Second-phase validation study of an alternative developmental toxicity test using mouse embryonic stem cell-derived embryoid bodies.

The embryoid body test (EBT) is a developmental toxicity test method that measures the size of embryoid bodies (EBs) and the viability of mouse embryonic stem cells (mESCs) and fibroblasts (3T3 cells). The previous pre-validation study confirmed the high accuracy (above 80%) of EBT using 26 coded test chemicals. This second-phase validation study assessed the inter-laboratory reproducibility (5 chemicals in common) and predictive capacity (10 chemicals in each laboratory) test using the coded test chemicals at three laboratories. For the prediction model, the accuracy is increased when more data is accumulated. Therefore, we updated the prediction model and analyzed the results of the second year with the newly created-prediction model. Statistical analysis of the inter-laboratory reproducibility test results indicated that accuracy, sensitivity, and specificity were 87%, 78%, and 100%, respectively. The results of the statistical analysis of the predictive capacity test showed an accuracy of 80%, sensitivity of 78%, and specificity of 81%. In conclusion, the EBT can accurately classify various embryotoxicants within a short period and with relatively little effort. Therefore, EBT can be used as a good way to test developmental toxicity.

Sleep duration and progression to diabetes in people with prediabetes defined by HbA1c concentration.

AIMS: To evaluate the association between sleep duration and the risk of progression to diabetes among people with prediabetes, defined by HbA1c values. METHODS: We conducted a cohort study in 17 983 adults who underwent health check-up examinations, including assessments of sleep duration and quality. Diabetes was defined as either HbA1c ≥48 mmol/mol (6.5%), or the use of antidiabetic medication. Time-dependent proportional hazards models were used to evaluate the association between sleep duration and the risk of progression to diabetes. RESULTS: During 31,582 person-years of follow-up, 664 incident cases of diabetes were identified; the incidence rate was 21.0 per 1000 person-years. The multivariate adjusted hazard ratios for progression to diabetes in people with sleep durations of ≤5, 6 and ≥8 h compared with 7 h were 1.68 (95% CI 1.30-2.16), 1.44 (95% CI 1.17-1.76) and 1.23 (95% CI 0.85-1.78), respectively (P for quadratic trend <0.001). This association was partially mediated by biomarkers of adiposity, fatty liver and insulin resistance. CONCLUSION: In this large study in young and middle-aged adults with prediabetes, we found an association between short sleep duration and the risk of progression to diabetes. Our findings suggest that sufficient sleep duration is important for delaying or preventing the progression of prediabetes to diabetes.

Anti-heparan sulfate antibody and functional loss of glomerular heparan sulfate proteoglycans in lupus nephritis.

Background The purpose of this study was to evaluate the features of heparan sulfate proteoglycans (HSPGs) as agrins of the glomerular basement membrane (GBM) and circulating anti-heparan sulfate (HS) antibodies in lupus nephritis, comparing titers among the following groups: lupus nephritis (LN), non-renal lupus, non-lupus nephritis, and healthy controls. Methods The stage of nephritis was determined based on the kidney biopsy. Alcian blue staining and immunohistochemical (IHC) staining for agrin were performed for histological evaluation of GBM HSPGs in normal glomeruli, non-lupus membranous glomerulonephritis (MGN), and lupus MGN. The results were used for measurement of the serum anti-HS antibody titers using an enzyme-linked immunosorbent assay (ELISA) in the following groups: 38 healthy controls, 38 non-lupus nephritis, 37 non-renal lupus, and 38 LN. Results Glomerulus HSPGs were stained bluish-green along the GBM with Alcian blue. However, IHC staining against agrin was almost completely negative in the lupus MGN group compared with the normal and non-lupus MGN groups, which showed brown staining of GBM. A higher level of anti-HS IgG was detected in LN compared with other groups, respectively. Higher titers were associated with the presence of SLE and nephritis. A higher degree of proteinuria normalized to glomerular filtration rate (eGFR) was observed in association with higher anti-HS antibody titers in LN. Conclusion This study demonstrated a functional loss of GBM HSPGs and higher levels of circulating anti-HS antibodies as a characteristic feature of lupus nephritis, suggesting their involvement in the pathogenesis of lupus nephritis and proteinuria.

