Applied anatomy of human periobital region / 中华整形外科杂志

Objective@#To observe the anatomical layers and important vascular structures in the main periorbital regions of the human body, and to provide some anatomical basis for clinical periorbital fat injection.@*Methods@#During January 2018 to December 2018, 12 (24 sides) cadavers (6 males and 6 females, 47.5±11.7 years old) were selected. Their orbital tissues were dissected routinely and microdissected. The important blood vessels and tissues around the orbit were measured by electronic vernier caliper. The related matters needing attention in fat injection filling were analyzed according to references.@*Results@#The main structural areas around the orbit included eyelid, eyebrow and lacrimal groove deformities. The thickness of eyelid skin was (0.09±0.03) mm. The thickness of eyebrow skin was (3.45±0.38) mm. Vascular (diameter ranged from 1 mm to 3 mm) distribution was abundant in this area. The inner diameter of dorsal nasal artery, supraorbital artery and trochlear artery were (0.73±0.42) mm, (0.88±0.37) mm and (0.71±0.51) mm respectively. Facial artery, maxillary artery and superficial temporal artery with internal diameters of (2.96±0.88) mm, (1.92±0.33) mm and (1.35±0.15) mm, respectively.@*Conclusions@#The entrance of upper eyelid injection is usually in the eyebrow tail or middle eyebrow, and fat is injected into the deep surface of orbicularis oculi muscle. The injection range is limited to the medial 2/3 of upper eyelid, the medial 1/3 of lower eyebrow and the lateral part of eyebrow. It is suggested that single layer microinjection of fat (0.5 ml to 1.5 ml) could be used. Lower eyelid fat transplantation is mainly used to correct deformities at the eyelid-cheek junction. The aim is to reduce the V-shaped deformity at the eyelid-cheek junction by increasing the fullness. Injection can be made by blunt needle into the inner, outer and middle part of the deformity. Fat can be injected into SOOF layer or periosteum in the palpebral and cheek sulcus area. The injection volume is 0.5-1.0 ml.

Clinical observation of partial nasal alar cartilage reconstruction for nasal tip contour improvement / 中华整形外科杂志

Objective@#To observe the effect of partial nasal alar cartilage reconstruction with autogenous costal cartilage for nasal tip contour improvement.@*Methods@#From Feb. 2014 to Mar. 2016, 82 Chinese Han patients received rhinoplasty, including the requirement of nasal tip contour improvement. The cortical slices(0.1 cm in thickness) were used to augment the medial and middle crus of alar cartilage.@*Results@#Eighty-two cases were followed up for 11.7 months in average. One case(1.1%) with tip projection reduction and 2 cases(2.3%) with superior rotation of nasal tip underwent secondary operation with satisfactory result. Good result was achieved in all the other patients with no complication.@*Conclusions@#Partial nasal alar cartilage reconstruction with autogenous costal cartilage is effective for improvement of nasal tip contour in Orientals.

Clinical efficacy of short nose lengthening by using autologous costal cartilage / 中华医学美学美容杂志

Objective To explore the clinical efficacy of applying autologous costal cartilage in lengthening the short nose.Methods Bilateral extended spreader grafts (ESG) and columellar strut grafts were performed by using autologous costal cartilage in 253 patients with short nose,which increased nasal dorsal length and the support force of nasal tip;meanwhile,autologous costal cartilage was used for dorsal augmentation,alar rim retraction,and nasal tip modification.Results A total of 253 patients with short nose were satisfied with postoperative morphology,which presented elongated nasal dorsum,correction of nasal tip topspin,and normal nasal columella-lobular angle.6 months to 17 months follow-up was conducted,and nasal length and morphology showed stable,while 2 cases presented slight nasal tip decreasing,4 cases presented dorsal grafts warping;after revision surgery,the 6 patients had also got satisfactory results.Conclusions Correction of short nose using autologous costal cartilage can result in more stable nasal reconstruction structure,and can be used for the shape correction of other subunits of the nose,achieving at the comprehensive improvement of nasal morphology and functions.

