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1.
Neurosci Lett ; 696: 38-45, 2019 03 23.
Article in English | MEDLINE | ID: mdl-30528708

ABSTRACT

INTRODUCTION: The application of low-intensity electrical stimulation (LIES) to neural tissue increases neurochemical factors responsible for regeneration as nerve growth factor. Stem cell (SC) therapy for patients with Spinal cord injury (SCI) promote some increase functional improvement. OBJECTIVE: Investigate the electromyographic response in paraplegic dogs undergoing LIES and SC transplantation. METHODS: 27 dogs paraplegics with SCI were divided into three groups with different types of therapy. GADSC: two SC transplants (n = 9); GLIES: LIES (n = 8); GCOMB: two SC transplants and LIES (n = 10). Adipose derived mesenchymal stem cells (ADSCs) were transplanted by lumbar puncture in the amount of 1.2 × 106 cells/50 µL. Acupuncture needles positioned in the interspinous space were used for stimulation. The electrical stimulation was applied with a mean voltage ∼30 mV and four consecutive modulated frequencies (5 Hz, 10 Hz, 15 Hz and 20 Hz) within 5 min each. The patients motor performance was evaluated before (Pre) the procedure and after 30 (Post30) and 60 (Post60) days, from electromyography root mean square (EMGRMS) registered with subcutaneous electrodes in the vastus lateralis muscle, while the animals were in quadrupedal position. RESULTS: All three groups showed a significant intra-group increase of EMGRMS (Pre vs. Post30 or Pre vs. Post60). However, there were no statistically significant differences between Post30 and Post60. The inter-group test (GADSC X GLIES X GCOMB) did not present significance when compared the instants Pre (p = 0.34), Post30 (p = 0.78) and Post60 (p = 0.64). CONCLUSION: Some dogs recovered motor activity, expressed by the EMGRMS, in all groups, in pre vs. post (30 or 60 days) comparisons.


Subject(s)
Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/cytology , Spinal Cord Injuries/therapy , Spinal Cord/physiopathology , Animals , Disease Models, Animal , Dogs , Electric Stimulation/methods , Female , Male , Mesenchymal Stem Cell Transplantation/methods , Obesity/complications , Spinal Cord Injuries/physiopathology
2.
Neurogastroenterol Motil ; 28(1): 101-15, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26526599

ABSTRACT

BACKGROUND: Cachexia is a significant problem in patients with cancer. The effect of cancer on interstitial cells of Cajal (ICC) and neurons of the gastrointestinal tract have not been studied previously. Although supplementation with L-glutamine 2% may have beneficial effects in cancer-related cachexia, and be protective of ICC in models of oxidative stress such as diabetes, its effects on ICC in cancer have also not been studied. METHODS: Twenty-eight male Wistar rats were divided into four groups: control (C), control supplemented with L-glutamine (CG), Walker 256 tumor (WT), and Walker 256 tumor supplemented with L-glutamine (WTG). Rats were implanted with tumor cells or injected with saline in the right flank. After 14 days, the jejunal tissues were collected and processed for immunohistochemical techniques including whole mounts and cryosections and Western blot analysis. KEY RESULTS: Tumor-bearing rats demonstrate reduced numbers of Myenteric ICC and deep muscular plexus ICC and yet increased Ano1 protein expression and enhanced ICC networks. In addition, there is more nNOS protein expressed in tumor-bearing rats compared to controls. L-glutamine treatment had a variety of effects on ICC that may be related to the disease state and the interaction of ICC and nNOS neurons. Regardless, L-glutamine reduced the size of tumors and also tumor-induced cachexia that was not due to altered food intake. CONCLUSIONS & INFERENCES: There are significant effects on ICC in the Walker 256 tumor model. Although supplementation with L-glutamine has differential and complex effects of ICC, it reduces tumor size and tumor-associated cachexia, which supports its beneficial therapeutic role in cancer.


Subject(s)
Cachexia/metabolism , Carcinoma 256, Walker/metabolism , Chloride Channels/drug effects , Glutamine/pharmacology , Interstitial Cells of Cajal/drug effects , Jejunum/drug effects , Myenteric Plexus/drug effects , Nitric Oxide Synthase Type I/drug effects , Oxidative Stress/drug effects , Animals , Anoctamin-1 , Blotting, Western , Carcinoma 256, Walker/pathology , Chloride Channels/metabolism , Immunohistochemistry , Interstitial Cells of Cajal/metabolism , Male , Myenteric Plexus/cytology , Nitric Oxide Synthase Type I/metabolism , Rats , Rats, Wistar , Tumor Burden
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