复方利多卡因乳膏在儿童口腔颌面表浅小手术中的应用

目的：探讨复方利多卡因乳膏在儿童口腔颌面表浅小手术中应用的效果。方法：72例5～12岁口腔颌面表浅小手术患儿平均分为两组,分别给予复方利多卡因软膏表面麻醉和盐酸利多卡因注射液局部浸润麻醉,运用Wong—Baker面部表情分级量表比较两组麻醉时和手术时的疼痛情况。结果：使用复方利多卡因软膏组的患儿在实施麻醉过程中,疼痛评分明显低于盐酸利多卡因注射液组,而在手术过程中两组的疼痛评分没有统计学差异。结论：复方利多卡因软膏可以应用于儿童口腔颌面表浅小手术的表面麻醉。     

NBS1在口腔鳞癌组织中的表达及意义

目的:检测口腔鳞癌组织(OSCC)中NBS1的表达水平,探讨其与OSCC病理分化级别的相关性以及在肿瘤发生发展中的作用。方法:①采用免疫组化(SP法)检测NBS1蛋白在30例口腔鳞癌组织、9例癌旁组织中的表达。②应用RT-PCR技术检测组织中NBS1的mRNA表达水平。结果:在OSCC与癌旁正常组织中,NBS1 mRNA和蛋白表达差异显著,在口腔癌组织中均表达较高,并随着病理级别增高而增高(P<0.05)。结论:NBS1在不同病理分化程度OSCC中表达水平的差别与多种因素密切相关,与肿瘤的恶性生物学行为有关,其表达水平可成为判断口腔鳞癌侵袭转移和预后的指标之一。     

三种定位方法在腹腔镜结直肠肿瘤手术中的应用效果

目的评价术前亚甲蓝定位、金属夹定位和术中纤维结肠镜定位在腹腔镜结直肠肿瘤手术中的应用效果。方法复旦大学附属肿瘤医院2009年12月至2012年6月间收治的64例结直肠肿瘤患者在行腹腔镜手术前进行了肿瘤定位,其中术前2h内4点法亚甲蓝定位23例,术前1d金属夹定位20例,术中纤维结肠镜定位21例,定位后行腹腔镜结直肠肿瘤根治性手术、肠段切除或局部切除术。结果所有手术均获成功,无手术死亡和并发症发生。术前亚甲蓝定位标记成功率为82．6％（19／23）,2例因亚甲蓝弥散导致组织界限不清行中转开腹手术,2例肿瘤因腹腔面肠壁无亚甲蓝显色而无法定位,遂于术中加行纤维结肠镜定位。术前金属夹定位标记成功率为85．0％（17／20）,2例乙状结肠肿瘤和1例直肠上段肿瘤因无法确定下切缘而于术中加行纤维结肠镜定位。术中肠镜定位标记成功率为95．2％（20／21）,1例因病灶为长蒂腺瘤未能准确定位。对于术前亚甲蓝和金属夹定位失败而加行术中结肠镜定位的5例患者中,2例准确定位并成功施行腹腔镜手术;1例因病灶为长蒂腺瘤未准确定位;2例定位准确但因小肠和结肠胀气明显,手术空间不足致中转开腹手术。结论上述3种定位方法用于腹腔镜结直肠肿瘤手术均可获得较为满意的定位效果。临床实践中应根据肿瘤位置和拟行的手术方式来选择适宜的肿瘤定位方法。     

氟通过胞外信号调控激酶通路对成骨细胞增殖作用的影响

目的 观察氟通过胞外信号调控激酶(ERK)通路对成骨细胞(MC3T3-E1)增殖作用的影响.方法 取小鼠成骨细胞(MC3T3-E1)进行体外培养,加入不同浓度的氟(Fˉ,0、200、400、600、1000、2000、4000、8000、10 000 μmol/L)培养24、48 h,甲基噻唑蓝(MTT)法筛选出促进细胞增殖的最适浓度.根据最适浓度,将成骨细胞单纯随机分为3组:对照组(Fˉ,0 μmol/L)、染氟组(Fˉ,400 μmol/L)、染氟抑制组(Fˉ,400 μmol/L+PD9805,10 μmmol/L).培养48 h后应用流式细胞术检测各组细胞周期;Western bolt法和免疫荧光法检测各组磷酸化ERK(P-ERK)蛋白表达.结果 400 μmol/L的氟是促进成骨细胞增殖的最适合浓度.与对照组比较[(76.12±10.08)％、(2.06±0.31)％],染氟组G0/G1期细胞数[(63.04±8.12)％]明显减少,S期细胞数[(9.13±2.08)％]明显增多(P均＜ 0.05);而染氟抑制组G0/G1期细胞数[(92.11±9.01)％]明显增多(P＜0.05).Western blot结果表明,与对照组[(100.00±0.00)％]比较,染氟组成骨细胞P-ERK蛋白表达水平[(131.24±13.88)％]明显增高(P＜0.05),染氟抑制组P-ERK蛋白表达[(91.33±9.68)％]未见明显改变(P＞0.05);免疫荧光法检测结果与Western blot法相似.结论 400 μmol/L氟可以促进成骨细胞增殖,ERK通路在氟促进成骨细胞的增殖作用中起到了关键的作用.     

