Biomedical subjects

Robert J Milner

Publications and source records attributed to Robert J Milner.

3 recordsLinked to original sources

PubMed2006

Empowering junior faculty: Penn State's faculty development and mentoring program.

Empowerment of faculty is essential for academic success. The Junior Faculty Development Program (JFDP), sponsored by the Office of Professional Development of the Penn State College of Medicine, was established in 2003 with the goal of promoting the development and advancement of junior faculty so they can achieve success in their academic careers. The program consists of two components: a curriculum in research, education, clinical practice, and career development, and an individual project completed under the guidance of a senior faculty mentor. The curriculum provides faculty with knowledge, skills, and resources. Mentoring provides relationships and support. Together, these elements combine to empower junior faculty to better manage their careers. The effectiveness of the program has been demonstrated by several measures: participants evaluated the program highly, demonstrated increases in their perceptions of their own abilities, and completed tasks important to the advancement of their careers. Participants stated they were better prepared to advance their academic careers and that the individual projects would contribute to their career advancement. On the basis of this experience, the authors suggest that faculty development programs should empower faculty so that they can more effectively chart a successful career in academic medicine. This report describes an empowerment model, and the design, implementation, and evaluation of the Junior Faculty Development Program in 2003-04 and 2004-05. The authors offer this program as a model for the benefit of other institutions and for one of their most valuable assets: junior faculty.

Evaluation Studies as Topic↗

PubMed2003

Seven cDNAs enriched following hippocampal lesion: possible roles in neuronal responses to injury.

Synaptic plasticity is important for formation of long-term memories and in re-establishment of function following injury. Seven cDNAs enriched following lesion in the hippocampus of the rat have been isolated using a PCR-based cDNA suppression subtraction hybridization. Sequence analysis resulted in the identification of two genes with known roles in synaptic development and neuronal activities: astrotactin and calcineurin. These two neuron-specific genes have established roles in development or synaptogenesis. Sequence analysis of the other five additional genes shows that two are likely to be involved in G-protein signaling pathways, one is a WD repeat protein, and the remaining two are entirely novel. All seven candidates are expressed in the hippocampus and, in some cases, cortical layers of adult brains. RT-PCR data show that expression increases following synaptogenic lesion. Immunocytochemical analysis in primary hippocampal neurons showed that Calcineurin immunoreactivity was redistributed in neurons during 2 weeks in culture. This redistribution suggests that Calcineurin's role changes during neurite outgrowth immediately prior to synapse formation in vitro. In addition, inhibiting Calcineurin activity with cyclosporin A enhanced neurite outgrowth, suggesting that Calcineurin has a regulatory role in axon sprouting. The discovery of previously unknown genes involved in the response to neurodegeneration will contribute to our understanding of neural development, responses to CNS trauma, and neurodegenerative diseases.

Animals↗

PubMed2002

Differential expression of protein tyrosine kinase genes during microglial activation.

Protein tyrosine kinase (PTK) activity is abundant in microglia, but the PTKs that participate in their activation have not been identified. For these studies, we used three paradigms to characterize PTK expression during microglial activation: resting and activated microglia were bulk fractionated from the adult brain, cultured newborn microglia were treated with lipopolysaccharide (LPS) to model the transition from activated toward phagocytic microglia, and PTK expression was examined in activated microglia in situ after facial nerve axotomy. Two PCR-based strategies were used to show that 21 different PTK genes are expressed by rat brain microglia: 5 receptor PTKs, 10 nonreceptor PTKs, and 6 members of the src family. Seven of the 21 PTKs were examined in greater detail. Five PTK mRNAs (fgr, hck, fak, jak-2, and flk-1) increased expression across all three models of activation. We conclude that they represent key components in the cascades that participate in microglial activation. In contrast, expression of fes and fms correlated with stimuli that affect microglial proliferation. Four of the PTKs (hck, fgr, fes, and fms) are believed to be myeloid cell specific and were not expressed by cultured astrocytes. HCK and FAK protein were also not expressed in lysates of immature astrocytes and oligodendrocytes. Because of their putative specificity, these kinases represent potential targets for inhibitors of microglial activation. Because reactive microglia can exacerbate the severity of neurological diseases, the identification of specific kinases that participate in microglial activation represents an important advance toward the development of new therapeutics.

Animals↗