Waking Up to the Power of Reflection to Unlock Transformation in People, Teams and Organizations

In our busy and frenetic world, leaders face overwhelm. Never before has there been so much change on so many fronts, demanding attention, squeezing out critical reflective time and thinking space. This is time and space to develop the personal capacities to lead with greater clarity, humanity and wisdom in order for transformation to occur, to learn how to reflect on experience, to sense what is needed and to lean into the futures’ emerging potential, instead of problem solving based on habitual thinking and yesterday\u27s logic. This chapter will give reflection and reflective learning a rebranding, propelling it from dusty classrooms to become centre stage in a leader\u27s toolkit, and will show how to apply the findings of the authors’ important new research in the workplace. The new leadership process “Reflect to Create!” with its seven human capacities for inspiring, creating and leading transformational change in today\u27s VUCA world is introduced. The four core conditions and four key practices to embed the approach are also introduced

Modelling Human Activity Through Structural Vibrations with Alternate Computational Devices to Increase Cost Efficiency

Every event that occurs has a reaction, whether it be a pebble causing ripples in a pond or a bullet distressing a wall. Within a structure, these vibrations caused by a specific event in a medium can be measured with an accelerometer, and just as the vibrations caused by a bullet differ observably from those caused by a pebble, vibrations caused by walking vary from those caused by falling, running or jumping. To the eye, these differences are slight to severe, but when that signal is dissected, it is identifiably unique by its cause and location with extensive applications from home security to commercial monitoring of foot traffic to behavior analysis for medical care including fall detection. The focus of this study was to investigate how this signal is collected -- specifically, if a cheaper independent computer could replace a setup that currently costs thousands. The Raspberry Pi was used with an ADXL345 accelerometer as this alternate system. This study includes notes of development of the hardware and software as well as analysis of the developed system by comparison to the accepted system. The new system is enabled to continuously read the accelerometer’s z axis output value, maintaining a buffer and saving significant signals. These hypothesized capabilities were confirmed by collecting vibration data from the same impact and comparing how each system recorded the event

Factors that contribute to black students retention and graduation at Iowa State University

The purpose of this study was to examine the retention and graduation rates for 125 black students who had enrolled as freshmen at Iowa State University in 1984. The study examined student history data from the university\u27s data base and information on the college experience at Iowa State, based on telephone interviews with 95 former students. The study identified factors associated with black students who graduated and those who withdrew from Iowa State University;Information obtained from the Iowa State University data base determined that black students who graduated had higher ACT scores, high school rank, and grade point averages, than had the students who did not graduate. Generally, out-of-state students were more successful than were Iowa residents. The ACT scores were significantly greater for males as compared to females. The total ACT scores for males who graduated exceeded those of females who graduated or who withdrew. Females who graduated had higher average scores than females who withdrew; the significance level was also greater than that for males. Interestingly, the out-of-state subjects who graduated had significantly higher ACT composite scores than did the out-of-state subjects who withdrew;The second phase of the study involved a telephone interview with each former student to secure information about his or her experience at Iowa State University. Two major areas identified as significant factors of the students\u27 likelihood of success included involvement in campus organizations and activities, and positive interaction with faculty and staff. The major reason for Iowa State University\u27s high black student dropout rate, as cited by former black students included the following: lack of social and cultural outlets; small amount of black faculty, staff and students; and racial discrimination

Activation of the maternal immune system induces endocrine changes in the placenta via IL-6

Activation of the maternal immune system in rodent models sets in motion a cascade of molecular pathways that ultimately result in autism- and schizophrenia-related behaviors in offspring. The finding that interleukin-6 (IL-6) is a crucial mediator of these effects led us to examine the mechanism by which this cytokine influences fetal development in vivo. Here we focus on the placenta as the site of direct interaction between mother and fetus and as a principal modulator of fetal development. We find that maternal immune activation (MIA) with a viral mimic, synthetic double-stranded RNA (poly(I:C)), increases IL-6 mRNA as well as maternally-derived IL-6 protein in the placenta. Placentas from MIA mothers exhibit increases in CD69+ decidual macrophages, granulocytes and uterine NK cells, indicating elevated early immune activation. Maternally-derived IL-6 mediates activation of the JAK/STAT3 pathway specifically in the spongiotrophoblast layer of the placenta, which results in expression of acute phase genes. Importantly, this parallels an IL-6-dependent disruption of the growth hormone-insulin-like growth factor (GH-IGF) axis that is characterized by decreased GH, IGFI and IGFBP3 levels. In addition, we observe an IL-6-dependent induction in pro-lactin-like protein-K (PLP-K) expression as well as MIA-related alterations in other placental endocrine factors. Together, these IL-6-mediated effects of MIA on the placenta represent an indirect mechanism by which MIA can alter fetal development