Immune response gene function correlates with the expression of an Ia antigen. II. A quantitative deficiency in A(e):E(a), complex expression causes a corresponding defect in antigen-presenting cell function

A series of experiments were performed to explore the role of complementing major histocompatability complex (MHC)-linked immune response Ir genes in the murine T cell proliferative response to the globular protein antigen pigeon cytochrome c. The functional equivalence of I-E-subregion-encoded, structurally homologous E(a) chains from different haplotypes bearing the serologic specificity Ia.7 was demonstrated by the complementation for high responsiveness to pigeon cytochrome c of F(1) hybrids between low responder B 10.A(4R) (I-A (k)) or B 10.S (I-A(8)) mice and four low responder E(a)- bearing haplotypes. Moreover, this Ir gene function correlated directly with both the ability of antigen-pulsed spleen cells from these same F(1) strains to stimulate pigeon cytochrome c-primed T cells from B10.A or B10.S(9R) mice, and with the cell surface expression of the two-chain Ia antigenic complex, A(e):E(a), bearing the conformational or combinatorial determinant recognized by the monoclonal anti-Ia antibody, Y-17. The B 10.PL strain (H-2(u)), which expresses an Ia.7-positive I-E- subregion-encoded E(a) chain, failed to complement with B10.A(4R) or B10.S mice in the response to pigeon cytochrome c. However, (B10.A(4R) × B10.PL)F(1) and (B10.S × B10.PL)F(1) mice do express A(k)(e):E(u)(a) and A(8)(e):E(u)(a) on their cell surface, although in reduced amounts relative to A(k,s)(e):E(k,d,p,r)(a) complexes found in corresponding F(1) strains. This quantitative difference in Ia antigen expression correlated with a difference in the ability to present pigeon cytochrome c to B 10.A and B 10.S(9R) long-term T cell lines. Thus, (B10.A(4R) × B10.PL)F(1) spleen cells required a 10-fold higher antigen dose to induce the same stimulation as (B10.A(4R) × B10.D2)F(1) spleen cells. In addition, the monoclonal antibody, Y-17, which reacts with A(e):E(a) molecules of several strains, had a greater inhibitory effect on the proliferative response to pigeon cytochrome c of B10.A T cells in the presence of (B10.A(4R) X B10.PL)F(1) spleen cells than in the presence of (B10.A(4R) X B10.D2)F(1) spleen cells. These functional data, in concert with the biochemical and serological data in the accompanying report, are consistent with the molecular model for Ir gene complementation in which appropriate two-chain Ia molecules function at the antigen-presenting cell (APC) surface as restriction elements. Moreover, they clearly demonstrate that the magnitude of the T cell proliferative response is a function of both the concentration of nominal antigen and of the amount of Ia antigen expressed on the APC. Finally, the direct correlation of a quantitative deficiency in cell surface expression of an Ia antigen with a corresponding relative defect in antigen-presenting function provides strong independent evidence that the I-region-encoded Ia antigens are the products of the MHC-linked Ir genes.     

Unbound immunoglobulins are a major source of error in the quantitation of platelet surface-bound immunoglobulin levels

Analysis of assays for the determination of platelet-associated immunoglobulins (PAIgs) has led to disagreement over the amount of surface-bound Igs in both normal controls and patients with elevated platelet Ig levels. By the use of radiolabeled platelets and platelet counts, it was demonstrated that more than 10(8) platelets are disrupted after each centrifugation during platelet isolation procedures, releasing intraplatelet contents into the fluid phase of resuspended platelets in buffer. It was shown that suspensions of whole washed platelets contain a significant, but generally overlooked, amount of unbound Igs that have been liberated from platelets disrupted during processing. When platelet suspensions are evaluated for Igs with assays that fail to incorporate a final separation of whole platelets from the suspension fluid, unbound Igs as well as those bound to the platelet surface are measured, which yields a logarithmic overestimation of surface-bound Igs. It has been further demonstrated that patients infected with human immunodeficiency virus type 1 can have elevations of PAIgG, PAIgA, and PAIgM in both the thrombocytopenic and nonthrombocytopenic states. These elevations are due to increased internal platelet pools of Igs and not to increased surface-bound Igs.     