In vitro activation of bone marrow natural killer T cells of aplastic anemia patients / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the quantitative and qualitative changes of TCRVα24(+)Vβ11(+) natural killer T (NKT) cells from bone marrow (BM) of aplastic anemia (AA) after in vitro stimulation of α-galactosylceramide (α-Galcer).</p><p><b>METHODS</b>NKT cells in the bone marrow mononuclear cells (BMMNCs) from either AA patients or healthy controls were enumerated with flow cytometry. BMMNCs were cultured in RPMI1640 medium supplemented with either α-Galcer and rhIL-2 or α-Galcer, rhIL-2 and rhG-CSF. The proliferative capacity of NKT cells was determined by NKT cell numbers before and after in vitro culture. Expression of intracellular IFNγ and IL-4 in activated NKT cells was analyzed with flow cytometry.</p><p><b>RESULTS</b>In AA group, the percentage of NKT cells in BMMNCs was (0.19 ± 0.09)%. Addition of rhG-CSF into the α-Galcer/rhIL-2 culture medium resulted in significantly reduced expansion of NKT cells (67.45 ± 29.42-fold vs 79.91 ± 40.56 fold, P < 0.05). Meanwhile, addition of rhG-CSF reduced IFNγ positive NKT cells \[(37.45 ± 7.89)% vs (62.31 ± 14.67)%, P < 0.01\] and increased IL-4 positive NKT cells \[(55.11 ± 12.13)% vs (27.03 ± 9.88)%, P < 0.01\]. In healthy control group, the percentage of NKT cells in BMMNCs was (0.25 ± 0.12)%. Addition of rhG-CSF into the α-Galcer/rhIL-2 culture medium also significantly reduced expansion of NKT cells (97.91 ± 53.22-fold vs 119.58 ± 60.49-fold, P < 0.05), reduced IFNγ positive NKT cells \[(28.65 ± 10.63)% vs (50.87 ± 12.66)%, P < 0.01\], and increased IL-4 positive NKT cells \[(66.53 ± 14.96)% vs (31.11 ± 10.07)%, P < 0.01\].</p><p><b>CONCLUSION</b>Compared to those from healthy controls, BMMNCs from AA patiants have a reduced fraction of NKT cells, which possesses a decreased potential to expand in vitro in response to α-Galcer stimulation, and produce more IFNγ(+) NKT1 cells. rhG-CSF, in combination with α-Galcer, confers polarization of NKT cells towards IL-4(+) NKT2 subpopulation.</p>

Changes of gene expression profile in homoharringtonine-induced leukemia multi-drug resistant cell line K562/HHT / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the resistant related molecules of human leukemia drug resistant K562 cells (K562/HHT) induced by homoharringtonine (HHT).</p><p><b>METHODS</b>Gene expression profiles on K562/HHT, K562 and K562/HHT/RU486 (K562/HHT reversed by RU486) cells were detected by DNA microarray. The bone marrow tyrosine kinase gene in chromosome X (BMX) which changed dynamically among the three cells was confirmed by RT-PCR and Western blot. Then, BMX was transfected into K562 and K562/HHT cells, and the changes of daunorubicin (DNR) concentrations in these two cells were observed for BMX overexpression.</p><p><b>RESULTS</b>As compared with K562, there were changes in 117 gene expressions in K562/HHT, 57 of which were up-regulated and 60 down-regulated. The mdrl gene was significantly up-regulated. When compared with K562/HHT, 50 significantly differently expressed genes were screened out in the K562/HHT/RU486 cells, of which up- and down-regulated genes were 13 and 37 respectively. These genes involved in drug resistance, cell signaling, cell differentiation, cell proliferation, transcription regulator, ion transport and so on. Four genes [NM-001721 (BMX), NM-031459 (SESN2), NM-033642 (FGF13) and AL-049309 (SFRS12)] expressed significantly differently in the two group cells, BMX gene expression was higher in K562/HHT, than in K562, but lower than in K562/HHT/RU486 as confirmed by RT-PCR and Western blot. After the plasmid pCI-neo-BMX was transfected into K562 and K562/HHT cells, DNR concentration was significantly lower (79.28 +/- 4.04, 29.84 +/- 2.67) than those before transfection (158.52 +/- 8.08, 58.58 +/- 6.53).</p><p><b>CONCLUSION</b>BMX is associated with multi-drug resistance of K562/HHT cell line.</p>

Study of mifepristone on reversing multidrug resistance of leukemic cell line K562/A02 / 中华血液学杂志

