Chapter 28- Networked Mentoring Programs: Targeted Developmental Relationships and Building a Broader Community

We introduce a targeted approach to mentoring programs that considers students’ developmental stage and fosters an inclusive mentoring community. Using the case study of Babson College’s Center for Women’s Entrepreneurial Leadership Mentoring Programs, this chapter will detail evidence-based effective practice in delivering high-quality mentoring across distinctive student populations as well as connecting students and mentor volunteers to one another to cultivate a mentoring community. We highlight three mentoring programs: the Undergraduate Near Peer, Undergraduate Professional, and Graduate mentor programs. Each program is designed to match student mentees with developmentally appropriate mentors who provide support tailored to their needs. The Undergraduate Near Peer Mentoring Program pairs first-year students with third or fourth students for adjustment to college and integration with the broader community of diverse leaders. The Undergraduate Professional Mentoring Program pairs junior and senior students with early-career professionals (3–15 years of work experience) for vocational exploration and transition to work opportunities and challenges. The Graduate Mentoring Program pairs graduate students with seasoned professionals (15+ years of executive experience) for more advanced vocational exploration and sophisticated career transition strategies for diverse leaders. Programs are designed to incorporate industry best practices, including participant input for matching, required orientation, mentorship agreements, goal setting, and resources. Across all programs, students and mentors are encouraged to connect with one another through formal program opportunities and to develop a network of relationships to support their journey at Babson College and beyond

CRACM/Orai ion channel expression and function in human lung mast cells

BackgroundInflux of extracellular Ca2+ into human lung mast cells (HLMCs) is essential for the FcεRI-dependent release of preformed granule-derived mediators and newly synthesized autacoids and cytokines. However, the identity of the ion channels underlying this Ca2+ influx is unknown. The recently discovered members of the CRACM/Orai ion channel family that carries the Ca2+ release–activated Ca2+ current are candidates.ObjectivesTo investigate the expression and function of CRACM channels in HLMCs.MethodsCRACM mRNA, protein, and functional expression were examined in purified HLMCs and isolated human bronchus.ResultsCRACM1, -2, and -3 mRNA transcripts and CRACM1 and -2 proteins were detectable in HLMCs. A CRACM-like current was detected following FcεRI-dependent HLMC activation and also in HLMCs dialyzed with 30 μM inositol triphosphate. The Ca2+-selective current obtained under both conditions was blocked by 10 μM La3+ and Gd3+, known blockers of CRACM channels, and 2 distinct and specific CRACM-channel blockers—GSK-7975A and Synta-66. Both blockers reduced FcεRI-dependent Ca2+ influx, and 3 μM GSK-7975A and Synta-66 reduced the release of histamine, leukotriene C4, and cytokines (IL-5/-8/-13 and TNFα) by up to 50%. Synta-66 also inhibited allergen-dependent bronchial smooth muscle contraction in ex vivo tissue.ConclusionsThe presence of CRACM channels, a CRACM-like current, and functional inhibition of HLMC Ca2+ influx, mediator release, and allergen-induced bronchial smooth muscle contraction by CRACM-channel blockers supports a role for CRACM channels in FcεRI-dependent HLMC secretion. CRACM channels are therefore a potential therapeutic target in the treatment of asthma and related allergic diseases

Dietary calcium intake and Renin Angiotensin System polymorphisms alter the blood pressure response to aerobic exercise: a randomized control design

