Foundations in Wisconsin: A Directory [25th ed. 2006]

The 2006 production of Foundations in Wisconsin marks the 25th edition of the print directory and the 6th year of the online version (www.wifoundations.org). The directory is designed as a research tool for grantseekers interested in locating information on private, corporate, and community foundations registered in Wisconsin. Each entry in this new edition has been updated or reviewed to provide the most current information available. Most of the data was drawn from IRS 990-PF tax returns filed by the foundations. However, additional information was obtained from surveys, foundation Web sites, annual reports, and newsletters. Wisconsin foundations have shown continued growth in several key areas. The number of active grantmaking foundations has risen to 1227, with 77 new foundations identified since last year’s publication. Total grants increased by 15% to a total of $452 million, while assets increased by 6$5.5 billion.https://epublications.marquette.edu/lib_fiw/1004/thumbnail.jp

Local BDNF Delivery to the Injured Cervical Spinal Cord using an Engineered Hydrogel Enhances Diaphragmatic Respiratory Function.

We developed an innovative biomaterial-based approach to repair the critical neural circuitry that controls diaphragm activation by locally delivering brain-derived neurotrophic factor (BDNF) to injured cervical spinal cord. BDNF can be used to restore respiratory function via a number of potential repair mechanisms; however, widespread BDNF biodistribution resulting from delivery methods such as systemic injection or lumbar puncture can lead to inefficient drug delivery and adverse side effects. As a viable alternative, we developed a novel hydrogel-based system loaded with polysaccharide-BDNF particles self-assembled by electrostatic interactions that can be safely implanted in the intrathecal space for achieving local BDNF delivery with controlled dosing and duration. Implantation of BDNF hydrogel after C4/C5 contusion-type spinal cord injury (SCI) in female rats robustly preserved diaphragm function, as assessed b

Uspon ambasadora robne marke: društveni udio, korporativna društvena odgovornost i utjecaj među utjecajnim osobama na društvenim mrežama

One of social media’s influences on public relations has been the connection they provide organizations with stakeholder groups, and the need to recognize new and emerging stakeholder groups and their influence on the organization. One such stakeholder group with social media-borne influence and recognition in public relations is brand ambassadors, who distribute organizational content to social networks. This study examines the meanings and motivations of brand ambassadors in establishing relationships with an organization, and their considerations in representing and distributing content for an organization. In particular, we examined the consideration of corporate social responsibility (CSR) content among brand ambassadors. Findings suggest complex considerations of loyalties, commitments, and stakes within the brand ambassador-organization relationship. CSR content’s value among ambassadors was questionable. The ethical issues of organizational ties, including compensation, are discussed.Jedan od utjecaja društvenih medija na odnose s javnošću bila je veza koju osiguravaju organizacijama sa skupinama dionika te potreba za prepoznavanjem novih i novonastalih skupina dionika i njihovog utjecaja na organizaciju. Jedna takva skupina dionika s utjecajem na društvenim mrežama i prepoznatljivošću u odnosima s javnošću su ambasadori robnih marki, koji distribuiraju organizacijski sadržaj društvenim mrežama. Ova studija ispituje značenja i motivaciju ambasadora robne marke u uspostavljanju odnosa s organizacijom te njihova razmatranja u predstavljanju i distribuciji sadržaja za organizaciju. Konkretno, ispitali smo razmatranje sadržaja o društveno odgovornom poslovanju (CSR) među ambasadorima brendova. Nalazi upućuju na složena razmatranja lojalnosti, obveza i udjela unutar odnosa ambasadora marke i organizacije. Vrijednost sadržaja DOP-a među veleposlanicima bila je upitna. Razmatraju se etička pitanja organizacijskih veza, uključujući naknade

Early phrenic motor neuron loss and transient respiratory abnormalities following unilateral cervical spinal cord contusion

