Hydroxylation of dental zirconia surfaces: characterization and bonding potential

Bioinert zirconia surfaces exhibit a low chemical bonding potential to resin-based luting agents. The aim was to hydroxylate dental zirconia surfaces and to examine tensile bond strength using commercial luting agents. The measured bond strength was compared with established mechanical conditioning techniques. Five acidic and one alkaline hydroxylation pretreatments were applied and compared with air abrasion and tribochemical silica coating. For the chemical characterization of hydroxyl groups and hydroxyl value, zirconia powders were used, chemically modified, and analyzed using Fourier-transformed infrared spectroscopy and a titrimetric method according to the ISO 4629 standard. All acidic pretreatment procedures exhibited increased hydroxyl values. The highest values were recorded after treatment with phosphoric acid or Piranha solution. Tensile bond strength was examined in a universal testing machine using the commercial dual-cure luting agents Multilink (Ivoclar, Liechtenstein) and Panavia F2.0 (Kuraray, Japan). Surface hydroxylation with Piranha solution in combination with the luting agent Multilink led to a bond strength of 12.47 +/- 3.25 MPa. Tribochemical silica-coated/silanized zirconia surfaces with Multilink produced the highest bond strength of 19.33 +/- 3.65 MPa. Using the luting agent Panavia F2.0, statistically homogenous values for the untreated (11.60 +/- 1.68 MPa) and for the hydroxylated surface (12.46 +/- 3,81 MPa) were measured. Bioinert zirconia surfaces were successfully hydroxylated in terms of tensile bond strength. Resin bonding with Multilink can be strongly increased by acidic treatment with Piranha solution. Bonding with Panavia F2.0 is not affected by hydroxylation, which is likely due to the incorporation of specific functional monomers.     

Relaxin stimulates expression of vascular endothelial growth factor in normal human endometrial cells in vitro and is associated with menometrorrhagia in women

Although the role of the reproductive hormone, relaxin, in rodents is well documented, its potential contribution to human reproduction is less well defined. In this study, we examine the effects of relaxin on human endometrial cells in vitro and describe the clinical effects of relaxin on menstrual flow in women. In cultured endometrial cells, relaxin specifically induces the expression of an angiogenic agent, vascular endothelial growth factor (VEGF). cAMP is implicated as a second messenger involved in VEGF stimulation. VEGF expression is temporally regulated in the endometrium, and our results suggest that relaxin, which is secreted by the corpus luteum and is present in the endometrium during the menstrual cycle and pregnancy, may be involved in regulating endometrial VEGF expression. Relaxin was recently tested in a clinical trial for efficacy in the treatment of progressive systemic sclerosis, and was administered at levels up to 10 times higher than that measured during pregnancy. The most frequent relaxin-related adverse event reported during the course of the study was the onset of menometrorrhagia, defined in this study as heavier-than-usual or irregular menstrual bleeding. The intensification of menstrual flow observed in these patients is consistent with the hypothesis that relaxin mediates neovascularization of the endometrial lining.     

TRAF2 deficiency results in hyperactivity of certain TNFR1 signals and impairment of CD40-mediated responses.

Tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2) can interact with various members of the TNF receptor family. Previously, we reported that TRAF2-deficient mice die prematurely and have elevated serum TNF levels. In this study, we demonstrate that TRAF2-deficient macrophages produce increased amounts of nitric oxide (NO) and TNF in response to TNF stimulation. Furthermore, we could enhance the survival of TRAF2-deficient mice by eliminating either TNF or TNFR1. Using these double-knockout mice, we show that in the absence of TRAF2, the T helper-dependent antibody response, CD40-mediated proliferation, and NF-kappaB activation are defective. These data demonstrate two important roles of TRAF2, one as a negative regulator of certain TNFR1 signals and the other as a positive mediator of CD40 signaling.     

Novel Immunoblot Assay Using Four Recombinant Antigens for Diagnosis of Epstein-Barr Virus Primary Infection and Reactivation

A new immunoblot assay, composed of four Epstein-Barr virus (EBV)-encoded recombinant proteins (virus capsid antigen [VCA] p23, early antigen [EA] p138, EA p54, and EBNA-1 p72), was compared with an immunofluorescence assay on a total of 291 sera. The test was accurate in 94.5% of cases of primary EBV infection, while an immunoglobulin G anti-VCA p23 band with strong intensity correlated with reactivation.     