Maternal immune activation alters nonspatial information processing in the hippocampus of the adult offspring

The observation that maternal infection increases the risk for schizophrenia in the offspring suggests that the maternal immune system plays a key role in the etiology of schizophrenia. In a mouse model, maternal immune activation (MIA) by injection of poly(I:C) yields adult offspring that display abnormalities in a variety of behaviors relevant to schizophrenia. As abnormalities in the hippocampus are a consistent observation in schizophrenia patients, we examined synaptic properties in hippocampal slices prepared from the offspring of poly(I:C)- and saline-treated mothers. Compared to controls, CA1 pyramidal neurons from adult offspring of MIA mothers display reduced frequency and increased amplitude of miniature excitatory postsynaptic currents. In addition, the specific component of the temporoammonic pathway that mediates object-related information displays increased sensitivity to dopamine. To assess hippocampal network function in vivo, we used expression of the immediate-early gene, c-Fos, as a surrogate measure of neuronal activity. Compared to controls, the offspring of poly(I:C)-treated mothers display a distinct c-Fos expression pattern in area CA1 following novel object, but not novel location, exposure. Thus, the offspring of MIA mothers may have an abnormality in modality-specific information processing. Indeed, the MIA offspring display enhanced discrimination in a novel object recognition, but not in an object location, task. Thus, analysis of object and spatial information processing at both synaptic and behavioral levels reveals a largely selective abnormality in object information processing in this mouse model. Our results suggest that altered processing of object-related information may be part of the pathogenesis of schizophrenia-like cognitive behaviors

Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development

Maternal infection is a risk factor for autism spectrum disorder (ASD) and schizophrenia (SZ). Indeed, modeling this risk factor in mice through maternal immune activation (MIA) causes ASD- and SZ-like neuropathologies and behaviors in the offspring. Although MIA upregulates pro-inflammatory cytokines in the fetal brain, whether MIA leads to long-lasting changes in brain cytokines during postnatal development remains unknown. Here, we tested this possibility by measuring protein levels of 23 cytokines in the blood and three brain regions from offspring of poly(I:C)- and saline-injected mice at five postnatal ages using multiplex arrays. Most cytokines examined are present in sera and brains throughout development. MIA induces changes in the levels of many cytokines in the brains and sera of offspring in a region- and age-specific manner. These MIA-induced changes follow a few, unexpected and distinct patterns. In frontal and cingulate cortices, several, mostly pro-inflammatory, cytokines are elevated at birth, followed by decreases during periods of synaptogenesis and plasticity, and increases again in the adult. Cytokines are also altered in postnatal hippocampus, but in a pattern distinct from the other regions. The MIA-induced changes in brain cytokines do not correlate with changes in serum cytokines from the same animals. Finally, these MIA-induced cytokine changes are not accompanied by breaches in the blood–brain barrier, immune cell infiltration or increases in microglial density. Together, these data indicate that MIA leads to long-lasting, region-specific changes in brain cytokines in offspring—similar to those reported for ASD and SZ—that may alter CNS development and behavior

The Placental Interleukin-6 Signaling Controls Fetal Brain Development and Behavior

Epidemiological studies show that maternal immune activation (MIA) during pregnancy is a risk factor for autism. However, mechanisms for how MIA affects brain development and behaviors in offspring remain poorly described. To determine whether placental interleukin-6 (IL-6) signaling is required for mediating MIA on the offspring, we generated mice with restricted deletion of the receptor for IL-6 (IL-6R_) in placental trophoblasts (Cyp19-Cre^(+);Il6ra^(fl/fl)), and tested offspring of Cyp19-Cre^(+);Il6ra^(fl/fl) mothers for immunological, pathological and behavioral abnormalities following induction of MIA. We reveal that MIA results in acute inflammatory responses in the fetal brain. Lack of IL-6 signaling in trophoblasts effectively blocks MIA-induced inflammatory responses in the placenta and the fetal brain. Furthermore, behavioral abnormalities and cerebellar neuropathologies observed in MIA control offspring are prevented in Cyp19-Cre^(+);Il6ra^(fl/fl) offspring. Our results demonstrate that IL-6 activation in placenta is required for relaying inflammatory signals to the fetal brain and impacting behaviors and neuropathologies relevant to neurodevelopmental disease