Contusion-type cervical spinal cord injury (SCI) is one of the most common forms of SCI observed in patients. In particular, injuries targeting the C3-C5 region affect the pool of phrenic motor neurons (PhMNs) that innervates the diaphragm, resulting in significant and often chronic respiratory dysfunction. Using a previously described rat model of unilateral midcervical C4 contusion with the Infinite Horizon Impactor, we have characterized the early time course of PhMN degeneration and consequent respiratory deficits following injury, as this knowledge is important for designing relevant treatment strategies targeting protection and plasticity of PhMN circuitry. PhMN loss (48% of the ipsilateral pool) occurred almost entirely during the first 24 h post-injury, resulting in persistent phrenic nerve axonal degeneration and denervation at the diaphragm neuromuscular junction (NMJ). Reduced diaphragm compound muscle action potential amplitudes following phrenic nerve stimulation were observed as early as the first day post-injury (30% of pre-injury maximum amplitude), with slow functional improvement over time that was associated with partial reinnervation at the diaphragm NMJ. Consistent with ipsilateral diaphragmatic compromise, the injury resulted in rapid, yet only transient, changes in overall ventilatory parameters measured via whole-body plethysmography, including increased respiratory rate, decreased tidal volume, and decreased peak inspiratory flow. Despite significant ipsilateral PhMN loss, the respiratory system has the capacity to quickly compensate for partially impaired hemidiaphragm function, suggesting that C4 hemicontusion in rats is a model of SCI that manifests subacute respiratory abnormalities. Collectively, these findings demonstrate significant and persistent diaphragm compromise in a clinically relevant model of midcervical contusion SCI; however, the therapeutic window for PhMN protection is restricted to early time points post-injury. On the contrary, preventing loss of innervation by PhMNs and/or inducing plasticity in spared PhMN axons at the diaphragm NMJ are relevant long-term targets

New Insights into the Lactate Shuttle: Role of MCT4 in the Modulation of the Exercise Capacity.

Lactate produced by muscle during high-intensity activity is an important end product of glycolysis that supports whole body metabolism. The lactate shuttle model suggested that lactate produced by glycolytic muscle fibers is utilized by oxidative fibers. MCT4 is a proton coupled monocarboxylate transporter preferentially expressed in glycolytic muscle fibers and facilitates the lactate efflux. Here we investigated the exercise capacity of mice with disrupted lactate shuttle due to global deletion of MCT4 (MCT4−/−) or muscle-specific deletion of the accessory protein Basigin (iMSBsg−/−). Although MCT4−/− and iMSBsg−/− mice have normal muscle morphology and contractility, only MCT4−/− mice exhibit an exercise intolerant phenotype. In vivo measurements of compound muscle action potentials showed a decrement in the evoked response in the MCT4−/− mice. This was accompanied by a significant structural degeneration of the neuromuscular junctions (NMJs). We propose that disruption of the lactate shuttle impacts motor function and destabilizes the motor unit

Personal and reported partner pornography viewing by Australian women, and association with mental health and body image

Background: Personal and partner pornography viewing may affect health and wellbeing. This study aimed to improve understanding of the effects of pornography on mental health and body image, given emerging evidence of increasing use, particularly among young people. Methods: A cross-sectional survey was implemented, targeting people who had accessed health and fitness content via social media. Convenience sampling was used and participants were recruited via advertising on social media. Results: Overall, 76% (75/99) of women reported having ever viewed pornography, and 21% had viewed pornography frequently (monthly/weekly/daily) in the prior 12 months. The association between frequent viewing and higher-risk Kessler 10 Psychological Distress Scale scores lost significance once controlled for age (adjusted OR 2.30, 95%CI 0.82–6.49, P = 0.11). There was an association with frequent reported partner pornography use (monthly/weekly/daily) and increased Drive for Muscularity scores (adjusted OR 2.20, 95%CI 1.01–4.80, P = 0.048). There were no other associations found with pornography use (personal or partner) and body image or mental health, although this was limited by the small sample size. Most women (85%, 41/48) reported being happy with their partner’s pornography use, and in qualitative responses, indicated that pornography had minimal effect on their lives. Nevertheless, multiple qualitative responses indicated a multiplicity of perceived effects of pornography, including negative effects on body image. Conclusions: Pornography had a minor effect on mental health and body image in this study. Additional research is required to improve understanding of the effects of pornography on body image and mental health, particularly among vulnerable individuals

Human iPS cell-derived astrocyte transplants preserve respiratory function after spinal cord injury.

