BACKGROUND: In the process of bone defect repair, as their respective shortcomings, both autograft and al ograft cannot obtain satisfactory outcomes. OBJECTIVE: To observe the effect of soft composite materials for bone regeneration established in vitro in skul defect repair. METHODS: Soft composite materials for bone regeneration (bone morphogenetic protein 7-derived polypeptide, chitosan, nano hydroxyapatite and col agen) were established in vitro. Twenty-four Sprague-Dwley rats were enrol ed to prepare skul defect models, and were randomly equivalently divided into two groups. The rats were repaired with chitosan/nano hydroxyapatite/col agen composite materials as control group, and those repaired with soft composite materials of bone regeneration as experimental group. RESULTS AND CONCLUSION: The soft composite material of bone regeneration exhibited a loose and porous structure and bone morphogenetic protein 7-derived polypeptide was released in a gradual y rising trend. Compared with the control group, bone mineral density of the defect region in the experimental group was higher, which was similar with that of the normal bone tissue, and additional y numerous newborn bones could be found. These results show that the soft bone regeneration composite material exerts a better repair effect in skul defect.

BACKGROUND:Percutaneous vertebroplasty for treatment of osteoporotic vertebral compression fractures has achieved very good results.
OBJECTIVE:To discuss and resolve some problems related to thoracic and lumbar vertebroplasty.
METHODS:225 patients (78 males and 147 females) aged 53 to 92 years old were included in this study. They al accepted percutaneous vertebrolplasty and we observed and made a record about some questions related this surgery during perioperative period.
RESULTS AND CONCLUSION:Six cases (2.7%) missed diagnosis. More than two-third of the compression degree were found in sixteen cases (7.1%). Forty-five (12.8%) vertebrae suffered from bone cement leakage in twenty-nine cases (12.9%). Recurrent fractures appeared in ten cases (4.4%). Multiple vertebrae fractures appeared in seventy-nine cases (35.1%). (1) Strategies for missed diagnosis:conduct preoperative physical examination careful y;avoid missing the point of pain;increase MRI scanning when necessary. (2) Coping strategies for severe vertebral fractures:place the needle into the paral el endplates as far as possibly;puncture along the lumbar spine pedicle base and the lateral thoracic pedicle. (3) Coping strategies for cement leakage:when cement leakage over the lower edge of the end plate occurred in operation, we should immediately put the C-arm X-ray machine into anteroposterior position to determine the orientation of the leakage and stop injecting;we should continue to inject the bone cement into the no leak-side to ensure the fil ing amount of vertebral bone cement. (4) Coping strategies for recurrent fractures:reoperation. (5) Coping strategies for multiple fractures:patients with multiple fractures often have a feature of poor constitution and more complications. So, it is necessary to shorten the operation time, and determine unilateral or bilateral puncture ways depending on the degree of vertebral compression to save operation time.

OBJECTIVE To explore the key mechanism of Bazi Bushen capsule(BZBS)in delaying the senescence of mesenchymal stem cells(MSCs)through network pharmacology and in vitro experiments.METHODS Network phar-macology was used to predict the mechanism targets of BZBS in delaying MSCs senescence.A MSCs senescence model induced by D-galac-tose(D-gal)was used to investigate the effect and mechanism of BZBS on MSCs senescence in vitro.RESULTS Network pharmacology analy-sis showed that BZSB could delay MSCs senes-cence.The experiment showed that BZBS could significantly improve the survival activity of the aged MSCs.It significantly reduced the positive rate of β-galactosidase staining and p16,p21 expression in aged MSCs,enhanced the ability of adipogenic differentiation and osteogenic differ-entiation,and increased expression of Nanog,OCT4 and SOX2 in senescent MSCs.CONCLU-SIONS Network pharmacology and in vitro cell experiments verified that BZBS could delay MSCs senescence.