The outcomes of instrumented posterolateral lumbar fusion in patients with rheumatoid arthritis.

AIMS: The aims of this study were to evaluate the clinical and radiological outcomes of instrumented posterolateral fusion (PLF) performed in patients with rheumatoid arthritis (RA). METHODS: A total of 40 patients with RA and 134 patients without RA underwent instrumented PLF for spinal stenosis between January 2003 and December 2011. The two groups were matched for age, gender, bone mineral density, the history of smoking and diabetes, and number of fusion segments. The clinical outcomes measures included the visual analogue scale (VAS) and the Korean Oswestry Disability Index (KODI), scored before surgery, one year and two years after surgery. Radiological outcomes were evaluated for problems of fixation, nonunion, and adjacent segment disease (ASD). The mean follow-up was 36.4 months in the RA group and 39.1 months in the non-RA group. RESULTS: Both groups had significant improvement in symptoms one year after surgery, while the RA group showed some deterioration of outcome scores owing to complications during the second year after surgery. Complications occurred at a higher rate in the group with RA (19 patients, 47.5%) than in those without RA (23 patients, 17.1%) (p < 0.001). A total of 15 patients in the RA group (37.5%) required revision surgery, mainly for implant failure and post-operative infection. DISCUSSION: Multimodal approaches should be considered when performing instrumented PLF in patients with RA to reduce the rate of complications, such as problems of fixation, post-operative infection and nonunion. TAKE HOME MESSAGE: Specific strategies should be undertaken in order to optimise outcomes in patients with rheumatoid arthritis.

Ferritin is associated with neural differentiation of bone marrow-derived mesenchymal stem cells under extremely low-frequency electromagnetic field.

Extremely low-frequency electromagnetic field (ELFEF) is a well-known mechanical stimulation that induces neural differentiation. It is potentially an effective treatment for neurodegenerative diseases. In a previous study, ferritin light chain was upregulated in ELFEF-exposed human bone marrow-derived mesenchymal stem cells (BM-MSCs). Ferritin light chain is a component of ferritin, a highly conserved iron-binding protein. In this study, to identify molecules associated with ferritin during neural differentiation of BM-MSCs, we performed reverse transcription polymerase chain reaction (RT-PCR), western blotting, and ATP analysis. Our data indicated that ELFEF triggers the upregulation of ferritin light chain (FLC) and ferritin heavy chain (FHC) in BM-MSCs. The elevated levels of FLC and FHC correlated positively with the differentiation of BM-MSCs into neural cells. Moreover ELFEF induced the activation of iron regulatory protein-1 (IRP-1) and cofilin, which are downstream targets of ferritin. These results suggest that ELFEF induces neural differentiation through activation of a ferritin-regulated mechanism.

Mucin 1 enhances the tumor angiogenic response by activation of the AKT signaling pathway.

Although the hyper-glycosylated transmembrane protein Mucin 1 (MUC1) is aberrantly overexpressed in human breast carcinoma, the biological significance of MUC1 overexpression is unclear. This study showed that MUC1 expression promoted the synthesis and secretion of vascular endothelial growth factor (VEGF) through the AKT signaling pathway. Increase VEGF production through MUC1 expression had a number of effect. First, MUC1 transfection increased expression of VEGF in breast cancer cells. Second, MUC1-mediated VEGF induction was attenuated by a chemical inhibitor of AKT or MUC1 knock-down by MUC1 siRNA. Third, MUC1 expression led to the activation of insulin-like growth factor-1 receptor, which correlated with VEGF expression. In addition, when MDA-MB-231 human breast cancer cells were directly injected into NOD/SCID mice, MUC1 expression accelerated xenograft tumor growth in vivo. Finally, MUC1 expression enhanced tumor growth and angiogenesis in a PyMT-MMTV/hMUC1 transgenic mouse model. Concurrent with these results, analysis of a human tissue microarray identified a high correlation between MUC1 and VEGF expression in human breast carcinoma. The current report is the first to demonstrate that MUC1 expression promotes angiogenesis in human breast cancer in vivo and in vitro.