Transplantation-based replacement of lost and/or dysfunctional astrocytes is a promising therapy for spinal cord injury (SCI) that has not been extensively explored, despite the integral roles played by astrocytes in the central nervous system (CNS). Induced pluripotent stem (iPS) cells are a clinically-relevant source of pluripotent cells that both avoid ethical issues of embryonic stem cells and allow for homogeneous derivation of mature cell types in large quantities, potentially in an autologous fashion. Despite their promise, the iPS cell field is in its infancy with respect to evaluating in vivo graft integration and therapeutic efficacy in SCI models. Astrocytes express the major glutamate transporter, GLT1, which is responsible for the vast majority of glutamate uptake in spinal cord. Following SCI, compromised GLT1 expression/function can increase susceptibility to excitotoxicity. We therefore evaluated intraspinal transplantation of human iPS cell-derived astrocytes (hIPSAs) following cervical contusion SCI as a novel strategy for reconstituting GLT1 expression and for protecting diaphragmatic respiratory neural circuitry. Transplant-derived cells showed robust long-term survival post-injection and efficiently differentiated into astrocytes in injured spinal cord of both immunesuppressed mice and rats. However, the majority of transplant-derived astrocytes did not express high levels of GLT1, particularly at early times post-injection. To enhance their ability to modulate extracellular glutamate levels, we engineered hIPSAs with lentivirus to constitutively express GLT1. Overexpression significantly increased GLT1 protein and functional GLT1-mediated glutamate uptake levels in hIPSAs both in vitro and in vivo post-transplantation. Compared to human fibroblast control and unmodified hIPSA transplantation, GLT1-overexpressing hIPSAs reduced (1) lesion size within the injured cervical spinal cord, (2) morphological denervation by respiratory phrenic motor neurons at the diaphragm neuromuscular junction, and (3) functional diaphragm denervation as measured by recording of spontaneous EMGs and evoked compound muscle action potentials. Our findings demonstrate that hiPSA transplantation is a therapeutically-powerful approach for SCI

Increased hypolipidemic benefits of cis-9, trans-11 conjugated linoleic acid in combination with trans-11 vaccenic acid in a rodent model of the metabolic syndrome, the JCR:LA-cp rat

<p>Abstract</p> <p>Background</p> <p>Conjugated linoleic acid (<it>cis</it>-9, <it>trans</it>-11 CLA) and <it>trans</it>-11 vaccenic acid (VA) are found naturally in ruminant-derived foods. CLA has been shown to have numerous potential health related effects and has been extensively investigated. More recently, we have shown that VA has lipid-lowering properties associated with reduced hepatic lipidogenesis and chylomicron secretion in the JCR:LA<it>-cp </it>rat. The aim of this study was to evaluate potential additional hypolipidemic effects of purified forms of CLA and VA in an animal model of the metabolic syndrome (the JCR:LA-<it>cp </it>rat).</p> <p>Methods</p> <p>Twenty four obese JCR:LA-<it>cp </it>rats were randomized and assigned to one of three nutritionally adequate iso-caloric diets containing 1% w/w cholesterol and 15% w/w fat for 16 wk: 1) control diet (CD), 2) 1.0% w/w <it>cis</it>-9, <it>trans</it>-11 CLA (CLA), 3) 1.0% w/w VA and 1% w/w <it>cis</it>-9, <it>trans</it>-11 CLA (VA+CLA). Lean rats were fed the CD to represent normolipidemic conditions.</p> <p>Results</p> <p>Fasting plasma triglyceride (TG), total cholesterol and LDL-cholesterol concentrations were reduced in obese rats fed either the CLA diet or the VA+CLA diet as compared to the obese control group (p < 0.05, p < 0.001; p < 0.001, p < 0.01; p < 0.01, p < 0.001, respectively). The VA+CLA diet reduced plasma TG and LDL-cholesterol to the level of the normolipidemic lean rats and further decreased nonesterified fatty acids compared to the CLA diet alone. Interestingly, rats fed the VA+CLA diet had a higher food intake but lower body weight than the CLA fed group (P < 0.05). Liver weight and TG content were lower in rats fed either CLA (p < 0.05) or VA+CLA diets (p < 0.001) compared to obese control, consistent with a decreased relative protein abundance of hepatic acetyl-CoA carboxylase in both treatment groups (P < 0.01). The activity of citrate synthase was increased in liver and adipose tissue of rats fed, CLA and VA+CLA diets (p < 0.001) compared to obese control, suggesting increased mitochondrial fatty acid oxidative capacity.</p> <p>Conclusion</p> <p>We demonstrate that the hypolipidemic effects of chronic <it>cis</it>-9, <it>trans</it>-11 CLA supplementation on circulating dyslipidemia and hepatic steatosis are enhanced by the addition of VA in the JCR:LA-<it>cp </it>rat.</p

Overexpression of the astrocyte glutamate transporter GLT1 exacerbates phrenic motor neuron degeneration, diaphragm compromise, and forelimb motor dysfunction following cervical contusion spinal cord injury.

