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Irritable bowel syndrome(IBS)is a common functional gastrointestinal disorder disease in children, and it is also a common cause of chronic abdominal pain in children.It not only seriously affects the life quality of children and their families, but also places a great burden on the Health Care System.At present, the exact pathogenesis of IBS is not completely clear, and most of the studies on the pathophysiological mechanism of IBS are based on adults, which poses a certain challenge to the effective management of children with IBS.Recent research progress of the pathogenesis of IBS was reviewed briefly in this paper, so as to provide a better strategy for the treatment of children with IBS.
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Objective@#To investigate the correlation between blood glucose and aneurysm rupture, and analyze the correlation factors of aneurysm rupture.@*Methods@#The clinical data of 128 patients with intracranial aneurysms in the First Affiliated Hospital of Kunming Medical University from January 2017 to August 2018 were retrospectively analyzed. Among them, intracranial aneurysm rupture was in 85 cases (rupture group), and unruptured was in 43 cases (unruptured group). The patient′s clinical features and aneurysm morphological features were recorded.@*Results@#The blood glucose, daughter sac rate and regularity of morphology rate in ruptured group were significantly higher than those in unruptured group: (6.74 ± 2.61) mmol/L vs. (5.77 ± 2.11) mmol/L, 60.00% (51/85) vs. 11.63% (5/43), and 68.24% (58/85) vs. 30.23% (13/43), the aneurysm width was significantly smaller than that in unruptured group: (4.53 ± 2.25) mm vs. (5.67 ± 2.68) mm, and there were statistical differences (P<0.05 or <0.01). There were no statistical difference in gender, age, blood pressure, diabetes, hypertension, smoking history, glycosylated hemoglobin, blood lipids, aneurysm length, aneurysm neck, aneurysm length ratio to neck between 2 groups (P>0.05). Univariate Logistic regression analysis result showed that blood glucose, aneurysm width, daughter ascus and irregular shape were the risk factors of rupture of aneurysm (P<0.05 or <0.01). Multivariate Logistic regression analysis result showed that blood glucose, aneurysm width, daughter sac and irregular shape were the independent risk factors of rupture of aneurysm (OR = 1.364, 0.709, 9.441 and 3.935; 95% CI 1.073 to 1.734, 0.565 to 0.889, 2.879 to 30.963 and 1.330 to 11.646; P = 0.011, 0.003, 0.000 and 0.013). The patients were grouped again according to the aneurysm width, and univariate Logistic regression analysis result showed that aneurysm width ≤ 3 mm was the risk factors of rupture of aneurysm (OR = 0.294, 95% CI 0.094 to 0.916, P = 0.035).@*Conclusions@#Irregular shape and daughter sac of aneurysm are the independent risk factors of aneurysm rupture, but aneurysm rupture has nothing to do with recent blood sugar levels.
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Objective To investigate the changes and mechanisms of immune function after ischemic stroke by studying the reaction of C57BL/6mice's lung and spleen after ischemic stroke.Methods Sixteen mice C57BL/6 were randomly assigned to experiment group (n=8) and control group (n=8).The acute ischemic stroke model was established in experiment group by Middle Cerebral Artery Occlusion (MCAO) and no stroke was performed in control group.Then we observed the lung inflammation by HE staining of the lung.And we measured the spleen weight,spleen weight index,the count and the apoptosis index of spleen cells of mice in two groups.Results Compared with the control group,the count of the inflammatory cells in lung of mice in the experiment group was higher,the spleen weight,spleen weight index and spleen cells count of the experiment group were decreased and the apoptosis index of spleen cells of the experiment group was higher.Conclusion The mice in the experiment group have inflammatory reaction in lung,the spleen atrophied and the apoptosis index of spleen cells is increased,which suggest that stroke-induced apoptosis of immunocytes may cause immunodepression after ischemic stroke and easily lead to the infection.
