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Search Results: 1 - 10 of 154969 matches for " Maribeth H. Johnson "
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Cardiometabolic Biomarkers in Young Black Girls: Relations to Body Fatness and Aerobic Fitness, and Effects of a Randomized Physical Activity Trial
Bernard Gutin,Ryan A. Harris,Cheryl A. Howe,Maribeth H. Johnson,Haidong Zhu,Yanbin Dong
International Journal of Pediatrics , 2011, DOI: 10.1155/2011/219268
Abstract: There is little evidence from randomized trials showing that physical activity alone influences biomarker profiles in youths. This study tested two hypotheses: (i) that elevated body fatness and poor fitness would be associated with unfavorable levels of cardiometabolic biomarkers in 8–12-y-old black girls (=242) and (ii) that a 10-mo PA intervention would have favorable effects on the fatness-related cardiometabolic biomarkers. At baseline, all fatness indices (i.e., percent body fat, visceral adipose tissue, BMI, and waist circumference) were significantly (<0.05) associated with unfavorable levels of insulin, glucose, systolic BP, diastolic BP, triglycerides, C-reactive protein (CRP), and fibrinogen. Aerobic fitness was significantly (<0.05) associated with favorable levels of insulin, CRP, fibrinogen, and HDL2. The PA intervention had significant and favorable effects on fitness, fatness, and two biomarkers—resting heart rate and LDL cholesterol. More research is needed to clarify what types of interventions can enhance the cardiometabolic health of youths.
Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke
Alex K Harris, Adviye Ergul, Anna Kozak, Livia S Machado, Maribeth H Johnson, Susan C Fagan
BMC Neuroscience , 2005, DOI: 10.1186/1471-2202-6-49
Abstract: Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9) expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change.The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke.The matrix metalloproteinases (MMPs) are a family of some 23 zinc dependent proteases that, collectively, possess the ability to degrade nearly every component of the extra-cellular matrix [1-3]. The activity of the MMPs is tightly controlled through proteolytic activation of the zymogen forms and stoichiometric binding of tissue inhibitors of metalloproteinases (TIMPs). The MMPs play an important role in many physiological processes due to their inherent ability to remodel tissues [2,3]. However, in disease states such as vascular disease and stroke, the MMPs may become deleterious due to dysregulation and can result in tissue injury and inflammation. Specifically, the MMPs may be involved in the degradation of the basal lamina in reperfusion injury resulting in disruption of the blood brain barrier and hemorrhagic transformation [4].Recently, several lines of evidence have demonstrated the involvement of the MMPs in cerebral ischemia. Studies in rat, mouse, and baboon models have shown that MMP-9 is up-regulated following transient focal ischemia [5-8]. Additionally, Asahi et al. have shown that MMP-9 knockout as
Stromal Cell-Derived Factor-1β Mediates Cell Survival through Enhancing Autophagy in Bone Marrow-Derived Mesenchymal Stem Cells
Samuel Herberg, Xingming Shi, Maribeth H. Johnson, Mark W. Hamrick, Carlos M. Isales, William D. Hill
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0058207
Abstract: Bone marrow-derived mesenchymal stem/stromal cells (BMSCs) hold great potential for cell-based therapy, yet the therapeutic efficacy remains uncertain. Transplanted BMSCs often fail to engraft within the bone marrow (BM), in part due to the poor survival of donor cells in response to inflammatory reactions, hypoxia, oxidative stress, or nutrient starvation. Two basic cell processes, apoptosis and autophagy, could potentially be responsible for the impaired survival of transplanted BMSCs. However, the functional relationship between apoptosis and autophagy in BMSC homeostasis is complex and not well understood. The stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) signaling axis appears to be critical in maintaining proliferation and survival of BM stem cell populations through improving cell proliferation and survival in response to stress; however, the exact mechanisms remain unclear. We recently described novel genetically engineered Tet-Off-SDF-1β BMSCs, which over-express SDF-1β under tight doxycycline-control, thus providing an ideal model system to investigate the isolated effects of SDF-1β. In this study we tested the hypothesis that SDF-1β can mediate cell survival of BMSCs in vitro through increasing autophagy. We found that SDF-1β had no effect on BMSC proliferation; however, SDF-1β significantly protected genetically engineered BMSCs from H2O2-induced cell death through increasing autophagy and decreasing caspase-3-dependent apoptosis. Taken together, we provide novel evidence that the SDF-1/CXCR4 axis, specifically activated by the SDF-1β isoform, plays a critical role in regulating BMSC survival under oxidative stress through increasing autophagy.
