scholarly journals Dietary Genistein Influences Number of Acetylcholine Receptors in Female Diabetic Jejunum

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Sydney Schacht ◽  
Faisal Masood ◽  
Shawn Catmull ◽  
Robert Dolan ◽  
RussL Altabtabaee ◽  
...  
Keyword(s):  
Mouse Model ◽  
Gastrointestinal Motility ◽  
Wall Thickness ◽  
Acetylcholine Receptors ◽  
Imaging System ◽  
Intestinal Function ◽  
Gastrointestinal Dysfunction ◽  
Number Of Clusters ◽  
Video Imaging ◽  
Therapeutic Benefits

Background. Intestinal dysfunction in theob/obmouse model of diabetes mimics that seen clinically.Methods. We determined the effects of a 4-week genistein diet (600 mg genistein/kg food) on intestinal function (contractility, morphology, AChR, and motility) in femaleob/oband lean mice.Results. Contractility of the jejunum in response to incrementally increasing concentrations of KCl was comparable inob/obfemales and lean controls regardless of a genistein-diet. There were no changes in the wall thickness measured. We assessed the number of clusters of AChR in the jejunum wall; AChR were decreased by 48% inob/obmice versus leans, and the genistein diet reversed this. In utilizing a video-imaging system to evaluate gastrointestinal motility, we determined that the distance between consecutive contractile events was significantly increased by 1.87-fold inob/obmice versus leans, and the genistein diet was without effect.Conclusions. These data suggest that slowed intestinal transit in the diabeticob/obmouse may be due in part to decreased AChR and decreased contraction events occurring per unit time. A genistein diet rescues the number of AChR to levels of leans yet did not change the number of contractile events. Feedingob/obmice a genistein-rich diet has potential therapeutic benefits towards improving the debilitating diabetes-related gastrointestinal dysfunction.

scholarly journals Therapeutic Potential of Magnetic Nanoparticle-Based Human Adipose-Derived Stem Cells in a Mouse Model of Parkinson’s Disease

2021 ◽  
Vol 22 (2) ◽  
pp. 654
Author(s):  
Ka Young Kim ◽  
Keun-A Chang
Keyword(s):  
Parkinson’S Disease ◽  
Stem Cells ◽  
Parkinson's Disease ◽  
Magnetic Nanoparticles ◽  
Substantia Nigra ◽  
Mouse Model ◽  
Magnetic Nanoparticle ◽  
Imaging System ◽  
Therapeutic Potential ◽  
Adipose Derived Stem Cells

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra. Several treatments for PD have focused on the management of physical symptoms using dopaminergic agents. However, these treatments induce various adverse effects, including hallucinations and cognitive impairment, owing to non-targeted brain delivery, while alleviating motor symptoms. Furthermore, these therapies are not considered ultimate cures owing to limited brain self-repair and regeneration abilities. In the present study, we aimed to investigate the therapeutic potential of human adipose-derived stem cells (hASCs) using magnetic nanoparticles in a 6-hydroxydopamine (6-OHDA)-induced PD mouse model. We used the Maestro imaging system and magnetic resonance imaging (MRI) for in vivo tracking after transplantation of magnetic nanoparticle-loaded hASCs to the PD mouse model. The Maestro imaging system revealed strong hASCs signals in the brains of PD model mice. In particular, MRI revealed hASCs distribution in the substantia nigra of hASCs-injected PD mice. Behavioral evaluations, including apomorphine-induced rotation and rotarod performance, were significantly recovered in hASCs-injected 6-OHDA induced PD mice when compared with saline-treated counterparts. Herein, we investigated whether hASCs transplantation using magnetic nanoparticles recovered motor functions through targeted brain distribution in a 6-OHDA induced PD mice. These results indicate that magnetic nanoparticle-based hASCs transplantation could be a potential therapeutic strategy in PD.

scholarly journals Characterization and Evaluation of HGF-Loaded PLGA Nanoparticles in a CCl4-Induced Acute Liver Injury Mouse Model

