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991.
992.
Marie-Luise Friedemann Rhonda J. Montgomery Bedonna Maiberger A. Ann Smith 《Research in nursing & health》1997,20(6):527-537
Staff–family cooperation in caring for elders in nursing homes is recommended but poorly understood. Family involvement and staff–family interactions in nursing homes with differing family orientations were investigated. Friedemann's (1995) system-based family theory guided the study. Of all 208 licensed nursing homes in southern Michigan, 143 completed a survey about their family-oriented practices. Family orientation was ranked accordingly. Twenty-four nursing homes were randomly selected to conduct semistructured telephone interviews with 177 family members. Data were analyzed by thematic interpretation. Findings showed a wide range of involvement patterns that promoted family connectedness, maintenance of control, growth, and learning. Families desired various types of staff cooperation and were given such opportunities in homes with high family orientation. © 1997 John Wiley & Sons, Inc. Res Nurs Health 20: 527–537, 1997 相似文献
993.
Neil M. Montgomery Christopher Tyler Katherine V. Fite 《The Journal of comparative neurology》1998,402(2):222-237
Light microscopic analysis of the optic nerve, chiasm, and optic tracts of Rana pipiens after the anterograde and retrograde transport of horseradish peroxidase has shown that retinal ganglion-cell axons reach the optic nerve head in chronotopically organized fascicles that form bands across the intraocular optic nerve. These bands of fascicles are divided along the midline in a “zone of reorganization” to create two full maps of the retinal surface; however, this map is discontinuous in that nasal and temporal quadrants are adjacent to one another. In the intracranial portion of the optic nerve, axons undergo another reorganization such that peripheral retinal axons shift position and become localized laterally and ventrally, whereas centrally placed axons become localized dorsally. Within this reorganization, the nerve is reconfigured into laminae of axons, and each lamina consists of age-related axons organized into two retinal maps. In the ipsilateral chiasm, axons diverge to form three central, optic tracts: the medial optic tract, the projection to the corpus geniculatum, and the basal optic root. Ipsilateral axons leave the chiasm at the same level of the chiasm as do their contralateral counterparts. The remaining axons converge in the lateral diencephalon to form a fourth fascicle, the marginal optic tract. Thus, within the optic chiasm, a sequence of positional transformations occur that result in the formation of multiple optic pathways. The various changes in axonal trajectory always coincide with changes in the orientation of cell groups that lie within the nerve and optic chiasm. J. Comp. Neurol. 402:222–237, 1998. © 1998 Wiley-Liss, Inc. 相似文献
994.
995.
SHANK3 is a postsynaptic structural protein localized at excitatory glutamatergic synapses in which deletions and mutations have been implicated in patients with autism spectrum disorders (ASD). The expression of Shank3 ASD mutations causes impairments in ionotropic glutamate receptor‐mediated synaptic responses in neurons, which is thought to underlie ASD‐related behaviors, thereby indicating glutamatergic synaptopathy as one of the major pathogenic mechanisms. However, little is known about the functional consequences of ASD‐associated mutations in Shank3 on another important set of glutamate receptors, group I metabotropic glutamate receptors (mGluRs). Here, we further assessed how Shank3 mutations identified in patients with ASD (one de novo InsG mutation and two inherited point mutations, R87C and R375C) disrupt group I mGluR (mGluR1 and mGluR5) expression and function. To identify potential isoform‐specific deficits induced by ASD‐associated Shank3 mutations on group I mGluRs, we surface immunolabeled mGluR1 and mGluR5 independently. We also induced mGluR‐dependent synaptic plasticity (R,S‐3,5‐dihydroxyphenylglycine [DHPG]‐induced long‐term depression [LTD]) as well as N‐methyl‐D‐aspartate receptor (NMDAR)‐dependent LTD. ASD‐associated mutations in Shank3 differentially interfered with the ability of cultured hippocampal neurons to express mGluR5 and mGluR1 at synapses. Intriguingly, all ASD Shank3 mutations impaired mGluR‐dependent LTD without altering NMDAR‐dependent LTD. Our data show that the specific perturbation in mGluR‐dependent synaptic plasticity occurs in neurons expressing ASD‐associated Shank3 mutations, which may underpin synaptic dysfunction and subsequent behavioral deficits in ASD. 相似文献
996.
