Prevalence of Candida spp., xerostomia,and hyposalivation in oral lichen planus – A controlled study

Objective

To determine the frequency of Candida spp., xerostomia, and salivary flow rate (SFR) in three different groups: patients with OLP (OLP group), patients with oral mucosal lesions other than OLP (non‐OLP group), and subjects without oral mucosal lesions (control group).

Material and methods

Xerostomia as well as SFR was investigated in the three groups. Samples for isolation of Candida spp. were collected from OLP lesions (38 patients), non‐OLP lesions (28 patients), and healthy subjects (32 subjects).

Results

There was no statistically significant difference regarding the frequency of xerostomia and hyposalivation among the three groups (P > 0.05). A higher prevalence for colonization by Candida spp. was found in the healthy subject as compared to that of patients with OLP (P = 0.03) and non‐OLP (P = 0.02) groups. Low SFR was not a factor for colonization by Candida spp.

Conclusions

Xerostomia and hyposalivation occur with similar frequency in subjects with and without oral lesions; also, the presence of oral lesions does not increase the susceptibility to colonization by Candida spp. It seems that any study implicating Candida spp. in the malignant transformation of oral lesions should be carried out mostly on a biochemical basis, that is, by testing the capability of Candida spp. to produce carcinogenic enzyme.     

Strain‐dependent induction of allergic rhinitis without adjuvant in mice

BACKGROUND: To date, no murine models have been reported to show the induction of both antigen-specific IgE and nasal eosinophilia, two of the major hallmarks of allergic rhinitis, after local sensitization in the absence of adjuvants, a phenomenon which reflects natural exposure. In this report, we attempted to establish a murine model representing an initiation of allergic rhinitis. METHODS: BALB/c, CBA/J, and C57BL/6 mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA) solely. After repeated sensitization, serum Ab titers, nasal eosinophilia, and cytokine production by nasal lymphocytes were determined. RESULTS: BALB/c mice produced SEA-specific IgE after repeated sensitization. High-dose sensitization to SEA induced IgE production in CBA/J mice, while C57BL/6 mice did not show the production throughout the period observed, suggesting that IgE production was regulated genetically. BALB/c mice also exhibited nasal eosinophilia after the nasal challenge. In addition, nasal lymphocytes sensitized with SEA intranasally produced significant amount of IL-5 in vitro. CONCLUSIONS: These results suggest that intranasal sensitization with SEA in the absence of adjuvants induces a Th2 immune reaction, reflecting the hallmarks of the initiation of allergic rhinitis both in vivo and in vitro, which is genetically regulated.     

乳腺癌患者保乳术联合腔镜腋窝淋巴结清扫术的临床研究

目的 探讨保乳手术联合腔镜腋窝淋巴结清扫术(MALND)对乳腺癌患者上肢功能、应激反应及血管细胞黏附分子-1 (VCAM-1)、细胞间黏附分子-1(ICAM-1)水平的影响。方法 回顾性分析98例乳腺癌患者的临床资料,依据手术方式的不同分为研究组53例和对照组45例。对照组行保乳手术联合传统腋窝淋巴结清扫术(CALND),研究组行保乳手术联合MALND。比较2组术前、术后6个月上肢功能;收集2组患者术前、术后12 h焦虑自评量表(SAS)、抑郁自评量表(SDS)评分以及心率(HR)、平均动脉压(MAP)水平,并对比2组应激反应程度;比较2组患者术前、术后5 d VCAM-1、ICAM-1水平。结果 术后6个月,研究组前屈、后伸、内收、外展、内旋、外旋活动角度大于对照组,差异有统计学意义(P<0.05);术后12 h,研究组SAS、SDS评分及HR、MAP水平低于对照组,差异有统计学意义(P<0.05);术后5 d,研究组VCAM-1、ICAM-1水平低于对照组,差异有统计学意义(P<0.05)。结论 保乳手术联合MALND对乳腺癌患者上肢功能影响小,术后应激反应程度轻...     

A new response to heart disease in women

Explore current practices in the multidisciplinary management of cardiovascular disease in women and innovative educational approaches to health promotion and disease prevention.     

1140919448CD200-dependent suppression of human NK activity by IVIG requires CD200 receptor type 2

Problem: IVIG prepared from plasma of stored human blood can be efficacious in improving pregnancy success in a selected subgroup of patients but RCTs using an IVIG showing inferior suppression of NK activity in vitro have been negative (J Assist Reprod Genet 2006). A significant component of NK suppression by IVIG appears to be due to CD200 released into plasma from PBL during storage at 4C. CD200 receptors (CD200R) are expressed at the fetomaternal interface prior to onset of abortion; CD200R1 mediates direct effects on gamma‐delta T cell development and suppresses alpha‐beta T cell responses in vitro, whereas CD200R2 alters DC so as to facilitate development of alpha‐beta Treg cells. Which receptor(s) mediate NK cell suppression? Methods: Purified human PBL or the CD56⁺ NK cell subset of PBL were used to lyse 51Cr‐labeled K562 cells in vitro. Different IVIG preparations were tested for suppressive ability, and suppression was blocked by either anti‐huCD200 mAb or rabbit anti‐huCD200R1 or R2 antibodies. Results: CD200‐dependent IVIG NK suppressive potency differed among IVIG types (Gammagard>Gamunex>>Gamimmune). CD200‐dependent suppression was blocked by anti‐CD200R antibody able to react with the type 2 receptor. K562 cells did not express receptor, and purified CD56⁺ NK cells were suppressed effectively without the need for non‐NK cells. Conclusions: IVIG may directly express NK cell activity via CD200 binding to CD200R2.     