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Chuxi Lin ◽  
Xueer Wang ◽  
Nuyun Liu ◽  
Qing Peng ◽  
Yang Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Mouse Model ◽  
Acute Liver Injury ◽  
Redox Homeostasis ◽  
Plga Nanoparticles ◽  
Physical Characteristics ◽  
Sod Activity ◽  
Therapeutic Benefits ◽  
Antioxidant Proteins ◽  
Drug Free

Liver injury can be caused by various harmful factors since the liver is considered the key organ for detoxifying endogenous and exogenous substances. Hepatocyte growth factor (HGF) can regulate redox homeostasis through the expression of antioxidant proteins when the liver is under injury. However, HGF is easily degraded. In this study, we produced three kinds of HGF-loaded poly(lactic-co-glycolic) acid (PLGA) nanoparticles with an initial addition of 2 μg HGF (NPs-HGF-2 μg), 4 μg HGF (NPs-HGF-4 μg), and drug-free nanoparticles (NPs) using the W/O/W emulsion-solvent evaporation method in accordance with our patent. The morphology and physical characteristics were analyzed, and effects of HGF-loaded PLGA nanoparticles on a CCl4-induced acute liver injury mouse model were investigated and compared with HGF solutions. We observed that the morphology and the physical characteristics of the nanoparticles were almost the same, with similar sizes, polydispersity, and zeta potential. HGF-loaded PLGA nanoparticles maintained higher HGF concentrations for a longer period of time in blood and liver tissues. HGF-loaded PLGA nanoparticles increased the SOD activity and GPX levels, decreased the MDA levels in the liver, reduced the necrotic areas of the liver, and decreased the levels of AST, ALT, ALP, T-BIL, BUN, and Scr in blood. In conclusion, our technique for preparing HGF-loaded PLGA nanoparticles was stable and the products were of good quality. HGF-loaded PLGA nanoparticles could provide greater therapeutic benefits on CCl4-induced acute liver injury, including antilipid peroxidation and a reduction in indicator enzymes of liver injury.

scholarly journals Tart Cherry Extract and Omega Fatty Acids Reduce Behavioral Deficits, Gliosis, and Amyloid-Beta Deposition in the 5xFAD Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 11 (11) ◽  
pp. 1423
Author(s):  
Zackary Bowers ◽  
Panchanan Maiti ◽  
Ali Bourcier ◽  
Jarod Morse ◽  
Kenneth Jenrow ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Mouse Model ◽  
Neuronal Morphology ◽  
Omega Fatty Acids ◽  
Tart Cherry ◽  
Therapeutic Benefits ◽  
Model Of Alzheimer’S Disease ◽  
5Xfad Mice

Combined treatments using polyphenols and omega fatty acids provide several therapeutic benefits for a variety of age-related disorders, including Alzheimer’s disease (AD). Previously, we found a commercial product, Total Body Rhythm (TBR), consisting of tart cherry extract, a potent polyphenol, and omega fatty acids, significantly reduced memory, and neuropathological deficits in the 192 IgG-saporin mouse model of AD. The present study assessed the efficacy of TBR for treating behavioral and neuropathological deficits in the 5xFAD model of AD. Both 6- and 12-month-old 5xFAD mice and age-matched wild-type controls received TBR (60 mg/kg) or the equivalent dose of vehicle (0.5% methylcellulose) via oral administration, every other day for two months. All mice were tested in the open field (OF), novel object recognition (NOR), and the Morris water maze (MWM) tasks. In addition, neuronal morphology, neurodegeneration, Aβ plaque load, and glial activation were assessed. TBR treatment reduced memory deficits in the MWM and NOR tests and lessened anxiety levels in the OF task, mostly in the 6-month-old male mice. TBR also protected against neuron loss, reduced activation of astrocytes and microglia, primarily in 6-month-old mice, and attenuated Aβ deposition. These results suggest that the combination of tart cherry extract and omega fatty acids in TBR can reduce AD-like deficits in 5xFAD mice.