Objective:To investigate the role of dendritic cells (DC) in Chlamydia muridarum ( Cm) respiratory infection and their effect on adaptive immune response. Methods:C57BL/6 mice were exposed to 1×10 3 inclusion-forming units (IFU) of Cm through inhalation to establish the mouse model of Cm respiratory infection. The proportion of CD11c + MHCⅡ + DC and the expression of costimulatory molecules (CD40, CD80 and CD86) in spleen tissues were detected by flow cytometry on 0, 3 and 7 d after infection. The expression of IL-12p40, IL-10 and IL-6 at mRNA level in spleen tissues was detected by qPCR. Mouse splenic DC isolated on 7 d after Cm infection were sorted by magnetic beads and then transferred to recipient mice. Th1 response in the recipient mice was measured using intracellular cytokine staining 14 d after infection. Results:Cm respiratory infection induced massive infiltration of DC and promoted the expression of costimulatory molecules on splenic DC. The expression of IL-12 and IL-10 at mRNA level in splenic DC reached the peak on 3 d after infection. Transferring the splenic DC of Cm-infected mice into the recipient mice could alleviate the disease condition in the recipient mice after Cm infection with reduced Cm inclusion-forming units in lung tissues and significantly increased proportion of Th1 cells in lung and spleen tissues. Conclusions:Cm respiratory infection could induce the maturation and activation of DC, which promoted Th1 immune response. DC played an important role in Cm infection.

Objective:To investigate the effects of Chlamydia muridarum ( Cm) respiratory tract infection on the infiltration and polarization of alveolar macrophages (AMs) and pulmonary interstitial macrophages (IMs). Methods:A C57BL/6 mouse model of Cm respiratory tract infection was established through nasal inhalation. Flow cytometry was used to detect AMs (CD45 + F4/80 + CD11c + ) and IMs (CD45 + F4/80 + CD11c -) in lung tissues at 0, 3, 7 and 14 d after Cm respiratory tract infection. The proportions of M1 (CD80 + , CD86 + , MHCⅡ + , iNOS + ) and M2 (CD206 + , Arg1 + ) macrophages in AMs and IMs were also detected. Results:(1) Cm respiratory tract infection induced the infiltration of AMs and IMs. Compared with the uninfected group (0 d), the proportions and the numbers of AMs and IMs of were significantly increased 3 d after infection ( P<0.05, P<0.01). The numbers of AMs and IMs reached the peak 7 d after infection ( P<0.001). (2) Compared with the uninfected group, the proportions of CD80 + and CD86 + cells in AMs were significantly up-regulated 3 d after infection ( P<0.05, P<0.01); the proportion of MHCⅡ + cells in AMs increased after infection and reached the peak at 14 d ( P<0.05), while the proportion of CD206 + cells decreased after infection ( P<0.05). (3) Compared with the uninfected group, the proportions of CD80 + and CD86 + cells in IMs were increased 3 d after infection ( P<0.05, P<0.001) and the proportion of MHCⅡ + cells was significantly increased 14 d after infection ( P<0.01), while there was no significant change in the proportion of CD206 + cells. (4) In AMs, the proportion of iNOS + cells increased continuously after infection ( P<0.01), while the proportion of Arg1 + cells decreased continuously after infection, especially at 7 d and 14 d ( P<0.05). In IMs, the proportion of iNOS + cells reached the peak at 7 d ( P<0.001), but the proportion of Arg1 + cells showed no significant change after infection. Conclusions:Cm respiratory tract infection induced the infiltration of AMs and IMs, stimulated the polarization of AMs and IMs towards the M1 phenotype and weakened the polarization of AMs to M2 macrophages, but had no significant influence on the polarization of IMs towards the M2 phenotype.

Objective:To investigate the infiltration and polarization of macrophages in mice during Chlamydia muridarum ( Cm) respiratory infection. Methods:C57BL/6 mice were intranasally infected with 1×10 3 inclusion-forming units (IFU) of Cm to establish the mouse model of Cm respiratory tract infection. The percentages of CD45 + F4/80 + cells and the macrophages expressing CD86, major histocompatibility complex Ⅱ (MHC), inducible nitric oxide synthase (iNOS) and CD206 were detected by flow cytometry. Expression of iNOS, CD206 and CCL2 at mRNA level was detected by real-time quantitative PCR. Results:Cm respiratory tract infection induced the increase of macrophages in mouse lung tissues. Compared with uninfected group, CD45 + F4/80 + macrophages were increased significantly from day 3 and reached the peak on day 7 after Cm infection. Moreover, the expression of CD86, MHCⅡ and CCL2 was increased, and the macrophages were polarized to M1 phenotype. However, the expression of M2 macrophage marker CD206 was decreased gradually. Further studies showed that iNOS expression, the indicator of M1 macrophage activation, was increased after Cm infection and reached to the top on day 7. Conclusions:Cm respiratory infection could induce the infiltration of macrophages in lung tissues and promote the polarization of macrophages to M1 phenotype.

Child ; Consensus ; Drugs, Chinese Herbal ; Humans ; Medicine, Chinese Traditional ; Respiratory System