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Houston, TX, United States

Ferguson D.P.,Childrens Nutritional Research Center | Ferguson D.P.,Texas A&M University | Dangott L.J.,Texas A&M University | Schmitt E.E.,Texas A&M University | And 2 more authors.
Journal of Applied Physiology | Year: 2014

Physical inactivity contributes to cardiovascular disease, type II diabetes, obesity, and some types of cancer. While the literature is clear that there is genetic regulation of physical activity with existing gene knockout data suggesting that skeletal muscle mechanisms contribute to the regulation of activity, actual differences in end-protein expression between high- and low-active mice have not been investigated. This study used two-dimensional differential gel electrophoresis coupled with mass spectrometry to evaluate the proteomic differences between high-active (C57L/J) and low-active (C3H/HeJ) mice in the soleus and extensor digitorum longus (EDL). Furthermore, vivo-morpholinos were used to transiently knockdown candidate proteins to confirm their involvement in physical activity regulation. Proteins with higher expression patterns generally fell into the calcium-regulating and Krebs (TCA) cycle pathways in the high-active mice (e.g., annexin A6, P = 0.0031; calsequestrin 1; P = 0.000025), while the overexpressed proteins in the low-active mice generally fell into cytoskeletal structure- and electron transport chain-related pathways (e.g., ATPase, P = 0.031; NADH dehydrogenase, P = 0.027). Transient knockdown of annexin A6 and calsequestrin 1 protein of high-active mice with vivo-morpholinos resulted in decreased physical activity levels (P = 0.001). These data suggest that high- and low-active mice have unique protein expression patterns and that each pattern contributes to the peripheral capability to be either high- or low-active, suggesting that different specific mechanisms regulate activity leading to the high- or low-activity status of the animal. Copyright © 2014 the American Physiological Society. Source

Elbjeirami W.M.,King Hussein Cancer Center | Truong L.D.,Methodist Hospital | Tawil A.,Childrens Nutritional Research Center | Wang W.,Baylor College of Medicine | And 5 more authors.
Journal of Interferon and Cytokine Research | Year: 2010

Interstitial fibrosis plays a major role in progression of renal diseases. Oncostatin M (OSM) is a cytokine that regulates cell survival, differentiation, and proliferation. Renal tissue from patients with chronic obstructive nephropathy was examined for OSM expression. The elevated levels in diseased human kidneys suggested possible correlation between OSM level and kidney tissue fibrosis. Indeed, unilateral ureteral obstruction (UUO), a model of renal fibrosis, increased OSM and OSM receptor (OSM-R) expression in a time-dependent manner within hours following UUO. In vitro, OSM overexpression in tubular epithelial cells (TECs) resulted in epithelial-myofibroblast transdifferentiation. cDNA microarray technology identified up-regulated expression of immune modulators in obstructed compared with sham-operated kidneys. In vitro, OSM treatment up-regulated CC chemokine ligand CCL7, and CXC chemokine ligand (CXCL)-14 mRNA in kidney fibroblasts. In vivo, treatment of UUO mice with neutralizing anti-OSM antibody decreased renal chemokines expression. In conclusion, OSM is up-regulated in kidney tissue early after urinary obstruction. Therefore, OSM might play an important role in initiation of renal fibrogenesis, possibly by inducing myofibroblast transdifferentiation of TECs as well as leukocyte infiltration. This process may, in turn, contribute in part to progression of obstructive nephropathy and makes OSM a promising therapeutic target in renal fibrosis. © Mary Ann Liebert, Inc. Source

Chen K.,Childrens Nutritional Research Center | Zhang X.,Chongqing Medical University | Li T.-Y.,Childrens Nutritional Research Center | Chen L.,Chongqing Medical University | And 3 more authors.
Nutrition | Year: 2011

Objective: Improvement of hemoglobin and serum retinol and facilitation of the mobilization of iron storage were achieved with a multiple-micronutrient-fortified diet in preschoolers for 6 mo in a suburb of Chongqing, China. We investigated whether fortification with multiple micronutrients in a diet for preschool children results in changes in children's infectious morbidity compared with diets fortified solely with vitamin A and with vitamin A plus iron. Methods: From December 2005 to June 2006, 226 2- to 6-y-old preschool children were recruited from three nurseries randomly assigned to three different fortified-diet groups for 6 mo. Group I was fortified with vitamin A; groups II and III were fortified with vitamin A plus iron and vitamin A plus iron, thiamine, riboflavin, folic acid, niacinamide, zinc, and calcium, respectively. The secondary functional outcomes, morbidity of diarrhea and respiratory infection, were collected during supplementation. Results: The groups were comparable concerning compliance and loss to follow-up. There was evidence of a lower incidence rate of respiratory-related illnesses, diarrhea-related illness, fewer symptoms of runny nose, cough, and fever, and shorter duration of respiratory-related illnesses and cough for children in group III compared with children in groups I and II. However, there was no significantly or clinically important difference between children in groups I and II. Conclusion: The beneficial effects on infectious morbidity over 6 mo, in addition to some biochemical improvements, highlight the potential of this micronutrient-fortified seasoning powder supplied in a diet for preschool children. © 2011 Elsevier Inc. Source

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