<p><b>OBJECTIVE</b>To study whether progestogen antagonist mifepristone could reverse multidrug resistance of K562/A02 cells and its mechanisms.</p><p><b>METHODS</b>MTT was used to study the proliferation of K562/A02 cells and sensitivity of K562/A02 cells to ADM after 72 hours treatment with mifepristone. Flow cytometry was used to assay the expression of P-glycoprotein and the mean fluorescent intensity of intracellular daunorubicin. The expressions of apoptosis related proteins (bcl-2, Bax and caspase-3) were assayed by immunohistochemistry and the glucosylceramide synthase mRNA expression by RT-PCR before and after mifepristone treatment.</p><p><b>RESULTS</b>MTT assay revealed that 2.5, 5.0 and 10 micromol/L mifepristone did not affect the proliferation of K562/A02 cells, but enhanced the sensitivity of K562/A02 cells to ADM, by 1. 68-, 4.17- and 10.71- fold increase, respectively. Expression of P-gp in K562/A02 cells was (49.03 +/- 5.32)%, and was decreased to (28.60 +/- 2.13)% (P < 0.01) after 10 micromol/L mifepristone treatment for 72 hours. and intracellular DNR accumulation in K562/A02 was (61.07 +/- 8.61)%, and was increased to (92.72 +/- 3.48)% (P < 0.01). After 10 micromol/L mifepristone treatment, the expression of bcl-2 protein was decreased from (56 +/- 9)% to (37 +/- 6)% (P < 0.05), Bax and caspase-3 proteins was increased from (40 +/- 5)% to (87 +/- 10)% (P < 0.01), and from (36 +/- 7)% to (89 +/- 6)% (P < 0.01) respectively. RT-PCR analysis revealed that expression of glucosylceramide synthase mRNA was higher in K562/A02 than in K562 cells, whereas 10 micromol/L mifepristone significantly down-regulated its expression in K562/A02 cells.</p><p><b>CONCLUSION</b>Mifepristone at 10 micromol/L could dose-dependently reverse the multidrug resistance of K562/A02 cells. The possible mechanisms are related with decreasing the expression of P-gp, regulating the expression of apoptosis related proteins and decreasing the expression of glucosylceramide synthase.</p>

Improvement effect of bacterium derived oligonucleotides on maturation of K562/A02 cells derived dendritic cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the maturation effect of CpG2006 and phosphodiester oligonucleotides on leukemia-derived dendritic cells.</p><p><b>METHODS</b>Leukemia cells K562/A02 were induced into dendritic cells by rhGM-CSF and rhIL-4. After 7 days induction, the cell-morphology was observed, the immunophenotype of cells was detected by flow cytometry and the cell function was evaluated by allogeneic mixed lymphocyte reactions, CTL responses and secretion of IL-12 and IL-6. Then a CpG oligonucleotide CpG2006, two synthetic bacterial phosphodiester oligonucleotides A-ODN and T-ODN were added to these leukemia-derived DCs. Three days later, the DCs were re-detected by the above-mentioned methods.</p><p><b>RESULTS</b>After induced by CpG2006, A-ODN or T-ODN, the leukemia-derived DCs with typical dendritic morphology were increased. The expressions of CD83, HLA-DR and CD86 were (65.5 +/- 8.4)%, (32.0 +/- 4.3)% and (18.6 +/- 3.2)% respectively in day 7 leukemia-derived DCs, raised to (88.9 +/- 3.6)%, (53.9 +/- 3.2)% and (39.9 +/- 7.3)% respectively after exposing CpG2006 for 3 days; increased to (97.0 +/- 5.3)%, (63.9 +/- 7.3)% and (40.2 +/- 7.4)% respectively after treated by A-ODN; and further increased to (93.26 +/- 4.65)%, (58.3 +/- 5.6)% and (36.2 +/- 6.8)% respectively after treated by T-ODN. These results was markedly different than unaffected cells did. These DCs induced by the above-mentioned three oligonucleotides could upregulate significantly the capacity for stimulating allogeneic T cells. They could also induce CTL to generate specific cytotoxic activity against K562/A02 cells. The secretion of IL-6 and IL-12 was increased remarkably.</p><p><b>CONCLUSION</b>CpG2006, as well as two phosphodiester oligonucleotides can induce leukemia-derived DCs maturation.</p>