Vascular Protection by Angiotensin Receptor Antagonism Involves Differential VEGF Expression in Both Hemispheres after Experimental Stroke
Weihua Guan, Payaningal R. Somanath, Anna Kozak, Anna Goc, Azza B. El-Remessy, Adviye Ergul, Maribeth H. Johnson, Ahmed Alhusban, Sahar Soliman, Susan C. Fagan
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0024551
Abstract: We identified that the angiotensin receptor antagonist, candesartan, has profound neurovascular protective properties when administered after ischemic stroke and was associated with a proangiogenic state at least partly explained by vascular endothelial growth factor A (VEGFA). However, the spatial distribution of vascular endothelial growth factor (VEGF) isoforms and their receptors remained unknown. Protein analysis identified a significant increase in vascular endothelial grow factor B (VEGFB) in the cerebrospinal fluid (CSF) and the ischemic hemispheres (with increased VEGF receptor 1 activation) of treated animals (p<0.05) which was co-occurring with an increase in protein kinase B (Akt) phosphorylation (p<0.05). An increase in VEGFA protein in the contralesional hemisphere corresponded to a significant increase in vascular density at seven days (p<0.01) after stroke onset. Vascular restoration by candesartan after stroke maybe related to differential regional upregulation of VEGFB and VEGFA, promoting a “prosurvival state” in the ischemic hemisphere and angiogenesis in the contralesional side, respectively. These vascular changes in both hemispheres after effective treatment are likely to contribute to enhanced recovery after stroke.
Sex-independent neuroprotection with minocycline after experimental thromboembolic stroke
Md Nasrul Hoda, Weiguo Li, Ajmal Ahmad, Safia Ogbi, Marina A Zemskova, Maribeth H Johnson, Adviye Ergul, William D Hill, David C Hess, Irina Y Sazonova
Experimental & Translational Stroke Medicine , 2011, DOI: 10.1186/2040-7378-3-16
Abstract: Five groups of mice were subjected to thromboembolic stroke: adult males, aged males, adult females, aged females, and adult ovariectomized females. They were treated with phosphate saline (vehicle) or minocycline (6 mg/kg) immediately after stroke onset. Behavioral outcomes, infarct volumes and cerebral blood flow were assessed. The effect of minocycline on expression and activity of MMP-9 was analyzed.The model resulted in reproducible infarct in the experimental groups. As expected, adult females were significantly more resistant to cerebral ischemic injury than males. This advantage was abolished by aging and ovariectomy. Minocycline significantly reduced the infarct volume (P < 0.0001) and also improved neurologic score (P < 0.0001) in all groups. Moreover, minocycline treatment significantly reduced mortality at 24 hours post stroke (P = 0.037) for aged mice (25% versus 54%). Stroke up-regulated MMP-9 level in the brain, and acute minocycline treatment reduced its expression in both genders (P < 0.0001).In a thromboembolic stroke model minocycline is neuroprotective irrespective of mouse sex and age.Interest in sex differences during acute stroke is an area of growing interest. A consistent finding in rodent models of cerebral ischemia is that young females have smaller infarct sizes and better outcomes than young male rodents [1]. This female protection is lost after ovariectomy. However, the sex difference in stroke is only present when the brain is reperfused; in permanent occlusion the sex difference vanishes [2]. Moreover, in older rodents, the sex difference seen in younger animals is lost [3]. Reproductively senescent older female and male mice have similar infarct sizes after 2 hours of ischemia and 22 hours of reperfusion [4].The effect of sex on stroke outcome may also be hormone independent [3]. Recent studies suggest the existence of sex-divergent cell death pathways operating during cerebral ischemia [5]. The neuronal nitric oxide (NO)/Poly ADP ri
Absence of Functional Leptin Receptor Isoforms in the POUND (Leprdb/lb) Mouse Is Associated with Muscle Atrophy and Altered Myoblast Proliferation and Differentiation
Phonepasong Arounleut, Matthew Bowser, Sunil Upadhyay, Xing-Ming Shi, Sadanand Fulzele, Maribeth H. Johnson, Alexis M. Stranahan, William D. Hill, Carlos M. Isales, Mark W. Hamrick
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072330
Abstract: Objective Leptin receptors are abundant in human skeletal muscle, but the role of leptin in muscle growth, development and aging is not well understood. Here we utilized a novel mouse model lacking all functional leptin receptor isoforms (POUND mouse, Leprdb/lb) to determine the role of leptin in skeletal muscle. Methods and Findings Skeletal muscle mass and fiber diameters were examined in POUND mice, and primary myoblast cultures were used to determine the effects of altered leptin signaling on myoblast proliferation and differentiation. ELISA assays, integrated pathway analysis of mRNA microarrays, and reverse phase protein analysis were performed to identify signaling pathways impacted by leptin receptor deficiency. Results show that skeletal muscle mass and fiber diameter are reduced 30–40% in POUND mice relative to wild-type controls. Primary myoblast cultures demonstrate decreased proliferation and decreased expression of both MyoD and myogenin in POUND mice compared to normal mice. Leptin treatment increased proliferation in primary myoblasts from muscles of both adult (12 months) and aged (24 months) wild-type mice, and leptin increased expression of MyoD and myogenin in aged primary myoblasts. ELISA assays and protein arrays revealed altered expression of molecules associated with the IGF-1/Akt and MAPK/MEK signaling pathways in muscle from the hindlimbs of mice lacking functional leptin receptors. Conclusion These data support the hypothesis that the adipokine leptin is a key factor important for the regulation of skeletal muscle mass, and that leptin can act directly on its receptors in peripheral tissues to regulate cell proliferation and differentiation.
