Information Systems and Healthcare XXIX: Information Technology Investments and Returns -- Uniqueness in the Healthcare Industry

The way in which information technology (IT) impacts firm productivity is an enduring question in organizational research and practice. Rather than adopting the common explanation that IT spending improves organizational performance, we hypothesize that IT spending determines the amount of IT assets, such as IT hardware, IT personnel, IT systems, and IT outsourcing, that can be acquired. These IT assets, in turn, affect productivity. The context of our study is the healthcare industry. Because of the unique set of managerial values, incentives, and constraints in this industry, we also hypothesize that IT personnel play a key role in determining hospital productivity. Analysis of panel data on acute-care centers provides support for our hypotheses. This paper contributes to literature by (1) refining earlier research that explains that IT spending improves organizational productivity; (2) examining the interrelationships between various types of IT assets; and (3) providing initial indications that outsourcing of the IT function may not have the beneficial effects in healthcare that it does in other industries

Evaluation of the Maser-equipped Radar Set AN/MPS-34 and Area Precipitation Measurement Indicator: Final Report

published or submitted for publicationis peer reviewedOpe

Ozone Response to Aircraft Emissions: Sensitivity Studies with Two-dimensional Models

Our first intercomparison/assessment of the effects of a proposed high-speed civil transport (HSCT) fleet on the stratosphere is presented. These model calculations should be considered more as sensitivity studies, primarily designed to serve the following purposes: (1) to allow for intercomparison of model predictions; (2) to focus on the range of fleet operations and engine specifications giving minimal environmental impact; and (3) to provide the basis for future assessment studies. The basic scenarios were chosen to be as realistic as possible, using the information available on anticipated developments in technology. They are not to be interpreted as a commitment or goal for environmental acceptability

Photoreceptor Outer Segment-like Structures in Long-Term 3D Retinas from Human Pluripotent Stem Cells.

The retinal degenerative diseases, which together constitute a leading cause of hereditary blindness worldwide, are largely untreatable. Development of reliable methods to culture complex retinal tissues from human pluripotent stem cells (hPSCs) could offer a means to study human retinal development, provide a platform to investigate the mechanisms of retinal degeneration and screen for neuroprotective compounds, and provide the basis for cell-based therapeutic strategies. In this study, we describe an in vitro method by which hPSCs can be differentiated into 3D retinas with at least some important features reminiscent of a mature retina, including exuberant outgrowth of outer segment-like structures and synaptic ribbons, photoreceptor neurotransmitter expression, and membrane conductances and synaptic vesicle release properties consistent with possible photoreceptor synaptic function. The advanced outer segment-like structures reported here support the notion that 3D retina cups could serve as a model for studying mature photoreceptor development and allow for more robust modeling of retinal degenerative disease in vitro

A model for the distribution of aftershock waiting times

In this work the distribution of inter-occurrence times between earthquakes in aftershock sequences is analyzed and a model based on a non-homogeneous Poisson (NHP) process is proposed to quantify the observed scaling. In this model the generalized Omori's law for the decay of aftershocks is used as a time-dependent rate in the NHP process. The analytically derived distribution of inter-occurrence times is applied to several major aftershock sequences in California to confirm the validity of the proposed hypothesis.Comment: 4 pages, 3 figure

Interleukin-1 signaling in the basolateral amygdala is necessary for heroin-conditioned immunosuppression

Heroin administration suppresses the production of inducible nitric oxide (NO), as indicated by changes in splenic inducible nitric oxide synthase (iNOS) and plasma nitrate/nitrite. Since NO is a measure of host defense against infection and disease, this provides evidence that heroin can increase susceptibility to pathogens by directly interacting with the immune system. Previous research in our laboratory has demonstrated that these immunosuppressive effects of heroin can also be conditioned to environmental stimuli by repeatedly pairing heroin administration with a unique environmental context. Re-exposure to a previously drug-paired context elicits immunosuppressive effects similar to heroin administration alone. In addition, our laboratory has reported that the basolateral amygdala (BLA) and medial nucleus accumbens shell (mNAcS) are critical neural substrates that mediate this conditioned effect. However, our understanding of the contributing mechanisms within these brain regions is limited. It is known that the cytokine interleukin-1 (IL-1) plays an important role in learning and memory. In fact, our laboratory has demonstrated that inhibition of IL-1β expression in the dorsal hippocampus (DH) prior to reexposure to a heroin-paired context prevents the suppression of measures of NO production. Therefore, the present studies sought to further investigate the role of IL-1 in heroin-conditioned immunosuppression. Blockade of IL-1 signaling in the BLA, but not in the caudate putamen or mNAcS, using IL-1 receptor antagonist (IL-1Ra) attenuated heroin-conditioned immunosuppression of NO production as measured by plasma nitrate/nitrite and iNOS mRNA expression in spleen tissue. Taken together, these findings suggest that IL-1 signaling in the BLA is necessary for the expression of heroin-conditioned immunosuppression of NO production and may be a target for interventions that normalize immune function in heroin users and patient populations exposed to opiate regimens

A Method to have Multi-Layer Thermal Insulation Provide Damage Detection

Design and testing of a multi-layer thermal insulation system that also provides debris and micrometeorite damage detection is presented. One layer of the insulation is designed as an array of passive open-circuit electrically conductive spiral trace sensors. The sensors are a new class of sensors that are electrically open-circuits that have no electrical connections thereby eliminating one cause of failure to circuits. The sensors are powered using external oscillating magnetic fields. Once electrically active, they produce their own harmonic magnetic fields. The responding field frequency changes if any sensor is damaged. When the sensors are used together in close proximity, the inductive coupling between sensors provides a means of telemetry. The spiral trace design using reflective electrically conductive material provides sufficient area coverage for the sensor array to serves as a layer of thermal insulation. The other insulation layers are designed to allow the sensor s magnetic field to permeate the insulation layers while having total reflective surface area to reduce thermal energy transfer. Results of characterizing individual sensors and the sensor array s response to punctures are presented. Results of hypervelocity impact testing using projectiles of 1-3.6 millimeter diameter having speeds ranging from 6.7-7.1 kilometers per second are also presented

CDK-dependent Hsp70 phosphorylation controls G1 cyclin abundance and cell-cycle progression

In budding yeast, the essential functions of Hsp70 chaperones Ssa1-4 are regulated through expression level, isoform specificity, and cochaperone activity. Suggesting a novel regulatory paradigm, we find that phosphorylation of Ssa1 T36 within a cyclin-dependent kinase (CDK) consensus site conserved among Hsp70 proteins alters cochaperone and client interactions. T36 phosphorylation triggers displacement of Ydj1, allowing Ssa1 to bind the G1 cyclin Cln3 and promote its degradation. The stress CDK Pho85 phosphorylates T36 upon nitrogen starvation or pheromone stimulation, destabilizing Cln3 to delay onset of S phase. In turn, the mitotic CDK Cdk1 phosphorylates T36 to block Cln3 accumulation in G2/M. Suggesting broad conservation from yeast to human, CDK-dependent phosphorylation of Hsc70 T38 similarly regulates Cyclin D1 binding and stability. These results establish an active role for Hsp70 chaperones as signal transducers mediating growth control of G1 cyclin abundance and activity