An inexpensive hybrid video imaging system

1995 ◽  
Vol 66 (11) ◽  
pp. 5385-5386 ◽  
Author(s):  
J. A. Walkenstein ◽  
W. B. Pardo ◽  
H. S. Robertson ◽  
M. Monti
Keyword(s):  
Imaging System ◽  
Video Imaging

Active illumination compressive 4D spectral video imaging system

2021 ◽  
Author(s):  
Xiao Ma ◽  
Xin Yuan ◽  
Chen Fu ◽  
Gonzalo R. Arce
Keyword(s):  
Imaging System ◽  
Video Imaging ◽  
Active Illumination

scholarly journals Overexpression of UBQLN1 reduces neuropathology in the P497S UBQLN2 mouse model of ALS/FTD

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Shaoteng Wang ◽  
Micaela Tatman ◽  
Mervyn J. Monteiro
Keyword(s):  
Mouse Model ◽  
Neuronal Loss ◽  
Body Weight Loss ◽  
Missense Mutations ◽  
Homologous Proteins ◽  
Female Mice ◽  
Beneficial Effects ◽  
Therapeutic Benefits ◽  
Gender Specific ◽  
Lateral Sclerosis

Abstract Missense mutations in UBQLN2 cause X-linked dominant inheritance of amyotrophic lateral sclerosis with frontotemporal dementia (ALS/FTD). UBQLN2 belongs to a family of four highly homologous proteins expressed in humans that play diverse roles in maintaining proteostasis, but whether one isoform can substitute for another is not known. Here, we tested whether overexpression of UBQLN1 can alleviate disease in the P497S UBQLN2 mouse model of ALS/FTD by crossing transgenic (Tg) mouse lines expressing the two proteins and characterizing the resulting genotypes using a battery of pathologic and behavioral tests. The pathologic findings revealed UBQLN1 overexpression dramatically reduced the burden of UBQLN2 inclusions, neuronal loss and disturbances in proteostasis in double Tg mice compared to single P497S Tg mice. The beneficial effects of UBQLN1 overexpression were primarily confirmed by behavioral improvements seen in rotarod performance and grip strength in male, but not female mice. Paradoxically, although UBQLN1 overexpression reduced pathologic signatures of disease in P497S Tg mice, female mice had larger percentage of body weight loss than males, and this correlated with a corresponding lack of behavioral improvements in the females. These findings lead us to speculate that methods to upregulate UBQLN1 expression may reduce pathogenicity caused by UBQLN2 mutations, but may also lead to gender-specific outcomes that will have to be carefully weighed with the therapeutic benefits of UBQLN1 upregulation.

scholarly journals Lactobacillus paracaseiReduces Intestinal Inflammation in Adoptive Transfer Mouse Model of Experimental Colitis

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Manuel Oliveira ◽  
Nabil Bosco ◽  
Genevieve Perruisseau ◽  
Jeanne Nicolas ◽  
Iris Segura-Roggero ◽  
...  
Keyword(s):  
Mouse Model ◽  
Adoptive Transfer ◽  
Immune Modulation ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Neutrophil Infiltration ◽  
Lactobacillus Paracasei ◽  
Therapeutic Benefits

Studies showed that specific probiotics provide therapeutic benefits in inflammatory bowel disease.In vitroevidence suggested thatLactobacillus paracaseialso called ST11 (CNCM I-2116) is a potent strain with immune modulation properties. However, little is known about its capacity to alleviate inflammatory symptomsin vivoIn this context, the main objective of this study was to investigate the role of ST11 on intestinal inflammation using the adoptive transfer mouse model of experimental colitis. Rag2-/-recipient mice were fed with ST11 (109CFU/day)a month prior toinduce colitis by adoptive transfer of naive T cells. One month later, in clear contrast to nonfed mice, weight loss was significantly reduced by 50% in ST11-fed mice. Further analysis of colon specimens revealed a significant reduction neutrophil infiltration and mucosal expression of IL1β, IL-6, and IL12 proinflammatory cytokines, whereas no consistent differences in expression of antibacterial peptides or tight junction proteins were observed between PBS and ST11-fed mice. All together, our results demonstrate that oral administration of ST11 was safe and had a significant preventive effect on colitis. We conclude that probiotics such asLactobacillus paracaseiharbor worthwhilein vivoimmunomodulatory properties to prevent intestinal inflammation by nutritional approaches.

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