Induction of apoptosis by the ginsenoside Rh2 by internalization of lipid rafts and caveolae and inactivation of Akt.

BACKGROUND AND PURPOSE: Lipid rafts and caveolae are membrane microdomains with important roles in cell survival signalling involving the Akt pathway. Cholesterol is important for the structure and function of these microdomains. The ginsenoside Rh2 exhibits anti-tumour activity. Because Rh2 is structurally similar to cholesterol, we investigated the possibility that Rh2 exerted its anti-tumour effect by modulating rafts and caveolae. EXPERIMENTAL APPROACH: A431 cells (human epidermoid carcinoma cell line) were treated with Rh2 and the effects on cell apoptosis, raft localization and Akt activation measured. We also examined the effects of over-expression of Akt and active-Akt on Rh2-induced cell death. KEY RESULTS: Rh2 induced apoptosis concentration- and time-dependently. Rh2 reduced the levels of rafts and caveolae in the plasma membrane and increased their internalization. Furthermore, Akt activity was decreased and consequently, Akt-dependent phosphorylation of Bad, a pro-survival protein, was decreased whereas the pro-apoptotic proteins, Bim and Bax, were increased upon Rh2 treatment. Unlike microdomain internalization induce by cholesterol depletion, Rh2-mediated internalization of rafts and caveolae was not reversed by cholesterol addition. Also, cholesterol addition did not restore Akt activation or rescue cells from Rh2-induced cell death. Rh2-induced cell death was attenuated in MDA-MB-231 cells over-expressing either wild-type or dominant-active Akt. CONCLUSIONS AND IMPLICATIONS: Rh2 induced internalization of rafts and caveolae, leading to Akt inactivation, and ultimately apoptosis. Because elevated levels of membrane rafts and caveolae, and Akt activation have been correlated with cancer development, internalization of these microdomains by Rh2 could potentially be used as an anti-cancer therapy.

Transglutaminase 2 suppresses apoptosis by modulating caspase 3 and NF-kappaB activity in hypoxic tumor cells.

The expression of hypoxia-inducible factor-1 (HIF-1) correlates with poor clinical outcomes and confers resistance to the apoptosis of the tumor cells that are exposed to hypoxia. Presently, the mechanism underlying this phenomenon is poorly understood. In this study we provide evidence that transglutaminase 2 (TG2), an enzyme that catalyses protein crosslinking reactions, is a transcriptional target of HIF-1 to enhance the survival of hypoxic cells. We found that hypoxia induces TG2 expression through an HIF-1 dependent pathway and concurrently activates intracellular TG2. The hypoxic cells overexpressing TG2 showed resistance to apoptosis. Conversely, the hypoxic cells treated with either TG2 inhibitor or small interfering RNA (siRNA) became sensitive to apoptosis. Activation of TG2 in response to hypoxic stress inhibited caspase-3 activity by forming crosslinked multimer, resulting in insoluble aggregates. TG2 also activates nuclear factor (NF)-kappaB pathway after hypoxic stress, and thereby induces the expression of cellular inhibitor of apoptosis 2. The anti-apoptotic role of TG2 was further confirmed in vivo using xenografts in athymic mice. Our results indicate that TG2 is an anti-apoptotic mediator of HIF-1 through modulating both apoptosis and survival pathways and may confer a selective growth advantage to tumor cells. These findings suggest that the inhibition of TG2 may offer a novel strategy for anticancer therapy.