Role of Matrix Metalloproteinase Activity in the Neurovascular Protective Effects of Angiotensin Antagonism
Tauheed Ishrat,Anna Kozak,Ahmed Alhusban,Bindu Pillai,Maribeth H. Johnson,Azza B. El-Remessy,Adviye Ergul,Susan C. Fagan
Stroke Research and Treatment , 2014, DOI: 10.1155/2014/560491
Abstract: Background and Purpose. Oxidative stress and matrix metalloproteinase (MMP) activity have been identified as key mediators of early vascular damage after ischemic stroke. Somewhat surprisingly, the angiotensin II type 1 receptor (AT1) blocker, candesartan, has been shown to acutely increase MMP activity while providing neurovascular protection. We aimed to determine the contribution of MMP and nitrative stress to the effects of angiotensin blockade in experimental stroke. Methods. Wistar rats (n?=?9–14/group; a total of 99) were treated in a factorial design with candesartan 1?mg/kg IV, alone or in combination with either a peroxynitrite decomposition catalyst, FeTPPs, 30?mg/kg IP or GM6001 50?mg/kg IP (MMP inhibitor). Neurological deficit, infarct, size and hemorrhagic transformation (HT) were measured after 3?h of middle cerebral artery occlusion (MCAO) and 21?h of reperfusion. MMP activity and nitrotyrosine expression were also measured. Results. Candesartan reduced infarct size and HT when administered alone ( ) and in combination with FeTPPs ( ). GM6001 did not significantly affect HT when administered alone, but the combination with candesartan caused increased HT ( ) and worsened neurologic score ( ). Conclusions. Acute administration of candesartan reduces injury after stroke despite increasing MMP activity, likely by an antioxidant mechanism. 1. Introduction Ischemic stroke, an obstruction of blood flow in a major cerebral vessel, remains a leading cause of adult disability and death in the United States [1]. Because of its complex pathology, a major research and clinical priority is to develop therapeutic interventions in the ischemic brain through the understanding of underlying mechanisms. Ischemia reperfusion leads to a cascade of pathophysiological processes, resulting in further brain damage. Accumulations of free radicals, oxygen/nitrogen species (ROS/RNS), not only increase the susceptibility of brain tissue to reperfusion-induced damage but also trigger numerous molecular cascades, leading to increased blood-brain barrier (BBB) permeability, brain edema, hemorrhage and inflammation, and brain death [2, 3]. As an important component of free radicals, RNS, including peroxynitrite (ONOO–), play important roles in the process of cerebral ischemia-reperfusion injury. Ischemia reperfusion results in the production of peroxynitrite in ischemic brain, which triggers numerous molecular cascades and leads to vascular damage. In vitro, peroxynitrite strongly activates matrix metalloproteinases (MMPs) [4, 5]. Peroxynitrite formation on
Relations of diet and physical activity to bone mass and height in black and white adolescents
Bernard Gutin,Inger Stallmann-Jorgensen,Anh Le,Maribeth Johnson
Pediatric Reports , 2011, DOI: 10.4081/pr.2011.e10
Abstract: Because the development of healthy bodies during the years of growth has life-long health consequences, it is important to understand the early influences of diet and physical activity (PA). One way to generate hypotheses concerning such influences is to conduct cross-sectional studies of how diet and PA are related to different components of body composition. The subjects were 660 black and white adolescents. Total body bone mineral content (BMC) was measured with dual-energy X-ray absorptiometry; free-living diet and PA were assessed with 4-7 separate 24-h recalls. The main dietary variables investigated were: total energy intake, macronutrient distribution (%), dairy servings, vitamin D, and calcium. The main PA variables were hours of moderate PA (3-6 METs) and vigorous PA (>6 METs). BMC was higher in blacks than in whites (P<0.01) and it increased more in boys than in girls (age by sex interaction) as age increased (P<0.01). After adjustment for age, race and sex, higher levels of BMC were associated with higher levels of energy intake, dairy servings, calcium, vitamin D, and vigorous PA (all P 's<0.05). In the multivariable model, significant and independent proportions of the variance in BMC were explained by race, the age by sex interaction, calcium, and vigorous PA (all P 's<0.01). When height was used as the outcome variable, similar diet results were obtained; however, there was a sex by vigorous PA interaction, such that vigorous PA was associated with height only in the girls. These data are consistent with the hypothesis that the bone mass and height of growing youths are positively influenced by higher dietary intake of energy and dairy foods, along with sufficient amounts of vigorous PA. This hypothesis needs to be tested in randomized controlled trials.
