tandem Beacon Experiment (TBEx) CubeSat mission by gathering 2.2x the beacons gathered by their home station alone. 93% of those additional beacons were collected by six SatNOGS stations. Augmenting MXL’s home station with these six stations increases access time to the TBEx satellites by a factor of 5 to15. This increased temporal coverage also enabled MXL operators to identify their spacecraft after deployment and correct an error causing the TBEx radios to function intermittently, saving the mission in its earliest days

O-mannosyl phosphorylation of alpha-dystroglycan is required for laminin binding.

Alpha-dystroglycan (alpha-DG) is a cell-surface glycoprotein that acts as a receptor for both extracellular matrix proteins containing laminin-G domains and certain arenaviruses. Receptor binding is thought to be mediated by a posttranslational modification, and defective binding with laminin underlies a subclass of congenital muscular dystrophy. Using mass spectrometry- and nuclear magnetic resonance (NMR)-based structural analyses, we identified a phosphorylated O-mannosyl glycan on the mucin-like domain of recombinant alpha-DG, which was required for laminin binding. We demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy, as well as mice with myodystrophy, commonly have defects in a postphosphoryl modification of this phosphorylated O-linked mannose, and that this modification is mediated by the like-acetylglucosaminyltransferase (LARGE) protein. These findings expand our understanding of the mechanisms that underlie congenital muscular dystrophy

Reinventing College Physics for Biologists: Explicating an epistemological curriculum

The University of Maryland Physics Education Research Group (UMd-PERG) carried out a five-year research project to rethink, observe, and reform introductory algebra-based (college) physics. This class is one of the Maryland Physics Department's large service courses, serving primarily life-science majors. After consultation with biologists, we re-focused the class on helping the students learn to think scientifically -- to build coherence, think in terms of mechanism, and to follow the implications of assumptions. We designed the course to tap into students' productive conceptual and epistemological resources, based on a theoretical framework from research on learning. The reformed class retains its traditional structure in terms of time and instructional personnel, but we modified existing best-practices curricular materials, including Peer Instruction, Interactive Lecture Demonstrations, and Tutorials. We provided class-controlled spaces for student collaboration, which allowed us to observe and record students learning directly. We also scanned all written homework and examinations, and we administered pre-post conceptual and epistemological surveys. The reformed class enhanced the strong gains on pre-post conceptual tests produced by the best-practices materials while obtaining unprecedented pre-post gains on epistemological surveys instead of the traditional losses.Comment: 35 pages including a 15 page appendix of supplementary material

Geographic and facility variation in initial use of non-tunneled catheters for incident maintenance hemodialysis patients

Abstract Background Non-tunneled (temporary) hemodialysis catheters (NTHCs) are the least-optimal initial vascular access for incident maintenance hemodialysis patients yet little is known about factors associated with NTHC use in this context. We sought to determine factors associated with NTHC use and examine regional and facility-level variation in NTHC use for incident maintenance hemodialysis patients. Methods We analyzed registry data collected between January 2001 and December 2010 from 61 dialysis facilities within 12 geographic regions in Canada. Multi-level models and intra-class correlation coefficients were used to evaluate variation in NTHC use as initial hemodialysis access across facilities and geographic regions. Facility and patient characteristics associated with the lowest and highest quartiles of NTHC use were compared. Results During the study period, 21,052 patients initiated maintenance hemodialysis using a central venous catheter (CVC). This included 10,183 patients (48.3 %) in whom the initial CVC was a NTHC, as opposed to a tunneled CVC. Crude variation in NTHC use across facilities ranged from 3.7 to 99.4 % and across geographic regions from 32.4 to 85.1 %. In an adjusted multi-level logistic regression model, the proportion of total variation in NTHC use explained by facility-level and regional variation was 40.0 % and 34.1 %, respectively. Similar results were observed for the subgroup of patients who received greater than 12 months of pre-dialysis nephrology care. Patient-level factors associated with increased NTHC use were male gender, history of angina, pulmonary edema, COPD, hypertension, increasing distance from dialysis facility, higher serum phosphate, lower serum albumin and later calendar year. Conclusions There is wide variation in NTHC use as initial vascular access for incident maintenance hemodialysis patients across facilities and geographic regions in Canada. Identifying modifiable factors that explain this variation could facilitate a reduction of NTHC use in favor of more optimal initial vascular access

Identification and functional characterization of a highly divergent N-acetylglucosaminyltransferase I (TbGnTI) in <em>Trypanosoma brucei</em>