BACKGROUND: Dietary calcium intake and the renin angiotensin system (RAS) regulate blood pressure (BP) by modulating calcium homeostasis. Despite similar BP regulatory effects, the influence of dietary calcium intake alone and combined with RAS polymorphisms on the BP response following acute aerobic exercise (i.e., postexercise hypotension) has not been studied. Thus, we examined the effect of dietary calcium intake and selected RAS polymorphisms on postexercise hypotension. METHODS: Subjects were men (n = 50, 43.8 ± 1.3 yr) with high BP (145.3 ± 1.5/85.9 ± 1.1 mm Hg). They completed three experiments: non-exercise control and two cycle bouts at 40% and 60% of maximal oxygen consumption (VO(2)max). Subjects provided 3 d food records on five protocol-specific occasions. Dietary calcium intake was averaged and categorized as low (<880 mg/d = LowCa) or high (≥ 880 mg/d = HighCa). RAS polymorphisms (angiotensin converting enzyme insertion/deletion, ACE I/D; angiotensin II type 1 receptor, AT(1)R A/C) were analyzed with molecular methods. Genotypes were reduced from three to two: ACE II/ID and ACE DD; or AT(1)R AA and AT(1)R CC/AC. Repeated measure ANCOVA tested if BP differed among experiments, dietary calcium intake level and RAS polymorphisms. RESULTS: Systolic BP (SBP) decreased 6 mm Hg after 40% and 60% VO(2)max compared to non-exercise control for 10 h with LowCa (p < 0.01), but not with HighCa (p ≥ 0.05). Under these conditions, diastolic BP (DBP) did not differ between dietary calcium intake levels (p ≥ 0.05). With LowCa, SBP decreased after 60% VO(2)max versus non-exercise control for 10 h among ACE II/ID (6 mm Hg) and AT(1)R AA (8 mm Hg); and by 8 mm Hg after 40% VO(2)max among ACE DD and AT(1)R CC/CA (p < 0.01). With HighCa, SBP (8 mm Hg) and DBP (4 mm Hg) decreased after 60% VO(2)max compared to non-exercise control for 10 h (p < 0.05), but not after 40% VO(2)max (p ≥ 0.05). CONCLUSION: SBP decreased after exercise compared to non-exercise control among men with low but not high dietary calcium intake. Dietary calcium intake interacted with the ACE I/D and AT(1)R A/C polymorphisms to further modulate postexercise hypotension. Interactions among dietary calcium intake, exercise intensity and RAS polymorphisms account for some of the variability in the BP response to exercise

The Role of Cooperative Extension in Chronic Disease Prevention and Management: Perspectives from Professionals in the Field

Chronic diseases are strongly associated with premature death and increased health care costs. Nearly half of American adults report they have one or more chronic health conditions. Cooperative Extension is calling for refocus to refine and align with broader efforts to promote public health by supporting the prevention and management of chronic disease. The success of this refocus is dependent on a shared vision between funding agencies, stakeholders, and Extension. As part of developing this shared vision, the Chronic Disease Health Implementation Team surveyed 152 Extension administrators, faculty, and Extension Agents/Educators to determine their perception of the role of Extension in chronic disease prevention and management in the next century. Respondents answered the open-ended question, “What role should Cooperative Extension have in working to reduce chronic diseases in America for the next 10, 25, and 100 years? Analysis with grounded theory identified three themes. The respondents perceived the role of Extension professionals as educators and collaborators in chronic disease prevention and management who focus on influencing individuals and environments. As educators, Extension should deliver evidence-based programs to communicate, inform, facilitate, and teach. As collaborators, Extension should facilitate and nurture partnerships to effect changes in chronic disease prevention and management

Cooperative Extension as a Partner in Creating Healthy Communities: An Environmental Scan

health and wellness, chronic disease prevention and management, curriculum, Cooperative Extension, Extension, health programming, Health and Wellness Framework, ECOP Action Team

Using a virtual environment to assess cognition in the elderly

YesEarly diagnosis of Alzheimer’s disease (AD) is essential if treatments are to be administered at an earlier point in time before neurons degenerate to a stage beyond repair. In order for early detection to occur tools used to detect the disorder must be sensitive to the earliest of cognitive impairments. Virtual reality (VR) technology offers opportunities to provide products which attempt to mimic daily life situations, as much as is possible, within the computational environment. This may be useful for the detection of cognitive difficulties. We develop a virtual simulation designed to assess visuospatial memory in order to investigate cognitive function in a group of healthy elderly participants and those with a mild cognitive impairment. Participants were required to guide themselves along a virtual path to reach a virtual destination which they were required to remember. The preliminary results indicate that this virtual simulation has the potential to be used for detection of early AD since significant correlations of scores on the virtual environment with existing neuropsychological tests were found. Furthermore, the test discriminated between healthy elderly participants and those with a mild cognitive impairment (MCI)

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin