We report the first beam-target double-polarization asymmetries in the \(\gamma + n(p) \rightarrow \pi^- + p(p)\) reaction spanning the nucleon resonance region from invariant mass \(W\)= \(1500\) to ...\(2300\) MeV. Circularly polarized photons and longitudinally polarized deuterons in \(H\!D\) have been used with the CLAS detector at Jefferson Lab. The exclusive final state has been extracted using three very different analyses that show excellent agreement, and these have been used to deduce the {\it{E}} polarization observable for an effective neutron target. These results have been incorporated into new partial wave analyses, and have led to significant revisions for several \(\gamma nN^*\) resonance photo-couplings.
We suggest that the error quoted in the Mainz determination of the E2/M1
ratio (at the resonance energy) should be enlarged. A term dropped in
expressions used by this group could be significant.
Background Despite substantive morbidity, unexplained nausea and vomiting has not been evaluated in a systematic manner via surgically obtained biopsies and direct electrophysiology of the gut, and ...this information has not been correlated with serologic information. We investigated consecutive patients with unexplained and refractory chronic nausea and vomiting to define the presence of morphologic, physiologic, and/or serologic abnormalities. Methods In all, 101 of 121 consecutive patients who experienced chronic nausea and vomiting of unknown etiology evaluated in 1 tertiary referral center over a 10-year period were profiled qualitatively by full-thickness small bowel biopsies with hematoxylin and eosin (H&E) and Smith's Silver stains, quantitatively by intraoperative gastric electrophysiology, and semiquantitatively, when it became available, by serum autoimmune Western blot analysis. Results Overall, 79 of 101 patients had abnormal full-thickness biopsy (70 neuropathies and 9 myopathies) and frequent serum autoimmune abnormalities (mean score = 13.2, normal < 3.0). In addition, 96 of 101 patients had abnormal frequency and/or uncoupling on gastric electrophysiology. Patients with small-intestinal myopathy showed a diversity of diagnoses; some patients with neuropathy had abdominal pain that correlated with autoimmune scores on Western blot. Conclusion Patients with refractory and unexplained nausea and vomiting have a high incidence of both small bowel morphologic abnormalities (primarily neuropathies) and gastric electrophysiologic abnormalities, which are associated commonly with serologic autoimmune activation. Similar histomorphologic, physiologic, and serologic measures should be considered in the diagnostic evaluation of any patient with refractory or unexplained nausea and vomiting.
At present a complex global patchwork of private and public monographs and reference materials is variously available to help ensure the quality of medicines and foods. The relationship of these ...monographs and reference materials, one to another, frequently is inconsistently understood and documented. This article considers the complexity of monographs and reference materials with a focus on qualifying one reference material relative to another.
Previously, we reported that histone H1 binding to nucleosome cores results in the repression of binding of the basic helix-loop-helix upstream stimulatory factor (USF) (Juan, L.-J., Utley, R. T., ...Adams, C. C., Vettese-Dadey, M., and Workman, J. L. (1994) EMBO J. 13, 6031-6040). We have tested whether this inhibition resulted from H1-mediated changes in nucleosome positioning (Ura, K., Hayes, J. J., and Wolffe, A. P. (1995) EMBO J. 14, 3752-3765) forcing the USF recognition sequence into less accessible locations within the nucleosome. Nucleosome boundaries were determined by assays combining micrococcal nuclease and restriction endonuclease digestion. A unique pair of boundaries were observed, indicating a single nucleosome translational position. This nucleosome position did not change on H1 or USF binding. Thus, H1 repression of USF binding was independent of nucleosome mobility, indicating an alternative mechanism of H1 repression. H1 repressed USF binding at a site 35 base pairs into the nucleosome core more effectively than at a site near the “linker” DNA, suggesting that inhibition by H1 was not simply due to steric occlusion. Instead, these data are consistent with a model by which H1 binding reduces transient dynamic exposure of the DNA from the histone octamer surface (Polach, K. L., and Widom, J. (1995) J. Mol. Biol. 254, 130-149).
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