997.
David F. Pinelli Andrea A. Zachary John J. Friedewald David W. Gjertson Michelle A. Evans Erik N. Chatroop Mary S. Leffell Ashley A. Vo Stanley C. Jordan Robert A. Montgomery Anat R. Tambur 《American journal of transplantation》2019,19(2):381-390
Currently, the ability to predict or monitor the efficacy of HLA antibody–removal therapies is deficient. We previously reported that titration studies are a consistent and accurate means of assessing antibody strength. To test whether titration studies can also predict which patients are better candidates for desensitization, we studied 38 patients from 3 centers (29 receiving plasmapheresis/low‐dose intravenous immunoglobulin [IVIg]; 9 patients receiving high‐dose IVIg). For patients undergoing plasmapheresis/low‐dose IVIg, antibody titer reduction correlated with number of treatment cycles for both class I and II antibodies but only up to approximately 4 cycles. Reduction in titer slowed with additional cycles, suggesting a limit to the efficacy of this approach. Furthermore, initial titer (predesensitization) can guide the selection of candidates for successful antibody‐removal treatment. In our experience, patients with antibodies at an initial titer >1:512 could not be reduced to the goal of a negative lymphocyte crossmatch, corresponding to a 1:16 titer, despite a significant increase in the number of treatment cycles. Change in mean fluorescence intensity (MFI) value did not correlate with success of treatment if initial MFI values were >10 000, likely due to single antigen bead saturation. Overall, we present a potential prognostic tool to predict candidacy and a monitoring tool to assess efficacy of desensitization treatment. 相似文献
998.
999.
Li JL Sainson RC Oon CE Turley H Leek R Sheldon H Bridges E Shi W Snell C Bowden ET Wu H Chowdhury PS Russell AJ Montgomery CP Poulsom R Harris AL 《Cancer research》2011,71(18):6073-6083
Resistance to VEGF inhibitors is emerging as a major clinical problem. Notch signaling has been implicated in tumor angiogenesis. Therefore, to investigate mechanisms of resistance to angiogenesis inhibitors, we transduced human glioblastoma cells with retroviruses encoding Notch delta-like ligand 4 (DLL4), grew them as tumor xenografts and then treated the murine hosts with the VEGF-A inhibitor bevacizumab. We found that DLL4-mediated tumor resistance to bevacizumab in vivo. The large vessels induced by DLL4-Notch signaling increased tumor blood supply and were insensitive to bevacizumab. However, blockade of Notch signaling by dibenzazepine, a γ-secretase inhibitor, disrupted the large vessels and abolished the tumor resistance. Multiple molecular mechanisms of resistance were shown, including decreased levels of hypoxia-induced VEGF and increased levels of the VEGF receptor VEGFR1 in the tumor stroma, decreased levels of VEGFR2 in large blood vessels, and reduced levels of VEGFR3 overall. DLL4-expressing tumors were also resistant to a VEGFR targeting multikinase inhibitor. We also observed activation of other pathways of tumor resistance driven by DLL4-Notch signaling, including the FGF2-FGFR and EphB4-EprinB2 pathways, the inhibition of which reversed tumor resistance partially. Taken together, our findings show the importance of classifying mechanisms involved in angiogenesis in tumors, and how combination therapy to block DLL4-Notch signaling may enhance the efficacy of VEGF inhibitors, particularly in DLL4-upregulated tumors, and thus provide a rational base for the development of novel strategies to overcome antiangiogenic resistance in the clinic. 相似文献
1000.
Yoon HH Catalano P Gibson MK Skaar TC Philips S Montgomery EA Hafez MJ Powell M Liu G Forastiere AA Benson AB Kleinberg LR Murphy KM 《Cancer chemotherapy and pharmacology》2011,68(4):863-870