Trypanosoma brucei expresses a diverse repertoire of N-glycans, ranging from oligomannose and paucimannose structures to exceptionally large complex N-glycans. Despite the presence of the latter, no obvious homologues of known β1–4-galactosyltransferase or β1–2- or β1–6-N-acetylglucosaminyltransferase genes have been found in the parasite genome. However, we previously reported a family of putative UDP-sugar-dependent glycosyltransferases with similarity to the mammalian β1–3-glycosyltransferase family. Here we characterize one of these genes, TbGT11, and show that it encodes a Golgi apparatus resident UDP-GlcNAc:α3-d-mannoside β1–2-N-acetylglucosaminyltransferase I activity (TbGnTI). The bloodstream-form TbGT11 null mutant exhibited significantly modified protein N-glycans but normal growth in vitro and infectivity to rodents. In contrast to multicellular organisms, where the GnTI reaction is essential for biosynthesis of both complex and hybrid N-glycans, T. brucei TbGT11 null mutants expressed atypical “pseudohybrid” glycans, indicating that TbGnTII activity is not dependent on prior TbGnTI action. Using a functional in vitro assay, we showed that TbGnTI transfers UDP-GlcNAc to biantennary Man(3)GlcNAc(2), but not to triantennary Man(5)GlcNAc(2), which is the preferred substrate for metazoan GnTIs. Sequence alignment reveals that the T. brucei enzyme is far removed from the metazoan GnTI family and suggests that the parasite has adapted the β3-glycosyltransferase family to catalyze β1–2 linkages

R|S Atlas: Identifying Existing Cohort Study Data Resources to Accelerate Epidemiological Research on the Influence of Religion and Spirituality on Human Health

OBJECTIVE: Many studies have documented significant associations between religion and spirituality (R/S) and health, but relatively few prospective analyses exist that can support causal inferences. To date, there has been no systematic analysis of R/S survey items collected in US cohort studies. We conducted a systematic content analysis of all surveys ever fielded in 20 diverse US cohort studies funded by the National Institutes of Health (NIH) to identify all R/S-related items collected from each cohort\u27s baseline survey through 2014. DESIGN: An R|S Ontology was developed from our systematic content analysis to categorise all R/S survey items identified into key conceptual categories. A systematic literature review was completed for each R/S item to identify any cohort publications involving these items through 2018. RESULTS: Our content analysis identified 319 R/S survey items, reflecting 213 unique R/S constructs and 50 R|S Ontology categories. 193 of the 319 extant R/S survey items had been analysed in at least one published paper. Using these data, we created the R|S Atlas (https://atlas.mgh.harvard.edu/), a publicly available, online relational database that allows investigators to identify R/S survey items that have been collected by US cohorts, and to further refine searches by other key data available in cohorts that may be necessary for a given study (eg, race/ethnicity, availability of DNA or geocoded data). CONCLUSIONS: R|S Atlas not only allows researchers to identify available sources of R/S data in cohort studies but will also assist in identifying novel research questions that have yet to be explored within the context of US cohort studies

A human embryonic kidney 293T cell line mutated at the Golgi -mannosidase II locus

Disruption of Golgi -mannosidase II activity can result in type II congenital dyserythropoietic anemia and can induce lupus-like autoimmunity in mice. Here, we isolate a mutant human embryonic kidney (HEK) 293T cell line, called Lec36, that displays sensitivity to ricin that lies between the parental HEK 293T cells, whose secreted and membrane-expressed proteins are dominated by complex-type glycosylation, and 293S Lec1 cells, which only produce oligomannose-type N-linked glycans. The stem cell marker, 19A, was transiently expressed in the HEK 293T Lec36 cells, and in parental HEK 293T cells with and without the potent Golgi -mannosidase II inhibitor, swainsonine. Negative-ion nano-electrospray ionization mass spectra of the 19A N-linked glycans from HEK 293T Lec36 and swainsonine-treated HEK 293T cells were qualitatively indistinguishable and, as shown by collision-induced dissociation spectra, dominated by hybrid-type glycosylation. Nucleotide sequencing revealed mutations in each allele of MAN2A1, the gene encoding Golgi -mannosidase II: a point mutation in one allele mapping to the active site and an in-frame deletion of twelve-nucleotides in the other. Expression of wild-type but not the mutant MAN2A1 alleles in Lec36 cells restored processing of the 19A reporter glycoprotein to complex-type glycosylation. The Lec36 cell line will be useful for expressing therapeutic glycoproteins with hybrid-type glycans and provides a sensitive host for detecting mutations in human MAN2A1 causing type II congenital dyserythropoietic anemia