VEGF-C表达和微淋巴管密度与胃癌淋巴转移的关系及意义

目的探讨胃癌组织血管内皮生长因子C(VEGF-C)表达和微淋巴管密度(MLVD)及两者与胃癌淋巴转移的关系。方法应用免疫组织化学方法检测208例人胃癌组织、40例癌浸润前缘组织及139例人胃正常粘膜组织中VEGF-C、D2-40的表达,对D2-40阳性脉管进行MLVD计数,并结合病理资料进行统计学分析。结果胃癌组织VEGF-C的表达明显高于正常胃粘膜组织(χ2=109.199,P<0.01);胃癌组织中有淋巴结转移(χ2=14.496,P<0.01)或浸润透浆膜(χ2=11.586,P<0.01)组VEGF-C表达水平分别较无转移或浸润未及浆膜组增高。癌浸润前缘组织中MLVD(18.36±15.60个/mm2)明显高于胃癌组(9.41±9.32个/mm2,t=-3.681,P<0.01)和胃正常粘膜组织(7.70±7.69个/mm2,t=-4.180,P<0.01);胃癌淋巴结转移组MLVD(9.81±9.97个/mm2)高于无转移组(6.41±7.85个/mm2,t=2.516,P<0.01),而在浸润透浆膜组(11.20±10.55个/mm2)和未及浆膜组(8.54±9.36个/mm2)MLVD无差别(t=1.467,P=0.472)。另外,在胃癌组织中VEGF-C表达与MLVD呈正相关(F=2.910,P<0.05)。结论VEGF-C在胃癌中的高表达与胃癌浸润深度、淋巴转移密切相关。     

Nanoscale presentation of cell adhesive molecules via block copolymer self-assembly

Precise control over the nanoscale presentation of adhesion molecules and other biological factors represents a new frontier for biomaterials science. Recently, the control of integrin spacing and cellular shape has been shown to affect fundamental biological processes, such as differentiation and apoptosis. Here, we present the self-assembly of maleimide functionalised polystyrene-block-poly (ethylene oxide) copolymers as a simple, yet highly precise method for controlling the position of cellular adhesion molecules. By manipulating the phase separation of the functional PS-PEO block copolymer used in this study, via a simple blending technique, we alter the nanoscale (on PEO domains of 8–14 nm in size) presentation of the adhesion peptide, GRGDS, decreasing lateral spacing from 62 nm to 44 nm and increasing the number density from ～450 to ～900 islands per μm². The results indicate that the spreading of NIH-3T3 fibroblasts increases as the spacing between domains of RGD binding peptides decreases. Further, the same functional PS-PEO surfaces have been utilised to immobilise, via a zinc chelating peptide sequence, poly-histidine tagged proteins and extracellular matrix (ECM) fragments. This method is seen as an ideal platform for investigations into the role of spatial arrangements of cell adhesion molecules and ECM molecules on cell function and, in particular, control of cell phenotype.     

Reciprocal effect of Waardenburg syndrome mutations on DNA binding by the Pax-3 paired domain and homeodomain

The Pax-3 protein contains two DNA-binding domains, a paired domain and a homeodomain. Mutations in Pax-3 cause Waardenburg syndrome (WS) in humans and the mouse Splotch (Sp) phenotype. In the Sp-delayed mouse, a mutation in the Pax-3 paired domain (G9R) abrogates the DNA-binding activity of both the paired domain and the homeodomain, suggesting that they may functionally interact. To investigate this possibility further, we have analyzed the DNA-binding properties of additional point mutants in the Pax-3 paired domain and homeodomain that occur in WS patients (F12L, N14H, G15S, P17L, R23L, G48A, S51F and G66D in the paired domain, V47F and R53G in the homeodomain), the Pax-1 un mutation (G15A) and a substitution associated with Peters' anomaly in the PAX-6 gene (R23G). Within the paired domain, seven of 10 mutations were found to abrogate DNA-binding by the paired domain. Remarkably, these seven mutations also affected DNA binding by the homeodomain, causing either a complete loss (P17L and G66D), a reduction (R23G, R23L, G15S and G15A) or an increase in DNA-binding activity (N14H). In addition, the effect of paired domain mutations occurred at the level of monomer formation by the homeodomain, while the dimerization potential of this domain seemed unaffected in mutants where it could be analyzed. Furthermore, while both homeodomain mutations were found to abolish DNA binding by this domain, the R53G mutation also abrogated DNA binding by the paired domain. The important observation that independent mutations in either domain can affect DNA binding by the other in the intact Pax- 3 protein strongly suggests that the two domains are not functionally independent but bind DNA through cooperative interactions. Modeling the deleterlous mutations on the three-dimensional structure of the paired domain of Drosophila Prd shows that these mutations cluster at the DNA interface, thus suggesting that a series of DNA contacts are essential for DNA binding by both the paired domain and the homeodomain of Pax-3.