The current status of HIV screening laboratories in Korea assessed by a questionnaire survey of participants in the KCDC HIV EQAS (2006).

Using a questionnaire, we assessed the current status of the quality management systems at HIV screening laboratories in Korea. The Korea Centres for Disease Control and Prevention HIV external quality assurance scheme (EQAS) questionnaire includes 18 items divided into five groups related to HIV testing: personnel, HIV test processes, participation in the Quality Assurance programme and HIV testing equipment. Five hundred and sixty-one HIV screening laboratories participated in this questionnaire investigation; data were collected from 233 public health centres, 309 hospitals or clinics, eight blood centres and 11 commercial laboratories. The total number of HIV screening tests was about 5.5 million in 2005. The average number of HIV tests per institution was highest in blood centres (308 561), followed by commercial laboratories (56 084), hospital or clinic laboratories (6756), and public health centres (1751). Equipment and HIV test methods varied between HIV screening laboratories, and, to manage the quality of their HIV testing, most laboratories participated in several evaluation programmes such as EQAS or a laboratory accreditation programme. This study is the first questionnaire survey of HIV testing laboratories in Korea. The results could be used to evaluate and promote the quality management of HIV testing laboratories.

Increased quantity of tumor-infiltrating FOXP3-positive regulatory T cells is an independent predictor for improved clinical outcome in extranodal NK/T-cell lymphoma.

BACKGROUND: Extranodal natural killer/T-cell lymphoma (NKTCL) is a clinically heterogeneous disease with a poor prognosis, requiring risk-stratified management in affected patients. Recently, tumor microenvironment including regulatory T cells (Tregs) has been implicated as a prognostic marker in certain types of lymphoma. PATIENTS AND METHODS: We collected 64 NKTCL cases and numerically quantified the amount of tumor-infiltrating FOXP3-positive Tregs by automated slide scanning and image analysis program after immunohistochemical staining using anti-FOXP3 antibody. RESULTS: Patients were able to be classified into two end groups by their level of Tregs. Twenty-eight (44%) patients had Tregs <50/0.40 mm(2), while 36 (56%) had Tregs > or =50/0.40 mm(2) within the tumor. The decreased number of Tregs (<50/0.40 mm(2)) was more common in patients with poor performance status or in those presented in non-upper aerodigestive tract. However, the level of Tregs was not associated with other prognostic factors, including stage, lactate dehydrogenase level, International Prognostic Index, and NKTCL Prognostic Index. Importantly, patients with increased numbers of Tregs (> or =50/0.40 mm(2)) showed prolonged overall and progression-free survival (P = 0.0005 and P = 0.0079, respectively). The number of FOXP3-positive Tregs was an independent prognostic factor (P = 0.001) by multivariate analysis. CONCLUSION: Increased quantity of tumor-infiltrating Tregs predicted improved clinical outcome in NKTCL patients.

Alpha-T-catenin (CTNNA3) gene was identified as a risk variant for toluene diisocyanate-induced asthma by genome-wide association analysis.

BACKGROUND: Toluene diisocyanate (TDI) is the most important cause of occupational asthma, but the genetic mechanism of TDI-induced asthma is still unknown. OBJECTIVE: The objective of the study was to identify susceptibility alleles associated with the TDI-induced asthma phenotype. METHODS: We conducted a genome-wide association study in 84 patients with TDI-induced asthma and 263 unexposed healthy normal controls using Affymetrix 500K SNPchip. We also investigated the relationships between genetic polymorphisms and transcript levels in Epstein-Barr virus-transformed lymphoblastoid cell lines from patients with TDI-induced asthma enrolled in this study. RESULTS: Genetic polymorphisms of CTNNA3 (catenin alpha 3, alpha-T catenin) were significantly associated with the TDI-induced asthma phenotype (5.84 x 10(-6) for rs10762058, 1.41 x 10(-5) for rs7088181, 2.03 x 10(-5) for rs4378283). Carriers with the minor haplotype, HT2 [GG], of two genetic polymorphisms (rs10762058 and rs7088181) showed significantly lower PC(20) methacholine level (P=0.041) and lower mRNA expression of CTNNA3 than non-carriers (P=0.040). A genetic polymorphism in the 3' downstream region of CTNNA3 (rs1786929), as identified by DNA direct sequencing, was significantly associated with the TDI-induced asthma phenotype (P=0.015 in recessive analysis model) and the prevalence of serum-specific IgG to cytokeratin 19 (P=0.031). CONCLUSION: These findings suggested that multiple genetic polymorphisms of CTNNA3 may be determinants of susceptibility to TDI-induced asthma.

