BACKGROUND:Al ogeneic bone has anatomical appearance and biological features similar to autogenous bone, which is an excel ent biological scaffold material. Mesenchymal stem cel s originating from autogenous bone marrow have mutli-lineage differentiation potential, can differentiate into osteoblasts and chondrocyte, and thus can accelerate the formation of bone tissue and cartilage tissue. OBJECTIVE:To establish the osteogenic ability of al ogeneic bone with autogenous bone marrow mesenchymal stem cel s for repairing major mandibular defects. METHODS:The left mandibular teeth of 24 beagles were extracted, and at 2 months after wound healing, mandibular defects were made artificial y. The beagles were divided into two groups:control group treated with lyophilized al ogeneic bone, and experimental group with autogenous bone marrow mesenchymal stem cel s and lyophilized al ogeneic bone. Densitometry with CT and Micro-CT was conducted 4, 12, and 24 weeks after surgery. RESULTS AND CONCLUSION:Compared with the control group, the bone density of the mandible was significantly higher in the experimental group at 12 weeks after transplantation (P<0.05). Over time, the bone densities in the two groups were both increased, but the bone density in the experimental group was always higher than that in the control group. Bone structure parameters were progressively increased or decreased in the two groups, especial y in the experimental group. At 24 weeks after surgery, the degree of trabecular separation in regions of interest was higher in the experimental group than the control group (P<0.05), but the bone volume fraction, number of trabecular bone, and bone trabecular thickness were significantly lower in the experimental group than the control group (P<0.05). These findings indicate that bone marrow mesenchymal stem cel s are capable of accelerating the reconstruction of al ogeneic bones.

Objective To investigate the effect of isoflurane preconditioning on rat learning and memory in cerebral ischemia-reperfusion injury and its possible mechanism.Methods Thirty-six adult male Sprague-Daw ley rats w ere randomly divided into a sham operation group, a cerebral ischemia-reperfusion group, and an isoflurane preconditioning group (n=12 in each group). A model of middle cerebral artery occlusion and ischemic-reperfusion w as induced by a modified intraluminal suture method. The rats of the isoflurane preconditioning group inhaled 1.5%isoflurane for 1 hour per day for 5 d. At 24 h after the last preconditioning, a model of MCAO w as made. At 24 h after MCAO, the infarct volume w as detected by using 2,3,5 chlorinated diphenyl tetrazolium staining. At day 1, 3, 7, and 14 after MCAO, the modified Neurological Severity Score (mNSS) were performed. At day 9 after MCAO, the Morris w ater maze test w as used to evaluate the learning and memory of rats. At day 14, Western blotting w as used to detect the protein expression level of hippocampal tissue glutamate receptor 1 (GluR1) on the side of ischemia. Results No obvious infarcts w ere observed in the rats of the sham operation group. The infarct volume in the isoflurane preconditioning group w as significantly smal er than that of the cerebral ischemia-reperfusion group (26.383%±3.128%vs.19.107%±1.661%;P<0.05). No neurological deficit w as observed in the sham operation group (score 0). The mNSS scores at day 1, 3, 7, and 14 after MCAO in the isoflurane preconditioning group w ere decreased significantly (day 1:9.000 ±1.195 vs.11.500 ±1.414;day 3:6.6250 ±1.407 vs.6.625 ±1.407vs.6.625 ±1.407; day 7: 5.875 ±0.707 vs.7.375 ±1.407; and day 14:3.375 ±1.187 vs.5.125 ±1.246;al P<0.05). The Morris w ater maze show ed that the escape latencies at day 1-5 after MCAO in the isoflurane preconditioning group w ere al significantly shorter than those in the cerebral ischemia-reperfusion group (day 1: 95.992 ±15.734 s vs.103.008 ±11.654 s; day 2: 70.949 ±14.708 s vs. 94.705 ±14.709 s;day 3:39.660 ±7.413 s vs.65.716 ±10.155 s;day 4:22.692 ±5.778 s vs.35.240 ±8.553 s;day 5: 14.906 ±4.336 s vs.22.890 ±10.381 s; al P<0.05). The numbers of crossing platform (4.556 ± 1.333 vs.2.889 ±1.536 ) and the percentages of time spent in the target quadrant ( 33.014%±5.223%vs. 21.978%±6.697%) in the isoflurane preconditioning group w ere significantly increased than in the cerebral ischemia-reperfusion group (al P<0.01). The levels of hippocampal GluR1 protein on the ischemic sides in the sham operation group, ischemia-reperfusion group, and isoflurane preconditioning group w ere 0.871 ±0.153, 0.456 ±0.130, and 0.689 ±0.126, respectively. There w ere significant differences among the 3 groups ( F=18.329, P<0.001) and the isoflurane preconditioning group w as significantly higher than the ischemia-reperfusion group (P<0.05). Conclusions Isoflurane preconditioning can improve the learning and memory in cerebral ischemia-reperfusion in rats, its mechanism may be associated w ith the uprelagating GluR1 expression in the hippocampus.

OBJECTIVETo investigate the effect of segmental defects reconstruction of canine mandible with allogenenic bone marrow mesenchymal stem cells (BMSC) combined with lyophilized bone.

