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1.  Publishing and sharing multi-dimensional image data with OMERO 
Mammalian Genome  2015;26(9-10):441-447.
Imaging data are used in the life and biomedical sciences to measure the molecular and structural composition and dynamics of cells, tissues, and organisms. Datasets range in size from megabytes to terabytes and usually contain a combination of binary pixel data and metadata that describe the acquisition process and any derived results. The OMERO image data management platform allows users to securely share image datasets according to specific permissions levels: data can be held privately, shared with a set of colleagues, or made available via a public URL. Users control access by assigning data to specific Groups with defined membership and access rights. OMERO’s Permission system supports simple data sharing in a lab, collaborative data analysis, and even teaching environments. OMERO software is open source and released by the OME Consortium at
PMCID: PMC4602067  PMID: 26223880
2.  Program Evaluation of Remote Heart Failure Monitoring: Healthcare Utilization Analysis in a Rural Regional Medical Center 
Telemedicine Journal and e-Health  2015;21(3):157-162.
Background: Remote monitoring for heart failure (HF) has had mixed and heterogeneous effects across studies, necessitating further evaluation of remote monitoring systems within specific healthcare systems and their patient populations. “Care Beyond Walls and Wires,” a wireless remote monitoring program to facilitate patient and care team co-management of HF patients, served by a rural regional medical center, provided the opportunity to evaluate the effects of this program on healthcare utilization. Materials and Methods: Fifty HF patients admitted to Flagstaff Medical Center (Flagstaff, AZ) participated in the project. Many of these patients lived in underserved and rural communities, including Native American reservations. Enrolled patients received mobile, broadband-enabled remote monitoring devices. A matched cohort was identified for comparison. Results: HF patients enrolled in this program showed substantial and statistically significant reductions in healthcare utilization during the 6 months following enrollment, and these reductions were significantly greater compared with those who declined to participate but not when compared with a matched cohort. Conclusions: The findings from this project indicate that a remote HF monitoring program can be successfully implemented in a rural, underserved area. Reductions in healthcare utilization were observed among program participants, but reductions were also observed among a matched cohort, illustrating the need for rigorous assessment of the effects of HF remote monitoring programs in healthcare systems.
PMCID: PMC4365431  PMID: 25025239
mobile health; telemedicine; telecardiology; home health monitoring; cardiology/cardiovascular
3.  Using satellite remote sensing and household survey data to assess human health and nutrition response to environmental change 
Population and Environment  2014;36(1):48-72.
Climate change and degradation of ecosystem services functioning may threaten the ability of current agricultural systems to keep up with demand for adequate and inexpensive food and for clean water, waste disposal and other broader ecosystem services. Human health is likely to be affected by changes occurring across multiple geographic and time scales. Impacts range from increasing transmissibility and the range of vectorborne diseases, such as malaria and yellow fever, to undermining nutrition through deleterious impacts on food production and concomitant increases in food prices. This paper uses case studies to describe methods that make use of satellite remote sensing and Demographic and Health Survey data to better understand individual-level human health and nutrition outcomes. By bringing these diverse datasets together, the connection between environmental change and human health outcomes can be described through new research and analysis.
PMCID: PMC4131131  PMID: 25132700
DHS; NDVI; Environment; Health; Survey; Nutrition
4.  Disrupted Zinc-Binding Sites in Structures of Pathogenic SOD1 Variants D124V and H80R 
Biochemistry  2010;49(27):5714-5725.
Mutations in human copper-zinc superoxide dismutase (SOD1) cause an inherited form of the fatal neurodegenerative disease amyotrophic lateral sclerosis (ALS). Here, we present structures of the pathogenic SOD1 variants D124V and H80R, both of which demonstrate compromised zinc-binding sites. The disruption of the zinc-binding sites in H80R SOD1 leads to conformational changes in loop elements, permitting non-native SOD1-SOD1 interactions that mediate the assembly of these proteins into higher order filamentous arrays. Analytical ultracentrifugation sedimentation velocity experiments indicate that these SOD1 variants are more prone to monomerization than is the wild type enzyme. Although D124V and H80R SOD1 proteins appear to have fully functional copper-binding sites, inductively coupled plasma mass spectrometery (ICP-MS) and anomalous scattering X-ray diffraction analyses reveal that zinc (not copper) occupies the copper-binding sites in these variants. The absence of copper in these proteins, together with the results of covalent thiol modification experiments in yeast strains with and without the gene encoding the copper chaperone for SOD1 (CCS), suggest that CCS may not fully act on newly translated forms of these polypeptides. Overall, these findings lend support to the hypothesis that immature mutant SOD1 species contribute to toxicity in SOD1-linked ALS.
