Male Gender Expression Conflict Between Baby Boomers and Millennials

Ellen Degeneres cheerfully identifies herself as a Baby Boomer to her TV show audience, explaining that her generation was so-named because after World War II their parents said “We lived through the war, let’s make whoopee!” (Degeneres, 2016). Ellen then quips that “For you Millennials, making whoopee is like Netflix and Chill... But they were married,” (Degeneres, 2016). Here, Ellen has identified one of the key differences between two generations. Inasmuch as a person can be influenced by their parents, friends, or education, generations (or cohorts) can be impacted through the societal context surrounding their time of birth. Differences within cohort effects can reflect varied societal priorities and can persist throughout a person’s lifetime

RIPK3 activation leads to cytokine synthesis that continues after loss of cell membrane integrity

Necroptosis is a form of programmed cell death that is defined by activation of the kinase RIPK3 and subsequent cell membrane permeabilization by the effector MLKL. RIPK3 activation can also promote immune responses via production of cytokines and chemokines. How active cytokine production is coordinated with the terminal process of necroptosis is unclear. Here, we report that cytokine production continues within necroptotic cells even after they have lost cell membrane integrity and irreversibly committed to death. This continued cytokine production is dependent on mRNA translation and requires maintenance of endoplasmic reticulum integrity that remains after plasma membrane integrity is lost. The continued translation of cytokines by cellular corpses contributes to necroptotic cell uptake by innate immune cells and priming of adaptive immune responses to antigens associated with necroptotic corpses. These findings imply that cell death and production of inflammatory mediators are coordinated to optimize the immunogenicity of necroptotic cells

Investigating the Diabetic Brain: The Effects of Pioglitazone and Insulin on the Cellular Processes and Pathology of Alzheimer's Disease

Alzheimer’s disease (AD) is the sixth leading cause of death in the US. Some researchers refer to AD as “Type III Diabetes” because of reported glucose metabolism dysfunction. Preclinical studies suggest increasing insulin decreases AD pathology, although the mechanism remains unclear. To sensitize insulin signaling, this study activated Peroxisome Proliferator-Activated Receptor Gamma using intranasal co-administration of pioglitazone (PGZ) and insulin. This method targeted the site of action to reduce peripheral effects and to maximize impact in transgenic mice expressing AD pathology. Data from GC-MS fluxomics analysis suggested that PGZ+Insulin increased glucose metabolism in the brain. Immunohistochemistry with relevant antibodies was used to identify AD pathological markers in the subiculum, indicating that PGZ+Insulin decreased pathology compared to Insulin and Saline. This suggests that increasing glucose uptake in the brain alleviated AD pathology, further clarifying the role of insulin signaling in AD pathology.Gemston

Genetic and molecular characterization of <italic>CORONA</italic>, a novel regulator of meristem development in <italic>Arabidopsis thaliana</italic>.

The shoot meristem (SM) in higher plants is responsible for all above-ground organ formation. The SM maintains a population of stem cells and directs progenitor cells towards differentiation and organ formation. I have used Arabidopsis thaliana as a model system to study SM function. Previous work had shown that the CLV loci promote cell differentation at the shoot meristem, and that clv mutants accumulate stem cells. Mutations in CORONA (CNA) were identified in genetic screens for modifiers of the Clv- phenotype. cna clv double mutant plants, when compared to clv single mutants, exhibit dynamic and dramatic changes in SM structure as they proceed through development. These changes include an often massive enlargement of the shoot meristem. This clv cna enlargement differs from that observed in clv single mutants in that most of the additional cells are not stem cells. This is based on three lines of evidence. (1) The SMs of clv cna plants fully differentiate into carpelloid structures at approximately 4 weeks. (2) clv cna shoots lose the ability to initate new organs early in development. (3) clv cna shoots show variable but early loss of expression of key meristem regulators WUS and CLV3. The CNA gene was isolated by positional cloning and encodes a member of the plant-specific homeodomain - leucine zipper III class of transcription factors. The lesion found in the dominant-negative cna-1 is a missense mutation in a conserved domain of unknown function. The null cna-2 allele contains a T-DNA insertion in the THIRD exon. CNA is expressed in developing vascular tissue, as well as diffusely through developing SMs and flower meristems. The primary defect in clv cna plants remains to be determined. Perhaps clv cna plants are unable to maintain a population of stem cells resulting in premature organ termination and eventual differentiation. Alternatively, premature organ termination might lead to the subsequent breakdown of meristem identity. Whichever mechanism best describes the function of CNA, it is a novel component of meristem development representing a new pathway likely regulating the balance between stem cell identity and differentiation.Ph.D.Biological SciencesGeneticsMolecular biologyPlant biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/123594/2/3096100.pd

Alginate-PEG Sponge Architecture and Role in the Design of Insulin Release Dressings

Wound healing is a natural process involving several signaling molecules and cell types over a significant period of time. Although current dressings help to protect the wound from debris or infection, they do little in accelerating the healing process. Insulin has been shown to stimulate the healing of damaged skin. We have developed an alginate sponge dressing (ASD) that forms a hydrogel capable of providing a moist and protective healing environment. By incorporating insulin-loaded poly­(d,l-lactide-<i>co</i>-glycolide) (PLGA) microparticles into ASD, we successfully stabilized and released insulin for up to 21 days. Insulin release and water absorption and transfer through the ASD were influenced by altering the levels of poly­(ethylene glycol) (PEG) in the dressing matrix. Bioactivity of released insulin can be maintained for at least 10 days, demonstrated using a human keratinocyte migration assay. Results showed that insulin-loaded PLGA microparticles, embedded within PEG-ASD, functioned as an effective long-term delivery platform for bioactive insulin