METHODSA 30 mm segmental defect was created on the left mandibles of beagles. Beagles were randomly divided into three groups. Allogeneic bone marrow mesenchymal stem cells with lyophilized bone were used for segmental defects reconstruction in group A. Autologous bone marrow mesenchymal stem cells with freeze- dried bone were used for segmental defects reconstruction in group B. The defects of group C were repaired with lyophilized bone only. Every three beagles were sacrificed 4, 12, 24, and 48 weeks after surgery respectively. The reconstruction effect was evaluated by CT and histopathological examination.

RESULTSCT examination showed that new bones formed in group A and group B 12 weeks after surgery, but not in group C. The form of the reconstructed mandibles in the three groups recovered in 48 weeks. The small pores on the bone graft were filled with new bones in group A and group B. In group C, the pores were still evident. Histopathological examination showed that bone trabecula between allogeneic bone and autogenous bone was completely joined in group A and group B. A large number of fibrous tissue appeared around the implanted bone and new bones were formed. In group C, the lyophilized bone resorption was still not obvious, the new bone formation was significantly slower than the other two groups. There was no difference between group A and group B.

CONCLUSIONSBoth allogeneic bone marrow mesenchymal stem cells and autologous mesenchymal stem cells could accelerate the bone formation.

Allografts ; Animals ; Bone Transplantation ; Dogs ; Mandibular Reconstruction ; methods ; Mesenchymal Stem Cell Transplantation ; Osteogenesis ; Time Factors ; Tissue Engineering ; methods

Objective To explore the repair of the open compound wounds in lower extremities caused by multiple factors. Methotis Transplantation of cutaneous.musculo-cutaneous or greater omentum flaps were applied to 155 patients of open compound lower extremity wounds. Results The wound healing rate following first operation was 50% and that following two operations was 14.8%.While the wounds were healed in 7.7% of patients after three operations. Conclusion Transplantations of cutaneous,musculo-cutaneous or greater omentum flaps ale effective to repair and reconstruct the open compound lower extremity wounds.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

OBJECTIVETo present a new method for correction of prominent malar complex by L-shaped osteotomy through an intraoral incision.

METHODSBased on the anatomical characteristics of the malar complex, we designed a new L-shaped osteotomy for malar eminence reduction. The procedure includes oblique incision of the upper part of the mala, vertical incision of the anterior part of the mala and "greenstick" fracture of the zygomatic arches. According to the severity of malar prominence, we resect part of the anterior-inferior part of the mala and lower the malar complex.

RESULTSThis method was used in 39 patients with prominent malar complex. Of them, 32 were symmetrical and 7 were unsymmetrical. All the patients obtained good results.

CONCLUSIONL-shaped osteotomy for correction of prominent malar complex is a relatively ideal surgical method with the advantages of simpler manipulation, fewer complications, better result, and ensuring the intactness of the structural characteristics of the malar complex.

Adult ; Female ; Humans ; Male ; Osteotomy ; methods ; Surgery, Plastic ; methods ; Treatment Outcome ; Zygoma ; surgery

OBJECTIVES: To explore the effects of hypoxic and hypobaric conditions on blood gas and erythrocyte-related indicators in rats. METHODS: SD male rats were exposed to low-pressure hypoxic conditions simulating an altitude of 6500 m in a small or a large experimental cabin. Abdominal aortic blood samples were collected and blood gas indicators, red blood cells (RBCs) count, and hemoglobin (Hb) content were measured. The effects of exposure to different hypoxia times, different hypoxia modes, normal oxygen recovery after hypoxia, and re-hypoxia after hypoxia preconditioning on blood gas indicators, RBCs count and Hb content were investigated. RESULTS: The effect of blood gas indicators was correlated with the length of exposure time of hypoxia and the reoxygenation after leaving the cabin. Hypoxia caused acid-base imbalance and its severity was associated with the duration of hypoxia; hypoxia also led to an increase in RBCs count and Hb content, and the increase was also related to the time exposed to hypoxia. The effects of reoxygenation on acid-base imbalance in rats caged in a small animal cabin were more severe that those in a large experimental cabin. Acetazolamide alleviated the effects of reoxygenation after leaving the cabin. Different hypoxia modes and administration of acetazolamide had little effect on RBCs count and Hb content. Normal oxygen recovery can alleviate the reoxygenation and acid-base imbalance of hypoxic rats after leaving the cabin and improve the increase in red blood cell and hemoglobin content caused by hypoxia. The improvement of hypoxia preconditioning on post hypoxia reoxygenation is not significant, but it can alleviate the acid-base imbalance caused by hypoxia in rats and to some extent improve the increase in red blood cell and hemoglobin content caused by hypoxia. CONCLUSIONS Due to excessive ventilation and elevated RBCs count and Hb content after hypoxia reoxygenation, oxygen partial pressure and other oxygenation indicators in hypoxic rats are prone to become abnormal, while blood gas acid-base balance indicators are relatively stable, which are more suitable for evaluating the degree of hypoxia injury and related pharmacological effects in rats.
Rats ; Animals ; Male ; Acetazolamide ; Hypoxia ; Oxygen ; Erythrocytes ; Hemoglobins ; Acid-Base Imbalance