男护士在妇产科实习体验的质性研究

目的探讨男护士在妇产科的实习体验。方法采用现象学研究方法,深入访谈2012年3月~2013年5月在妇产科实习的男护士12名,并用Colaizzi的7步分析法分析访谈资料。结果男护士在妇产科实习的主要体验有：得不到患者的理解与支持、失落感、学习积极性下降、生活学习不方便、对专科操作不满意等。结论男护士在妇产科实习期间有着多种不良体验,临床带教老师要积极采取措施帮助他们顺利完成在妇产科的实习。     

HPLC法测定葛根提取物片中葛根素含量的不确定度评定

目的建立HPLC法测定葛根提取物片中的葛根素的不确定度评定方法。方法采用HPLC法测定葛根素 含量,分析影响其不确定度的因素来源,量化不确定度分量,最终计算合成不确定度,并得出测量结果的扩展不确定度。结果 葛根素的不确定度评估为±6. 66%。结论本方法可用于HPLC法测定药物含量的不确定度分析,使测定结果更加可靠。     

Effect of hormone replacement therapy,tibolone and raloxifene on serum lipids,apolipoprotein A1, apolipoprotein B and lipoprotein(a) in Greek postmenopausal women

The aim of this study was to assess the effect of estrogen, two regimens of continuous combined hormone replacement therapy (HRT), tibolone and raloxifene on serum lipid, apolipoprotein A1 and B and lipoprotein(a) levels in Greek postmenopausal women. A total of 350 postmenopausal women were studied in a prospective open design. Women were assigned to one of the following regimens depending on the presence of risk factors for osteoporosis, climacteric symptoms and an intact uterus: conjugated equine estrogen 0.625 mg (CEE, n=34), continuous combined CEE 0.625 mg plus medroxyprogesterone acetate (MPA) 5 mg, (n=80), continuous combined 17β-estradiol 2 mg plus norethisterone acetate (NETA) 1 mg (n=58), tibolone 2.5 mg (n=83) and raloxifene HCl 60 mg (n=50). Forty-five postmenopausal women with no indications for HRT served as controls. Total cholesterol (TC), low-density lipoprotein (LDL) cholestrol and high-density lipoprotein (HDL) cholesterol, triglyceride (TG), apolipoprotein A1 (ApoA₁), apolipoprotein B (ApoB) and lipoprotein(a) (Lp(a)) levels were assessed in each subject at baseline, and at 6 and 12 months of therapy. All therapy regimens lowered TC levels compared to baseline (4.2-8.0% decrease). This effect was more prominent in the subgoup of women with high baseline TC levels (9.1-20.4% decrease). LDL cholesterol decreased significantly in CEE, CEE/MPA and raloxifene groups (?11.2%, ?11.9% and ?11.0%, respectively). Hypercholesterolemic women exhibited a steeper decrease in LDL cholesterol (10.6-27.8% in all therapy groups). TG levels increased significantly in the CEE and CEE/MPA groups (23.7% and 21.8%, respectively), while estradiol/NETA had no effect on TG levels. Tibolone decreased TG levels markedly, by 20.6%, while raloxifene had no TG-lowering effect. HDL cholesterol and ApoA₁ were increased by CEE and CEE/MPA (HDL cholesterol, 7.4% and 11.8%, respectively; ApoA₁, 17.8% and 7.9%, respectively) and decreased by tibolone (HDL cholesterol, ?13.6%; and ApoA₁, ?9.9%). All therapy regimens except raloxifene lowered Lp(a) levels, with tibolone having the more pronounced effect (?13.2 to ?29.0%). In conclusion, each therapy regimen had a different effect on lipid-lipoprotein levels, exerting favorable and unfavorable modifications. Hypercholesterolemic women seemed to benefit more from the cholesterol-lowering effect of estrogen replacement therapy/HRT. The choice for a particular regimen should be based on individual needs, indications and lipid-lipoprotein profile.