PMCID: PMC3037816  PMID: 20515040
5.  Innovation Networks for Improving Access and Quality Across the Healthcare Ecosystem 
Telemedicine Journal and e-Health  2010;16(1):107-111.
Partnerships between patient communities, healthcare providers, and academic researchers are key to stepping up the pace and public health impact of clinical and translational research supported by the National Institutes of Health. With emphasis shifting toward community engagement and faster translation of research advances into clinical practice, academic researchers have a vital stake in widening the use of health information technology systems and telehealth networks to support collaboration and innovation. However, limited interaction between academic institutions and healthcare providers hinders the ability to form and sustain the integrated networks that are needed to conduct meaningful community-engaged research that improves public health outcomes. Healthcare providers, especially those affiliated with smaller practices, will need sustainable infrastructure and real incentives to utilize such networks, as well as training and additional resources for ongoing technical assistance.
PMCID: PMC3016866  PMID: 20043702
business administration/economics; distance learning; e-health; home health monitoring; policy
6.  Innovation in Indian Healthcare: Using Health Information Technology to Achieve Health Equity for American Indian and Alaska Native Populations 
The US Indian health system utilizes a diverse range of health information technology and innovative tools to enhance health service delivery for American Indians and Alaska Natives. This article provides an overview of efforts and experience using such tools to achieve health equity for American Indian and Alaska Native communities. Specific attention is given to the Indian Health Service Electronic Health Record and to two examples of telehealth innovation.
PMCID: PMC3035828  PMID: 21307987
Indian Health Service; American Indians; Alaska Natives; telehealth
7.  Structural and Biophysical Properties of the Pathogenic SOD1 Variant H46R/H48Q 
Biochemistry  2009;48(15):3436-3447.
Over 100 mutations in the gene encoding human copper-zinc superoxide dismutase (SOD1) cause an inherited form of the fatal neurodegenerative disease amyotrophic lateral sclerosis (ALS). Two pathogenic SOD1 mutations, His46Arg (H46R) and His48Gln (H48Q), affect residues that act as copper ligands in the wild type enzyme. Transgenic mice expressing a human SOD1 variant containing both mutations develop paralytic disease akin to ALS. Here we show that H46R/H48Q SOD1 possesses multiple characteristics that distinguish it from the wild type. These properties include: 1) an ablated copper-binding site; 2) a substantially weakened affinity for zinc; 3) a binding site for calcium ion; 4) the ability to form stable heterocomplexes with the Copper Chaperone for SOD1 (CCS); and 5) compromised CCS-mediated oxidation of the intrasubunit disulfide bond in vivo. The results presented here, together with data on pathogenic SOD1 proteins coming from cell culture and transgenic mice, suggest that incomplete posttranslational modification of nascent SOD1 polypeptides via CCS may be a characteristic shared by fALS SOD1 mutants, leading to a population of destabilized, off-pathway folding intermediates that are toxic to motor neurons.
PMCID: PMC2757159  PMID: 19227972
8.  The Effects of Glutaredoxin and Copper Activation Pathways on the Disulfide and Stability of Cu,Zn Superoxide Dismutase*… 
The Journal of biological chemistry  2006;281(39):28648-28656.
Mutations in Cu,Zn superoxide dismutase (SOD1) can cause amyotrophic lateral sclerosis (ALS) through mechanisms proposed to involve SOD1 misfolding, but the intracellular factors that modulate folding and stability of SOD1 are largely unknown. By using yeast and mammalian expression systems, we demonstrate here that SOD1 stability is governed by post-translational modification factors that target the SOD1 disulfide. Oxidation of the human SOD1 disulfide in vivo was found to involve both the copper chaperone for SOD1 (CCS) and the CCS-independent pathway for copper activation. When both copper pathways were blocked, wild type SOD1 stably accumulated in yeast cells with a reduced disulfide, whereas ALS SOD1 mutants A4V, G93A, and G37R were degraded. We describe here an unprecedented role for the thiol oxidoreductase glutaredoxin in reducing the SOD1 disulfide and destabilizing ALS mutants. Specifically, the major cytosolic glutaredoxin of yeast was seen to reduce the intramolecular disulfide of ALS SOD1 mutant A4V SOD1 in vivo and in vitro. By comparison, glutaredoxin was less reactive toward the disulfide of wild type SOD1. The apo-form of A4V SOD1 was highly reactive with glutaredoxin but not SOD1 containing both copper and zinc. Glutaredoxin therefore preferentially targets the immature form of ALS mutant SOD1 lacking metal co-factors. Overall, these studies implicate a critical balance between cellular reductants such as glutaredoxin and copper activation pathways in controlling the disulfide and stability of SOD1 in vivo.
