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As a cellular bulk degradation and survival mechanism, autophagy is implicated in diverse biological processes. Genome-wide association studies have revealed the link between autophagy gene polymorphisms and susceptibility of autoimmune diseases including systemic lupus erythematosus (SLE) and inflammatory bowel disease (IBD), indicating that autophagy dysregulation may be involved in the development of autoimmune diseases. A series of autophagy modulators have displayed protective effects on autoimmune disease models, highlighting the emerging role of autophagy modulators in treating autoimmune diseases. This review explores the roles of autophagy in the autoimmune diseases, with emphasis on four major autoimmune diseases [SLE, rheumatoid arthritis (RA), IBD, and experimental autoimmune encephalomyelitis (EAE)]. More importantly, the therapeutic potentials of small molecular autophagy modulators (including autophagy inducers and inhibitors) on autoimmune diseases are comprehensively analyzed.
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BACKGROUND: Previous findings show that osteoblast-specific peptides can promote the repair and regeneration of skull defects in rabbits, and β-tricalcium phosphate (β-TCP) is used as a scaffold to carry osteoblast-specific polypeptides. Both of them not only complement each other, but also fully exert dual effects of osteoinduction and bone conduction. OBJECTIVE: To investigate the effect of osteoblast-specific peptide on the preservation of the anterior tooth extraction site in rabbits, and to study the effect on the alveolar bone remodeling. METHODS: Twenty-seven New Zealand white rabbits were randomly divided into three groups (n=9 per group), and the right mandibular incisors were removed to establish the animal models of tooth extraction. β-TCP/osteoblast-specific peptide compounds were implanted in the experimental group, and pure β-TCP meal was implanted into the material group. The blank control group had no implantation. Three rabbits from each group were scarified at 4, 8 and 12 postoperative weeks, and tissue samples were prepared for gross observation, histomorphology measurements, and radiographic measurements of extraction socket healing. RESULTS AND CONCLUSION: (1) Imaging results showed that the relative length of residual alveolar bone after modeling was ranked as follows: the experimental group > the material group > the blank control group, and the difference was statistically significant among groups (P < 0.05). Cone-beam CT findings in the three groups changed as time went on. At 4 and 8 postoperative weeks, the implanted materials in the experimental and material groups gradually degraded; the bone mass in the experimental group was significantly higher than that in the material and blank control groups. At 12 postoperative weeks, the experimental group had basically completed the reconstruction of tooth socket, but there were still some bone defects in the material and blank control groups. (2) Histomorphological findings showed that at 4 postoperative weeks, the experimental group exhibited obvious bone deposition lines, and the bone trabecula was widened; in the material and blank control groups, the new bone was less. At 8 postoperative weeks, a small amount of undegraded scaffold was found in the experimental group, with mature lamellar bone, the amount of new bone tissues in the material group increased and osteoblasts were obviously detected in the blank control group. At 12 postoperative weeks, the bone remodeling in the extraction socket of the experimental group was basically completed; in the material group, there were still a small amount of scaffold materials and dense plate-like new bone; and in the blank control group, the new bone tended to be mature, and there was obvious lamellar structure. To conclude, osteoblast-specific peptides can effectively preserve the length of the residual alveolar bone after tooth extraction, promote the formation of new bone, and have the function of preserving the tooth extraction site.
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<p><b>OBJECTIVE</b>To suggest a chemical surface treatment for titanium and to initiate the formation of hydroxycarbonated apatite (HCA) on titanium surface during in vitro bioactivity tests in simulated body fluid (SBF).</p><p><b>METHODS</b>To improve the bone-bonding ability of Ti implants, commercially pure titanium (cpTi) by a simple chemical pre-treatment in orthophosphoric acid (H(3)PO(4)) with different density was activated, and then the phosphorylation specimens were soaked in SBF to investigate the function of biomineralization.</p><p><b>RESULTS</b>The scanning electron microscope (SEM) photographs showed that the surfaces of the pre-treated samples were characterized by a complex construction, which consisted of a mesh-like morphology matrix (a micro-roughened surface) and an uniform surface with different morphous of titanium dihydrogen orthophosphate [Ti(H(2)PO(4))(3)] crystal. After 14 days in SBF a homogeneous biomimetic apatite layer precipitated.</p><p><b>CONCLUSIONS</b>These data suggest that the treatment of titanium by acid etching in orthophosphoric acid is a suitable method to provide the titanium implant with bone-bonding ability.</p>
Subject(s)
Acid Etching, Dental , Methods , Biomimetics , Body Fluids , Coated Materials, Biocompatible , Dental Bonding , Dental Implants , Microscopy, Electron, Scanning , Phosphoric Acids , Chemistry , Phosphorylation , Surface Properties , Titanium , ChemistryABSTRACT
Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.
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Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.
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<p><b>OBJECTIVE</b>To investigate the association of estrogen receptor (ER) gene polymorphism and primary trigeminal neuralgia.</p><p><b>METHODS</b>By polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), ER gene polymorphism was analyzed in 20 trigeminal neuralgia (TR) patients and 20 control individuals, and the distribution of ER genotype was compared in TR group and control group.</p><p><b>RESULTS</b>There was no significant difference in frequencies of allele and genotype in XbaI or PvuII polymorphism or XbaI with PvuII polymorphisms together between TR group and control group (P > 0.05). The genotypic distribution of Xx or PpXx in TR group was higher than control group, and it was contary to xx, ppxx or Ppxx in TR group and control group.</p><p><b>CONCLUSION</b>XbaI or PvuII polymorphism may be related to TR. Women with PpXx genotype may be a dangerous factor to primary trigeminal neuralgia.</p>