395 results on '"Guan, Zhi-Zhong"'
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2. Exposure to fluoride exacerbates the cognitive deficit of diabetic patients living in areas with endemic fluorosis, as well as of rats with type 2 diabetes induced by streptozotocin via a mechanism that may involve excessive activation of the poly(ADP ribose) polymerase-1/P53 pathway
3. Periploca forrestii Schltr. ameliorate liver injury caused by fluorosis in rat
4. Resveratrol Attenuates the Disruption of Lipid Metabolism Observed in Amyloid Precursor Protein/Presenilin 1 Mouse Brains and Cultured Primary Neurons Exposed to Aβ
5. Extract of Ginkgo biloba leaves attenuates neurotoxic damages in rats and SH-SY5Y cells exposed to a high level of fluoride
6. Improvement of the Health Condition of Local Residents After Comprehensive Treatments of Coal-Burning Type of Endemic Fluorosis
7. Drug Development
8. Changes in Gene Expression
9. Biological Indicators for Early Diagnosis of Endemic Fluorosis
10. Changes of Receptors
11. Mitochondrial Changes
12. Modification of Urinary System
13. Altering of Carbohydrate Metabolism
14. Modification of Digestive System
15. Enhanced Oxidative Stress
16. Discovery and Concept of Endemic Fluorosis
17. Medical Imaging Manifestation of Skeletal Fluorosis
18. Skeletal Fluorosis
19. Epidemic Status of Coal-burning Type of Endemic Fluorosis
20. Damage in Nervous System
21. Damage of Endocrine System
22. Alterations in Neuronal Nicotinic Acetylcholine Receptors in the Pathogenesis of Various Cognitive Impairments.
23. An inexpensive anaerobic chamber for the genetic manipulation of strictly anaerobic bacteria
24. Integrated transcriptomic and proteomic analysis indicated that neurotoxicity of rats with chronic fluorosis may be in mechanism involved in the changed cholinergic pathway and oxidative stress
25. Protections against toxicity in the brains of rat with chronic fluorosis and primary neurons exposed to fluoride by resveratrol involves nicotinic acetylcholine receptors
26. Silent Mating–Type Information Regulation 2 Homolog 1 Attenuates the Neurotoxicity Associated with Alzheimer Disease via a Mechanism Which May Involve Regulation of Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-α
27. Exposure to fluoride exacerbates the cognitive deficit of diabetic patients living in areas with endemic fluorosis, as well as of rats with type 2 diabetes induced by streptozotocin via a mechanism that may involve excessive activation of the poly(ADP ribose) polymerase-1/P53 pathway
28. Berberine Ameliorates Oxygen-glucose Deprivation/Reperfusion-induced Apoptosis by Inhibiting Endoplasmic Reticulum Stress and Autophagy in PC12 Cells
29. Changes of DNA repair gene methylation in blood of chronic fluorosis patients and rats
30. Protection against the Neurotoxic Effects of β-Amyloid Peptide on Cultured Neuronal Cells by Lovastatin Involves Elevated Expression of α7 Nicotinic Acetylcholine Receptors and Activating Phosphorylation of Protein Kinases
31. Changed expressions of N-methyl-d-aspartate receptors in the brains of rats and primary neurons exposed to high level of fluoride
32. Resveratrol Attenuates the Disruption of Lipid Metabolism Observed in APP/PS1 Mouse Brains and Cultured Primary Neurons Exposed to Aβ
33. Exposure to fluoride aggravates the impairment in learning and memory and neuropathological lesions in mice carrying the APP/PS1 double-transgenic mutation
34. The influence of NQO2 on the dysfunctional autophagy and oxidative stress induced in the hippocampus of rats and in SH‐SY5Y cells by fluoride
35. The decreased expression of mitofusin-1 and increased fission-1 together with alterations in mitochondrial morphology in the kidney of rats with chronic fluorosis may involve elevated oxidative stress
36. Inhibited Expression of α4β2 Nicotinic Acetylcholine Receptor in Blood Leukocytes of Chinese Patients with Vascular Dementia and in Blood Leukocytes as Well as the Hippocampus of Brain from Ischemic Rats
37. The neurotoxicity of β-amyloid peptide toward rat brain is associated with enhanced oxidative stress, inflammation and apoptosis, all of which can be attenuated by scutellarin
38. The influence of inhibiting or stimulating the expression of the α3 subunit of the nicotinic receptor in SH-SY5Y cells on levels of amyloid-β peptide and β-secretase
39. Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors
40. Increased level of apoptosis in rat brains and SH-SY5Y cells exposed to excessive fluoride—A mechanism connected with activating JNK phosphorylation
41. An Extract of Ginkgo Biloba Leaves Attenuates Neurotoxic Changes in Rats with Chronic Fluorosis, as Well as in Sh-Sy5y Cells Exposed to a High Level of Fluoride
42. Alterations of nAChRs and ERK1/2 in the brains of rats with chronic fluorosis and their connections with the decreased capacity of learning and memory
43. Amyloid precursor protein gene mutated at Swedish 670/671 sites in vitro induces changed expression of nicotinic acetylcholine receptors and neurotoxicity
44. Activation of α7 Nicotinic Acetylcholine Receptor by its Selective Agonist Improved Learning and Memory of Amyloid Precursor Protein/Presenilin 1 (APP/PS1) Mice via the Nrf2/HO-1 Pathway
45. LiCl attenuates impaired learning and memory of APP/PS1 mice, which in mechanism involves α7 nAChRs and Wnt/β‐catenin pathway
46. Myeloperoxidase Activity and Its Corresponding mRNA Expression as well as Gene Polymorphism in the Population Living in the Coal-Burning Endemic Fluorosis Area in Guizhou of China
47. Preventing Expression of the Nicotinic Receptor Subunit α7 in SH-SY5Y Cells with Interference RNA Indicates that this Receptor may Protect Against the Neurotoxicity of Aβ
48. The influence of chronic fluorosis on mitochondrial dynamics morphology and distribution in cortical neurons of the rat brain
49. Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia
50. Oxidative stress might be a mechanism connected with the decreased α7 nicotinic receptor influenced by high-concentration of fluoride in SH-SY5Y neuroblastoma cells
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