Osteoblast Response to Copper-Doped Microporous Coatings on Titanium for Improved Bone Integration.

Due to their excellent mechanical properties and good biocompatibility, titanium alloys have become a popular research topic in the field of medical metal implants. However, the surface of the titanium alloy does not exhibit biological activity, which may cause poor integration between the interface of the titanium implant and the interface of the bone tissue and subsequently may cause the implant to fall off. Therefore, surface biological inertness is one of the problems that titanium alloys must overcome to become an ideal orthopedic implant material. Surface modification can improve the biological properties of titanium, thereby enhancing its osseointegration effect. Copper is an essential trace element for the human body, can promote bone formation and plays an important role in maintaining the physiological structure and function of bone and bone growth and development. In this study, a microporous copper-titanium dioxide coating was prepared on the surface of titanium by microarc oxidation. Based on the evaluation of its surface characteristics, the adhesion, proliferation and differentiation of MC3T3-E1 cells were observed. A titanium rod was implanted into the rabbit femoral condyle, and the integration of the coating and bone tissue was evaluated. Our research results show that the microporous copper-titanium dioxide coating has a nearly three-dimensional porous structure, and copper is incorporated into the coating without changing the structure of the coating. In vitro experiments found that the coating can promote the adhesion, proliferation and differentiation of MC3T3-E1 cells. In vivo experiments further confirmed that the titanium copper-titanium dioxide microporous coating can promote the osseointegration of titanium implants. In conclusion, copper-titanium dioxide microporous coatings can be prepared by microarc oxidation, which can improve the biological activity and biocompatibility of titanium, promote new bone formation and demonstrate good osteoinductive properties. Therefore, the use of this coating in orthopedics has potential clinical application.

Ulinastatin protects brain against cerebral ischemia/reperfusion injury through inhibiting MMP-9 and alleviating loss of ZO-1 and occludin proteins in mice.

BACKGROUND: The effects of Ulinastatin (UTI) on the blood-brain barrier (BBB) in the acute phase of cerebral ischemia/reperfusion (I/R) are not clear. This study was to investigate the potential protective effects of UTI on the BBB and the underlying mechanisms. METHODS: Male CD-1 mice were subjected to transient middle cerebral artery occlusion (tMCAO) and randomly assigned to four groups: Sham (sham-operated), tMCAO (tMCAO+0.9% saline), UTI-L (tMCAO+UTI 1500U/100g) and UTI-H (tMCAO+UTI 3000U/100g) group. UTI was administered immediately after reperfusion in the UTI-L and UTI-H groups. At 24h after reperfusion, the neurological deficit, brain water content, and infarct volume were determined. Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to examine the expression of matrix metalloproteinase (MMP)-9, Zonula occludens-1 (ZO-1) and occludin in ischemic cerebral cortex. The integrity of the BBB was assessed by the leakage of Evans blue. RESULTS: Compared with tMCAO group, both UTI-L and UTI-H groups showed significantly (P<0.001) ameliorated the neurological deficit (2.00±0.71 and 1.60±0.55 vs. 4.60±0.55), lessened brain water content (82.99%±0.21% and 82.05%±0.59% vs. 84.28%±0.0.57%) and decreased the infarct volume (38.52%±1.72% and 24.78%±1.20% vs. 49.48%±1.93%). In addition, significantly (P<0.001) decreased expression of MMP-9 (0.48±0.06 and 0.37±0.05 vs.0.76±0.10 for protein and 2.88±0.23 and 2.17±0.16 vs. 3.90±0.24 for mRNA) and alleviated loss of ZO-1 (0.19±0.04 and 0.24±0.05 vs. 0.25±0.03) and occludin (0.74±0.08 and 0.87±0.07 vs. 0.94±0.06) proteins were observed in both UTI-L and UTI-H groups. CONCLUSION: UTI protects the brain against ischemic injury potentially via down-regulating the expression of MMP-9 and alleviating loss of ZO-1 and occludin proteins to restore the BBB permeability.

[Analysis of ring chromosome 9 syndrome with fluorescence in situ hybridization].

OBJECTIVE: To investigate the mechanism of the ring chromosome 9 formation by cytogenetic analysis of one case affected with ring chromosome 9 syndrome. METHODS: Routine chromosome GTG-binding analysis and dual-color fluorescence in situ hybridization (FISH) with TelVision 9p and 9q probes were applied to characterize the case. RESULTS: The G-binding revealed that the patient had ring chromosome 9 with the following karyotype: 45,X,-9/46,XX,r(9)(p24q34)/46,XX,r(9;9)(p24q34;p24q34)[4/92/4]. The dual-color FISH analysis with TelVision 9p and TelVision 9q probes failed to detect a hybridization signal on the ring chromosome in the case, which indicated that at least 115 kb were deleted on the terminal 9p and 95 kb were deleted on the terminal 9q. Comparing to the cases reported in the literatures, our patient shared some common features of the 9p- and 9q- syndrome. CONCLUSION: The clinical features of patients with identical r(9) breakpoints present variable phenotypes. The possible cause might be the submicroscopic variation in the deletion breakpoints, variation in the ring stability, the modification of the expression of the deleted by the individual's genetic background, or the effect of changes in the fetal environment. The haploinsufficiency of genes located in the deleted regions may play critical roles in the patient phenotype as well.

[Analysis of the small supernumerary marker chromosome in Turner syndrome with 45, X/46, X, + mar karyotype].

OBJECTIVE: To identify the origin and study the morphology of small supernumerary marker chromosome (sSMC) in Turner syndrome with 45, X/46, X, + mar karyotype. METHODS: Using the conventional chromosome G-banding technique, 10 cases of Turner syndrome with 45, X/46, X, + mar chromosome karyotype were obtained, dual-color fluorescence in situ hybridization was applied to study the origin and morphology of the sSMC. RESULTS: In the 10 cases of Turner syndrome with 45, X/46, X, + mar karyotype, the sSMC of 7 cases was derived from X chromosome [sSMC(X)], the sSMC of 2 cases was derived from Y chromosome [sSMC(Y)] and the remaining 1 case was derived from the autosome. There were 4 cases of ring(r) chromosomes and 3 of centric minutes (min) in the 7 sSMC (X) cases. In the 2 sSMC(Y), one case was dicentric (dic) and the other was centric minute (min). The sSMC originated from the autosome was a centric minute (min). CONCLUSION: The origin of sSMC of Turner syndrome with 45, X/46, X, + mar karyotype was almost all from sex chromosomes, and rarely from autosomes. sSMC can exist as isodicentric, ring, or centric minute. The molecular cytogenetic features of the sSMC can provide useful information for genetic counseling, prenatal diagnosis and treatment of the Turner syndrome patients with a 45, X/46, X, + mar karyotype.

[Cytogenetic analysis and phenotype location analysis on the karyotype of a ring chromosome 21 syndrome].

OBJECTIVE: To search the forming cause and the correlation between the clinical phenotype and chromosome band by the cytogenetic analysis on a case of ring chromosome 21 syndrome. METHODS: Identification and location of 21 ring chromosome were performed with the G-banding, C-banding, N-banding, high-resolution banding and fluorescence in situ hybridization (FISH) techniques. RESULTS: It was found that the karyotypes of the patient's parents are normal. The patient's karyotype is 46,XY, r(21)[91]/46,XY,r(21;21)(p11q22.3;p11q22.3) [5]/45,XY,-21[4]. CONCLUSION: The clinical phenotype of ring chromosome 21 syndrome is related to the deletion of distal segment of 21q, and the abnormal sexual development of male is related with the deletion of 21q22.3.