微弱电流耦合信号在人体上臂传输的建模与分析

背景：基于人体组织的导电特性,研究微弱电流耦合信号在人体内的传输特性,对实现植入式医疗仪器的人体充电和通信具有重要意义。 目的：分析微弱电流耦合信号在人体上臂的分布及衰减情况。 方法：将人体上臂抽象成由皮肤、脂肪、肌肉、骨骼4层组织构成的同心圆柱体,采用有限元方法建立微弱电流耦合信号在上臂传输的准静态场模型,分析了多种情况下模型中电流密度的分布,并将体表电位的衰减率与仿真结果进行比较。 结果与结论：仿真结果表明肌肉层是人体内耦合电流传导的主要路径,皮肤层中的电流随频率提高而增大;人体内的传导电流远大于位移电流,但随频率的提高,位移电流逐步增大,传导电流减小;皮肤干湿程度对肌肉层中总电流密度大小有一定影响,湿皮肤时肌肉层中总的电流密度大于干皮肤时的情况;耦合电流的体表电位具有较大衰减,随频率提高成一定的高通特性,且是否考虑人体组织电容效应对建模的准确性具有显著影响;人体实验与仿真实验结果具有较好的一致性。     

Noncontact Evaluation of Articular Cartilage Degeneration Using a Novel Ultrasound Water Jet Indentation System

We previously reported a noncontact ultrasound water jet indentation system for measuring and mapping tissue mechanical properties. The key idea was to utilize a water jet as an indenter as well as the coupling medium for high-frequency ultrasound. In this paper, the system was employed to assess articular cartilage degeneration, using stiffness ratio as an indicator of the mechanical properties of samples. Both the mechanical and acoustical properties of intact and degenerated bovine patellar articular cartilage (n = 8) were obtained in situ. It was found that the stiffness ratio was reduced by 44 ± 17% after the articular cartilage was treated by 0.25% trypsin at 37 °C for 4 h while no significant difference in thickness was observed between the intact and degenerated samples. A significant decrease of 36 ± 20% in the peak-to-peak amplitude of ultrasound echoes reflected from the cartilage surface was also found for the cartilage samples treated by trypsin. The results also showed that the stiffness obtained with the new method highly correlated with that measured using a standard mechanical testing protocol. A good reproducibility of the measurements was demonstrated. The present results showed that the ultrasound water jet indentation system may provide a potential tool for the non-destructive evaluation of articular cartilage degeneration by simultaneously obtaining mechanical properties, acoustical properties, and thickness data.     

Prevalence and correlates of bipolar II disorder in major depressive patients at a psychiatric outpatient clinic in Hong Kong

BackgroundWestern studies indicate a high prevalence of bipolar II disorder defined by a Research Diagnostic Criteria 2-day hypomania duration criterion (30 to 61%) amongst clinically depressive patients. The situation in Chinese patients with depression is unknown.Methods64 (52.5% response rate) patients first presenting to a Hong Kong public psychiatric outpatient clinic in 2005 with a diagnosis of major depression were recruited. The SCID and Family History Screen were administered.ResultsDSM-IV bipolar II was found in 20.5% of depressive outpatients; 35.9% had bipolar II disorder defined by RDC 2-day duration criterion for hypomania. Family bipolarity, age of onset, and depressive recurrence distinguished bipolar II subjects from unipolar depressives irrespective of duration criteria chosen for hypomania.LimitationsSample size was limited.ConclusionsBipolar II disorder is common amongst Chinese depressive outpatients. The evaluation method and 2-day duration criterion for hypomania were supported by bipolar validators. Replication using larger samples is needed to arrive at a more representative prevalence estimate and to enable more refined nosological evaluation.     

