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Biomedical subjects

Scott Nelson

Publications and source records attributed to Scott Nelson.

8 recordsLinked to original sources
PubMed2006

Capillary-based, serial-loading, parallel microreactor for catalyst screening.

Soluble metal-ligand complexes are useful as catalysts for many organic reactions. The large number of metals and ligands available suggests a combinatorial approach to catalyst discovery. Carrying out reactions in very small (microliter) volumes in capillaries has many advantages in this regard, including material conservation, isolation from the atmosphere, and ease of transport of species by using pressure-induced flow. We have developed a capillary reactor in which separate zones of catalyst and reactants are combined and react. Zones are loaded serially into the capillary reactor from an autosampler, they react in parallel in the capillary reactor (at elevated temperature) and are ejected serially and under computer control for analysis by online GC. Offline analysis following sample collection is also possible. The Stille cross-coupling reaction has been the focus of our recent activity. Known palladium-based precatalysts and phosphine or arsine ligands were screened to validate the approach taken here. The results largely agree with results obtained by traditional organic synthesis, validating the method. The throughput of the nonoptimized system is over two 5-h reactions/h. For example, 40 5-h reactions examining the effect of catalyst loading were performed in 2 9-h runs requiring a total of 2 h of operator time.

Arsenicals↗
PubMed2004

The zebrafish Pard3 ortholog is required for separation of the eye fields and retinal lamination.

The vertebrate retina develops from a sheet of neuroepithelial cells. Because adherens and tight junctions are critical for epithelial and neuronal differentiation in a variety of eukaryotic systems, we examined the role of Par-3, a PDZ scaffold protein that is critical in cellular membrane junction formation. We cloned the zebrafish Par-3 ortholog (pard3), which encodes two Pard3 proteins (150 and 180 kDa) that differ in their carboxyl-terminus. Immunohistochemistry revealed that Pard3 localized to the apical region of the retinal and brain neuroepithelium, partially overlapping the adherens junction-associated actin bundles. After retinal lamination, the Pard3 protein was restricted to the outer limiting membrane and the outer and inner plexiform layers in the retina. Reducing Pard3 expression with antisense morpholinos caused loss of the retinal pigmented epithelia, disruption of retinal lamination, and cell death in the ventral diencephalon, which resulted in cyclopia. Overexpressing Pard3 by injection of wild-type pard3 mRNA resulted in cyclopia and eyeless embryos. Thus, Pard3 plays a critical role in the origination and separation of zebrafish eye fields and retinal lamination.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Influenza virus-induced sleep responses in mice with targeted disruptions in neuronal or inducible nitric oxide synthases.

Influenza viral infection induces increases in non-rapid eye movement sleep and decreases in rapid eye movement sleep in normal mice. An array of cytokines is produced during the infection, and some of them, such as IL-1beta and TNF-alpha, are well-defined somnogenic substances. It is suggested that nitric oxide (NO) may mediate the sleep-promoting effects of these cytokines. In this study, we use mice with targeted disruptions of either the neuronal NO synthase (nNOS) or the inducible NO synthase (iNOS) gene, commonly referred to as nNOS or iNOS knockouts (KOs), to investigate sleep changes after influenza viral challenge. We report that the magnitude of viral-induced non-rapid eye movement sleep responses in both nNOS KOs and iNOS KOs was less than that of their respective controls. In addition, the duration of rapid eye movement sleep in nNOS KO mice did not decrease compared with baseline values. All strains of mice had similar viral titers and cytokine gene expression profiles in the lungs. Virus was not isolated from the brains of any strain. However, gene expression in the brain stem differed between nNOS KOs and their controls: mRNA for the interferon-induced gene 2',5'-oligoadenylate synthase 1a was elevated in nNOS KOs relative to their controls at 15 h, and IL-1beta mRNA was elevated in nNOS KOs relative to their controls at 48 h. Our results suggest that NO synthesized by both nNOS and iNOS plays a role in virus-induced sleep changes and that nNOS may modulate cytokine expression in the brain.

2',5'-Oligoadenylate Synthetase↗
PubMedDate not supplied

The histologic host response to liquid silicone injections for prevention of pressure-related ulcers of the foot: a 38-year study.

This study analyzed the histologic effects of and host response to subdermally injected liquid silicone to augment soft-tissue cushioning of the bony prominences of the foot. A total of 148 postmortem and surgical specimens of pedal skin with attached soft tissue were obtained from 49 patients between July 1, 1974, and November 30, 2002. The longest period that silicone was in vivo was 38 years. The specimens were then processed into paraffin blocks and examined for specific findings. The variables considered included distribution of silicone within the tissue, host response, migration to regional lymph nodes, and viability of the host tissue after treatment. The host response to silicone therapy consisted primarily of delicate-to-robust fibrous deposition and histiocytic phagocytosis, with eventual formation of well-formed elliptic fibrous pads. The response in the foot appears different from that in the breast and other areas of the body previously studied. No examples of granulomas, chronic lymphoplasmacytic inflammation, or granulation tissue formation were seen, with only rare foreign-body giant cells present. Silicone injections in fat pads for the treatment of atrophy and loss of viable tissue show a histologically stable and biologically tolerated host response that is effective, with no evidence of any systemic changes.

Adipose Tissue↗