Cerebral Neovascularization and Remodeling Patterns in Two Different Models of Type 2 Diabetes
Roshini Prakash, Maribeth Johnson, Susan C. Fagan, Adviye Ergul
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056264
Abstract: We previously reported intense pial cerebral collateralization and arteriogenesis in a mild and lean model of type 2 diabetes (T2D), Goto-Kakizaki (GK) rats. Increased cerebral neovascularization differed regionally and was associated with poor vessel wall maturity. Building upon these findings, the goals of this study were to determine whether a) glycemic control prevents this erratic cerebral neovascularization in the GK model, and b) this pathological neovascularization pattern occurs in Leprdb/db model, which is the most commonly used model of T2D for studies involving cerebral complications of diabetes. Vascular volume, surface area and structural parameters including microvessel/macrovessel ratio, non-FITC (fluorescein) perfusing vessel abundance, vessel tortuosity, and branch density were measured by 3D reconstruction of FITC stained vasculature in GK rats or Leprdb/db mice. GK rats exhibited an increase in all of these parameters, which were prevented by glycemic control with metformin. In Leprdb/db mice, microvascular density was increased but there was no change in nonFITC-perfusing vessels. Increased PA branch density was associated with reduced branch diameter. These results suggest that T2D leads to cerebral neovascularization and remodeling but some structural characteristics of newly formed vessels differ between these models of T2D. The prevention of dysfunctional cerebral neovascularization by early glucose control suggests that hyperglycemia is a mediator of this response.
Secondary Mapping of Lymphatic Filariasis in Haiti-Definition of Transmission Foci in Low-Prevalence Settings
Naomi Drexler ,Charles H. Washington,Maribeth Lovegrove,Caroline Grady,Marie Denise Milord,Thomas Streit,Patrick Lammie
PLOS Neglected Tropical Diseases , 2012, DOI: 10.1371/journal.pntd.0001807
Abstract: To eliminate Lymphatic filariasis (LF) as a public health problem, the World Health Organization (WHO) recommends that any area with infection prevalence greater than or equal to 1% (denoted by presence of microfilaremia or antigenemia) should receive mass drug administration (MDA) of antifilarial drugs for at least five consecutive rounds. Areas of low-antigen prevalence (<1%) are thought to pose little risk for continued transmission of LF. Five low-antigen prevalence communes in Haiti, characterized as part of a national survey, were further assessed for transmission in this study. An initial evaluation of schoolchildren was performed in each commune to identify antigen-positive children who served as index cases for subsequent community surveys conducted among households neighboring the index cases. Global positioning system (GPS) coordinates and immunochromatographic tests (ICT) for filarial antigenemia were collected on approximately 1,600 persons of all ages in the five communes. The relationship between antigen-positive cases in the community and distance from index cases was evaluated using multivariate regression techniques and analyses of spatial clustering. Community surveys demonstrated higher antigen prevalence in three of the five communes than was observed in the original mapping survey; autochthonous cases were found in the same three communes. Regression techniques identified a significantly increased likelihood of being antigen-positive when living within 20 meters of index cases when controlling for age, gender, and commune. Spatial clustering of antigen-positive cases was observed in some, but not all communes. Our results suggest that localized transmission was present even in low-prevalence settings and suggest that better surveillance methods may be needed to detect microfoci of LF transmission.
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