Modulatory Effects and Action Mechanisms of Tryptanthrin on Murine Myeloid Leukemia Cells

Leukemia is the disorder of hematopoietic cell development and is characterized by an uncoupling of cell proliferation and differentiation. There is a pressing need for the development of novel tactics for leukemia therapy as conventional treatments often have severe adverse side effects. Tryptanthrin （6,12-dihydro-6,12-dioxoindolo- （2,1-b）-quinazoline） is a naturally-occurring, weakly basic alkaloid isolated from the dried roots of medicinal indigo plants （Ban-Lan-Gen）. It has been reported to have various biological and pharmacological activities, including anti-microbial, anti-inflammatory, immunomodulatory and anti-tumor effects. However, its modulatory effects and action mechanisms on myeloid cells remain poorly understood. In this study, tryptanthrin was shown to suppress the proliferation of the murine myeloid leukemia WEHI-3B JCS cells in a dose- and time-dependent manner. It also significantly reduced the growth of WEHI-3B JCS cells in vivo in syngeneic BALB/c mice. However, it exhibited no significant direct cytotoxicity on normal murine peritoneal macrophages. Flow cytometric analysis showed an obvious cell cycle arrest of the tryptanthrin-treated WEHI-3B JCS cells at the G0/G1 phase. The expression of cyclin D2, D3, Cdk 2, 4 and 6 genes in WEHI-3B JCS cells was found to be down-regulated at 24 h as measured by RT-PCR. Morphological and functional studies revealed that tryptanthrin could induce differentiation in WEHI-3B JCS cells, as shown by the increases in vacuolation, cellular granularity and NBT-reducing activity in tryptanthrin-treated cells. Collectively, our findings suggest that tryptanthrin might exert its anti-tumor effect on the murine myelomonocytic leukemia WEHI-3B JCS cells by causing cell cycle arrest and by triggering cell differentiation.     

iRhom2 regulates CSF1R cell surface expression and non‐steady state myelopoiesis in mice

CSF1R (colony stimulating factor 1 receptor) is the main receptor for CSF1 and has crucial roles in regulating myelopoeisis. CSF1R can be proteolytically released from the cell surface by ADAM17 (A disintegrin and metalloprotease 17). Here, we identified CSF1R as a major substrate of ADAM17 in an unbiased degradomics screen. We explored the impact of CSF1R shedding by ADAM17 and its upstream regulator, inactive rhomboid protein 2 (iRhom2, gene name Rhbdf2), on homeostatic development of mouse myeloid cells. In iRhom2‐/‐ mice, we found constitutive accumulation of membrane‐bound CSF1R on myeloid cells at steady state, although cell numbers of these populations were not altered. However, in the context of mixed bone marrow (BM) chimera, under competitive pressure, iRhom2‐/‐ BM progenitor‐derived monocytes, tissue macrophages and lung DCs showed a repopulation advantage over those derived from wild‐type (WT) BM progenitors, suggesting enhanced CSF1R signaling in the absence of iRhom2. In vitro experiments indicate that iRhom2‐/‐ Lin^?SCA‐1⁺c‐Kit⁺ (LSKs) cells, but not granulocyte‐macrophage progenitors (GMPs), had faster growth rates than WT cells in response to CSF1. Our results shed light on an important role of iRhom2/ADAM17 pathway in regulation of CSF1R shedding and repopulation of monocytes, macrophages and DCs.     

Application of diffusional kurtosis imaging to detect occult brain damage in multiple sclerosis and neuromyelitis optica

Multiple sclerosis (MS) and neuromyelitis optica (NMO) are two common types of inflammatory demyelinating disease of the central nervous system. Early distinction of NMO from MS is crucial but quite challenging. In this study, 13 NMO spectrum disorder patients (Expanded Disability Status Scale (EDSS) of 3.0 ± 1.7, ranging from 2 to 6.5; disease duration of 5.3 ± 4.7 years), 17 relapsing–remitting MS patients (EDSS of 2.6 ± 1.4, ranging from 1 to 5.5; disease duration of 7.9 ± 7.8 years) and 18 healthy volunteers were recruited. Diffusional kurtosis imaging was employed to discriminate NMO and MS patients at the early or stable stage from each other, and from healthy volunteers. The presence of alterations in diffusion and diffusional kurtosis metrics in normal‐appearing white matter (NAWM) and diffusely increased mean diffusivity (MD) in the cortical normal‐appearing gray matter (NAGM) favors the diagnosis of MS rather than NMO. Meanwhile, normal diffusivities and kurtosis metrics in all NAWM as well as increases in MD in the frontal and temporal NAGM suggest NMO. Our results suggest that diffusion and diffusional kurtosis metrics may well aid in discriminating the two diseases.