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1.
J Pharmacol Exp Ther ; 368(3): 490-502, 2019 03.
Article in English | MEDLINE | ID: mdl-30591528

ABSTRACT

The combination of decellularized nerve allograft and adipose-derived stromal cells (ASCs) represents a good alternative to nerve autograft for bridging peripheral nerve defects by providing physical guidance and biologic cues. However, the regeneration outcome of acellular nerve allograft (ANA) is often inferior to autograft. Therefore, we hypothesized that acetyl-l-carnitine (ALCAR) treatment and implantation of ASC-embedded ANA would work synergistically to promote nerve regeneration. Seventy rats were randomly allocated into seven experimental groups (n = 10), including the healthy control group, sham surgery group, autograft group, ANA group, ANA + ASCs group, ANA + ALCAR group (50 mg/kg for 2 weeks), and ANA + ASCs + ALCAR (50 mg/kg for 2 weeks) group. All grafts were implanted to bridge long-gap (10-mm) sciatic nerve defects. Functional, electrophysiological, and morphologic analysis was conducted during the experimental period. We found that ALCAR potentiated the survival and retention of transplanted ASCs and upregulated the expression of neurotrophic factor mRNAs in transplanted grafts. Sixteen weeks following implantation in the rat, the ANA supplemented by ASCs was capable of supporting reinnervation across a 10-mm sciatic nerve gap, with results close to that of the autografts in terms of functional, electrophysiological, and histologic assessments. Results demonstrated that ALCAR treatment improved regenerative effects of ANA combined with ASCs on reconstruction of a 10-mm sciatic nerve defect in rat comparable to those of autograft.


Subject(s)
Acetylcarnitine/administration & dosage , Adipose Tissue/transplantation , Allografts/transplantation , Nerve Regeneration/physiology , Sciatic Neuropathy/therapy , Stromal Cells/transplantation , Acellular Dermis/drug effects , Adipose Tissue/drug effects , Adipose Tissue/physiology , Allografts/drug effects , Allografts/physiology , Animals , Male , Nerve Regeneration/drug effects , Random Allocation , Rats , Rats, Wistar , Sciatic Neuropathy/drug therapy , Sciatic Neuropathy/pathology , Stromal Cells/drug effects , Stromal Cells/pathology , Vitamin B Complex/administration & dosage
2.
Article in English | WPRIM (Western Pacific) | ID: wpr-627970

ABSTRACT

Background: Helicobacter pylori infection is a major risk factor for chronic gastritis and gastric cancer. Some findings show increased frequencies of these diseases in individuals with type O blood and in secretors (expressing Leb antigen), but other studies have not found any relationship between blood groups and this infection. Given that H. pylori infection and gastric cancer are common in Iran, the assessment of the pathogenesis of this infection in relation to these blood groups could be valuable. Methods: In a cross-sectional study, we determined the ABO and Lewis blood groups of participants using the tube method and evaluated the level of anti-H. pylori immunoglobulin G using an enzyme-linked immunosorbent assay. This study included 171 Iranian blood donors from Mashhad, Iran, during 2010. The significance of the differences in the frequencies of the Lewis and ABO phenotypes between individuals infected with and without H. Pylori infection were tested using the chi-square test. A P-value < 0.05 was considered significant. Results: H. pylori infection was found in 76.6% of the study subjects (n = 131). The most common ABO blood group was O (33.9%), and the most common Lewis blood group was Le(a-b+) (54.7%). The frequencies of the ABO, Lewis, and secretion phenotypes were not significantly different between the infected and uninfected subjects. Conclusion: We did not find any significant relationship between the Lewis, ABO, and secretion phenotypes and H. pylori infection.

3.
Neurol Res ; 30(10): 1086-90, 2008 Dec.
Article in English | MEDLINE | ID: mdl-18768110

ABSTRACT

Huntington's disease is an inherited neurodegenerative disorder, characterized by loss of spiny neurons in the striatum and cortex, which usually happens in the third or fourth decades of life. In advanced form of the disease, progressive striatum atrophy happens and medium spiny neurons, which occupy more than 80% of the striatum, become atrophic. Gradually, the atrophy expands to the neocortex and other regions of the brain. To our knowledge, there is no effective therapeutic strategy for diminishing the motor disorders of Huntington's disease. In recent years, cellular transplantation has been an effective therapeutic method for neurodegenerative diseases. In the present study, the potential of bone marrow derived mesenchymal stem cells in amelioration of striatal degeneration was assessed in animal model of Huntington's disease. After unilateral lesion in striatum was caused by quinolinic acid (QA), bone marrow derived mesenchymal stem cells, which were isolated and purified from 4-6 weeks old rats, were transplanted into the damaged striatum. After 9 weeks of transplantation, the volume of striatum, lateral ventricles and hemispheres were measured in control (normal) and test (QA injected + cell transplanted) groups. After volume determination, the atrophy percentage of both striatum and damaged hemisphere and volume extension of lateral ventricles were calculated. Histologic results showed significant difference in amount of striatum atrophy between sham (only QA injected) and test groups. These results confirm the potential of bone marrow derived mesenchymal stem cells in treatment of microanatomical defects in motor disorders of Huntington's disease. According to our results, cell therapy by means of bone marrow derived adult stem cells could be considered as a good candidate for treatment of neurodegenerative diseases, especially Huntington's disease.


Subject(s)
Bone Marrow Transplantation/methods , Corpus Striatum/surgery , Huntington Disease/complications , Mesenchymal Stem Cells/physiology , Nerve Degeneration , Animals , Cerebral Ventricles/pathology , Corpus Striatum/pathology , Disease Models, Animal , Huntington Disease/chemically induced , Nerve Degeneration/etiology , Nerve Degeneration/pathology , Nerve Degeneration/surgery , Quinolinic Acid , Rats , Rats, Wistar , Time Factors
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