PMCID: PMC2757158  PMID: 16880213
9.  Down-Regulation of a Manganese Transporter in the Face of Metal Toxicity 
Molecular Biology of the Cell  2009;20(12):2810-2819.
The yeast Smf1p Nramp manganese transporter is posttranslationally regulated by environmental manganese. Smf1p is stabilized at the cell surface with manganese starvation, but is largely degraded in the vacuole with physiological manganese through a mechanism involving the Rsp5p adaptor complex Bsd2p/Tre1p/Tre2p. We now describe an additional level of Smf1p regulation that occurs with toxicity from manganese, but not other essential metals. This regulation is largely Smf1p-specific. As with physiological manganese, toxic manganese triggers vacuolar degradation of Smf1p by trafficking through the multivesicular body. However, regulation by toxic manganese does not involve Bsd2p/Tre1p/Tre2p. Toxic manganese triggers both endocytosis of cell surface Smf1p and vacuolar targeting of intracellular Smf1p through the exocytic pathway. Notably, the kinetics of vacuolar targeting for Smf1p are relatively slow with toxic manganese and require prolonged exposures to the metal. Down-regulation of Smf1p by toxic manganese does not require transport activity of Smf1p, whereas such transport activity is needed for Smf1p regulation by manganese starvation. Furthermore, the responses to manganese starvation and manganese toxicity involve separate cellular compartments. We provide evidence that manganese starvation is sensed within the lumen of the secretory pathway, whereas manganese toxicity is sensed within an extra-Golgi/cytosolic compartment of the cell.
PMCID: PMC2695789  PMID: 19369420
10.  The truth about proof 
Western Journal of Medicine  2000;173(2):142.
PMCID: PMC1071029  PMID: 10924447
11.  Sensing a purpose 
Western Journal of Medicine  2000;172(6):419.
PMCID: PMC1070942  PMID: 10854404
12.  Let the buyer beware 
Western Journal of Medicine  2000;172(5):347.
PMCID: PMC1070893  PMID: 18751294
13.  Our just desserts 
Western Journal of Medicine  2000;172(4):281.
PMCID: PMC1070852  PMID: 18751269
14.  A declaration of interdependence 
Western Journal of Medicine  2000;172(1):66.
PMCID: PMC1070739  PMID: 10695452
15.  Letter from the Southwest 
Western Journal of Medicine  1999;171(2):136.
PMCID: PMC1305784  PMID: 18751175
16.  Letter from the Southwest 
Western Journal of Medicine  1999;170(6):384.
PMCID: PMC1305714  PMID: 18751163
17.  Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion 
Molecular Ecology  2014;23(23):5904-5917.
Honey bee hives are filled with stored pollen, honey, plant resins and wax, all antimicrobial to differing degrees. Stored pollen is the nutritionally rich currency used for colony growth and consists of 40–50% simple sugars. Many studies speculate that prior to consumption by bees, stored pollen undergoes long-term nutrient conversion, becoming more nutritious ‘bee bread’ as microbes predigest the pollen. We quantified both structural and functional aspects associated with this hypothesis using behavioural assays, bacterial plate counts, microscopy and 454 amplicon sequencing of the 16S rRNA gene from both newly collected and hive-stored pollen. We found that bees preferentially consume fresh pollen stored for <3 days. Newly collected pollen contained few bacteria, values which decreased significantly as pollen were stored >96 h. The estimated microbe to pollen grain surface area ratio was 1:1 000 000 indicating a negligible effect of microbial metabolism on hive-stored pollen. Consistent with these findings, hive-stored pollen grains did not appear compromised according to microscopy. Based on year round 454 amplicon sequencing, bacterial communities of newly collected and hive-stored pollen did not differ, indicating the lack of an emergent microbial community co-evolved to digest stored pollen. In accord with previous culturing and 16S cloning, acid resistant and osmotolerant bacteria like Lactobacillus kunkeei were found in greatest abundance in stored pollen, consistent with the harsh character of this microenvironment. We conclude that stored pollen is not evolved for microbially mediated nutrient conversion, but is a preservative environment due primarily to added honey, nectar, bee secretions and properties of pollen itself.
PMCID: PMC4285803  PMID: 25319366
bee bread; fermentation; honey; Lactobacillus kunkeei; microbes; nutrition

Results 1-17 (17)