A major portion of spinal cord injury (SCI) cases affect midcervical levels, the location of the phrenic motor neuron (PhMN) pool that innervates the diaphragm. While initial trauma is uncontrollable, a valuable opportunity exists in the hours to days following SCI for preventing PhMN loss and consequent respiratory dysfunction that occurs during secondary degeneration. One of the primary causes of secondary injury is excitotoxic cell death due to dysregulation of extracellular glutamate homeostasis. GLT1, mainly expressed by astrocytes, is responsible for the vast majority of functional uptake of extracellular glutamate in the CNS, particularly in spinal cord. We found that, in bacterial artificial chromosome-GLT1-enhanced green fluorescent protein reporter mice following unilateral midcervical (C4) contusion SCI, numbers of GLT1-expressing astrocytes in ventral horn and total intraspinal GLT1 protein expression were reduced soon after injury and the decrease persisted for ≥6 weeks. We used intraspinal delivery of adeno-associated virus type 8 (AAV8)-Gfa2 vector to rat cervical spinal cord ventral horn for targeting focal astrocyte GLT1 overexpression in areas of PhMN loss. Intraspinal delivery of AAV8-Gfa2-GLT1 resulted in transduction primarily of GFAP(+) astrocytes that persisted for ≥6 weeks postinjury, as well as increased intraspinal GLT1 protein expression. Surprisingly, we found that astrocyte-targeted GLT1 overexpression increased lesion size, PhMN loss, phrenic nerve axonal degeneration, and diaphragm neuromuscular junction denervation, and resulted in reduced functional diaphragm innervation as assessed by phrenic nerve-diaphragm compound muscle action potential recordings. These results demonstrate that GLT1 overexpression via intraspinal AAV-Gfa2-GLT1 delivery exacerbates neuronal damage and increases respiratory impairment following cervical SCI

SYSTEMIC COADMINISTRATION OF CHLORAMPHENICOL WITH INTRAVENOUS BUT NOT INTRACEREBROVENTRICULAR MORPHINE MARKEDLY INCREASES MORPHINE ANTINOCICEPTION AND DELAYS DEVELOPMENT OF ANTINOCICEPTIVE TOLERANCE IN RATS 1

This paper is available online at http://www.dmd.org ABSTRACT: Chloramphenicol, an in vitro inhibitor of the glucuronidation of morphine to its putative antianalgesic metabolite, morphine-3-glucuronide (M3G), was coadministered with morphine in adult male Sprague-Dawley rats to determine whether it inhibited the in vivo metabolism of morphine to M3G, thereby enhancing morphine antinociception and/or delaying the development of antinociceptive tolerance. Parenteral chloramphenicol was given acutely (3-h studies) or chronically (48-h studies). Morphine was administered by the i.v. or i.c.v. route. Control rats received chloramphenicol and/or vehicle. Antinociception was quantified using the hotplate latency test. Coadministration of chloramphenicol with i.v. but not i.cv. morphine increased the extent and duration of morphine antinociception by Ϸ5.5-fold relative to rats that received i.v. morphine alone. Thus, the mechanism through which chloramphenicol enhances i.v. morphine antinociception in the rat does not directly involve supraspinal opioid receptors. Acutely, parenteral coadministration of chloramphenicol and morphine resulted in an Ϸ75% increase in the mean area under the serum morphine concentration-time curve but for chronic dosing there was no significant change in this curve, indicating that factors other than morphine concentrations contribute significantly to antinociception. Antinociceptive tolerance to morphine developed more slowly in rats coadministered chloramphenicol, consistent with our proposal that in vivo inhibition of M3G formation would result in increased antinociception and delayed development of tolerance. However, our data also indicate that chloramphenicol inhibited the biliary secretion of M3G. Whether chloramphenicol altered the passage of M3G and morphine across the blood-brain barrier remains to be investigated. Morphine is recommended by the World Health Organization as the drug of choice for the management of moderate to severe cancer pain (World Health Organization, 1986). However, chronic administration of morphine by systemic routes may result in the development of analgesic/antinociceptive tolerance, manifested as a diminution of the pain-relieving effect or the requirement for an increase in morphine dose to maintain satisfactory pain relief, without an underlying progression in the disease state. Sprague-Dawley (SD) 2 rats are commonly used for studies of morphine tolerance. In both rats and humans, more than half of every morphine dose is metabolized to morphine-3-glucuronide (M3G). However, in both SD and Wistar strains of rat (unlike humans), glucuronidation of morphine at the 6-position to form morphine-6-glucuronide (M6G), the analgesically active metabolite of morphine, does not occur in detectable quantitie