The heat-shock protein 90 inhibitor, geldanamycin, induces apoptotic cell death in Epstein-Barr virus-positive NK/T-cell lymphoma by Akt down-regulation.

NK/T-cell lymphoma (NKTL) is strongly associated with latent Epstein-Barr virus (EBV) infection. Recently, latent membrane protein 1 (LMP1), an EBV oncoprotein, was reported to activate the phosphatidylinositol-3 kinase (PI3K)/Akt pathway for cell survival. Because geldanamycin (GA) and its derivative, 17-allylamino-17-demethoxygeldanamycin (17-AAG), exhibit anti-tumour activity by degrading HSP90 client proteins, including Akt, we investigated the effect of GA and 17-AAG on the survival of NKTL cell lines. EBV-positive NKTL cell lines, Hank-1 and NK-YS, and an EBV-negative NK leukaemia cell line, NK-L, were treated with PI3K and Akt inhibitors, GA, and 17-AAG, and were subjected to apoptosis and cell viability assays, and immunoblot analysis. EBV-positive B-lymphoblastoid cell lines IM9 and LMP1-transfected IM9 (IM9-LMP1) were also included. Hank-1 and NK-YS cell viability was compromised and apoptosis was induced by LY294002 (PI3K inhibitor) or Akt inhibitor II. GA or 17-AAG administration resulted in the apoptosis of NKTL cells, accompanied by Akt and pAkt down-regulation, caspase 3 activation, and mitochondrial membrane potential disruption. The intrinsic level of pAkt was higher in EBV-positive NKTL cells than in EBV-negative NK-L, and GA or 17-AAG decreased the viability of NKTL cells more efficiently than NK-L. Moreover, IM9-LMP1 was more sensitive to Akt inhibitor II or HSP90 inhibitors than IM9. Importantly, GA showed little effect on the viability of normal peripheral NK cells as non-neoplastic counterparts for comparison. In conclusion, this study suggests that the PI3K/Akt pathway is frequently activated in EBV-positive NKTL and that therapeutic modalities based on targeting the PI3K/Akt pathway with HSP90 inhibitors could be useful for achieving NKTL control.

Interleukin-18 is a critical factor for vascular endothelial growth factor-enhanced migration in human gastric cancer cell lines.

Cell migration and angiogenesis are key steps in tumor metastasis. However, the mechanism of migration regulated by vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is not completely understood. This study examined the relationship between VEGF and migration, along with the mechanism involved in the VEGF-regulated migration of human gastric cancer cells. The level of cell migration was increased by recombinant human (rh)VEGF-165 in the VEGF receptor-2-expressing SNU-601 cells. Interleukin (IL)-18 is associated with the malignant progression of tumors. Accordingly, this study examined the effect of IL-18 on the migration of cancer cells in order to identify the factors involved in VEGF-enhanced migration. Inhibiting IL-18 markedly reduced the level of VEGF-enhanced migration, and IL-18 increased cell migration directly through filamentous-actin polymerization and tensin downregulation. It was confirmed that rhVEGF-165 increased IL-18 production significantly. An antioxidant and an extracellular signal-regulated kinase (ERK)1/2-specific inhibitor blocked rhVEGF-165-enhanced IL-18 production. Accordingly, rhVEGF-165 increased the generation of region of interest (ROI) and activated the ERK1/2 pathway. These results suggest that rhVEGF-165 enhances IL-18 production via the generation of ROI and ERK1/2 phosphorylation, which results in the increased migration of gastric cancer cells.