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BACKGROUND:Stromal cellderived factor 1 in chemotactic migration of endogenous neural stem cells plays a very important role, but the specific migration mechanism is unclear OBJECTIVE:To observe the effects of exogenous stromal cellderived factor 1 on chemotactic migration and proliferation of neural stem cells in the rat hippocampus METHODS:Exogenous stromal cellderived factor 1 (5μL, 500μ/L) was injected into the hippocampus of Sprague-Dawley rats to establish animal models. Brain tissues were taken after days 3, 7, 14 and 21 of perfusion to prepare paraffin sections. Thereafter, nestin expression in the injection region and hippocampus was detected using immunohistochemical method. Experimental control and blank control groups were set. RESULTS AND CONCLUSION:Paraffin section immunohistochemical results displayed the number of nestin-positive cells in the injection and the hippocampus was gradual y increased. At 3 and 7 days, nestin expression was a little and increased at 14 days, forming a migration tendency to the injection region. At 21 days, there were more nestin-positive cells in the injection area and hippocampus. However, there were no changes as above in the experimental control and blank control groups. The results showed that exogenous stromal cellderived factor 1 may induce the proliferation of neural stem cells in the hippocampus and may be involved in chemotactic migration of endogenous neural stem cells.
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@# Objective To apply the exogenous monocyte chemoattractant protein-1 (MCP-1) to induce the neural stem cells in vivo.Methods 64 adult male Sprague-Dawley rats were randomly divided into blank (n=4), control (n=30) and experimental (n=30) groups. The experimental group was injected with MCP-1 into the cerebra, and the control group with PBS, and the blank group with no intervention.The number of nestin positive cells in brain was observed with immunohistochemistry 3, 5, 7, 14, 21 days after injection. Results The number of nestin positive cells increased with time in the cortex and hippocampus in the experimental group (P<0.001). There was no significant difference between the control group and the blank group (P>0.05). Conclusion Exogenous MCP-1 may induce the increase of neural stem cells in vivo.
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BACKGROUND: Although previous studies have indicated that transplantation of marrow stromal cells (MSCs) has enhanced axonal regeneration and improved motor dysfunction induced by spinal cord injury. However, it is still unclear how transplanted MSCs promoted axonal regeneration and the relationship of transplanted cells and regenerated axons.OBJECTIVE: By immunofluorescence and immunoelectron microscopy, this study sought to elucidate the mechanism of promoting axonal sprouting following transplantation of MSCs into a completely transected spinal cord.DESIGN, TIME AND SETTING: The in vivo cytology randomized controlled animal experiment was performed at the Department of Anatomy of National University of Singapore from March 2006 to June 2007.MATERIALS: MSCs were isolated and purified from a Wistar neonatal rat. Model of completely transected spinal cord injury was established by transection at T_(10) segment with asepsis technique using 36 clean adult female Wistar rats.METHODS: MSCs were subcultured and purified. Thirty-six adult female Wistar rats were randomly divided into transplanted and control groups, with 18 animals in each group. Following 9 days of completely transected spinal cord injury, rats in the transplanted group were injected with MSCs (1×10~(11)/L), 5 μL in the defect region and 2.5 μL in 1 mm upper and lower the defect region. Rats in the control group were infused with an equal volume of DMEM, at the speed of 1 μL/min.MAIN OUTCOME MESSURES: Survival and differentiation of transplanted MSCs; Regeneration of axon and survival of host-derived nestin-, NF200-, GFAP-, and CNP-positive cells in control and transplanted groups; Relationship of regenerated axon and CNP-positive cells RESULTS: Two weeks after transplantation, a large number of CFDA-SE labeled MSCs were detected in the lesion site. Survival transplanted cell number was decreased over time. Abundant 0×42-positive phagocytes/activated microglia and cavity might affect the survival of transplanted cells. The number of MSCs was decreased, but MSC transplantation could promote axonal regeneration in the lesion site, and enhance the survival of host-derived nestin-, NF200-, GFAP-, and CNP-positive cells in lesion site, and host-derived CNP-positive cells and Schwann cells provided structural support to regenerated axons and promote their remyelination in spinal cord injury.CONCLUSION: Transplantation of MSCs enhances survival of host-derived CNP- positive cells and Schwann cells, and which may provide structural support to regenerated axons and promote their remyelination in spinal cord injury.