Relationship between neurokinin 2 receptor gene polymorphisms and serum vascular endothelial growth factor levels in patients with toluene diisocyanate-induced asthma.

BACKGROUND: Among the various pathogenic mechanisms of toluene diisocyanate (TDI)-induced asthma, a contribution from neurogenic inflammation has been suggested. OBJECTIVE: To evaluate neurokinin 2 receptor (NK2R) gene polymorphisms in association with the clinical phenotype of TDI-induced asthma, 70 TDI-induced occupational asthma (TDI-OA)patients, 59 asymptomatic exposed controls (AEC), and 93 unexposed healthy controls (NC) were enrolled in the study. METHODS: Two single-nucleotide polymorphisms (SNPs) of NK2R, 7853G>A (Gly231Glu) and 11 424G>A (Arg375His), were genotyped using a single base extension method. The levels of PC20 methacholine, specific IgE and IgG to TDI-human serum albumin conjugate, and serum vascular endothelial growth factor (VEGF), matrix metalloproteinase-9, and TGF-beta1 were compared according to the NK2R genotypes of the subjects with TDI-OA and AEC. RESULTS: No significant differences in allele, genotype, or haplotype frequencies of these two SNPs were noted among the three groups (P>0.05, respectively). Moreover, subjects with the NK2R 7853GG genotype had higher serum VEGF levels than those with GA or AA among the TDI-exposed workers (P=0.040). CONCLUSION: The NK2R 7853GG genotype may contribute to increased serum VEGF levels, which result in airway inflammation after TDI exposure.

HLA DRB1*15-DPB1*05 haplotype: a susceptible gene marker for isocyanate-induced occupational asthma?

BACKGROUND: There has been no study for evaluating the associations of human leukocyte antigen (HLA) class I and II alleles with toluene diisocyanate (TDI)-induced asthma in an Asian population. OBJECTIVE: The aim of this study was to investigate a susceptible or protective marker of HLA class I and II alleles in TDI-induced asthma. METHODS: Fifty-five patients with TDI-induced asthma patients (group I) showing positive responses on TDI bronchoprovocation test, 47 asymptomatic exposed subjects (group II) and 95 unexposed healthy nonatopic controls (group III) were enrolled in our study. HLA class I and II genotyping was done by the direct DNA sequencing method. RESULTS: The allelic frequency of C*09 (15.5%) was significantly higher in group I than in group III (6.8%, P = 0.019), but this statistical significance disappeared after correction was made for multiple comparisons. On two-locus and three-locus haplotype analysis, the allelic frequency of HLA DRB1*15-DPB1*05 in group I (10.6%) was significantly higher than that of group II (0%, P = 0.001) and group III (2.5%, P = 0.003). The allelic frequencies of HLA A*02-DRB1*15, A*02-DQB1*06, B*62-C*09 and A*02-DRB1*15-DQB1*06 were significantly higher in group I (8.5%, 10.3%, 8.2% and 6.8%, respectively) than those allelic frequencies of group III (1.3%, P = 0.002; 1.6%, P = 0.001; 0.6%, P < 0.0001; 0%, P < 0.0001, respectively). The allelic frequencies of HLA DQB1*06-DPB1*05 and DRB1*15-DQB1*06-DPB1*05 were significantly higher in group I (16.0% and 10.5%) than those in group II (2.5%, P = 0.001; 0%, P = 0.001), while the frequencies of DRB1*09-DPB1*05 and DRB1*09-DQB1*0303-DPB1*05 were significantly lower in group I (0% and 0%) than those of group II (7.4%, P = 0.004; 7.5%, P = 0.004). These differences remained statistically significant even after the correction for multiple comparisons. CONCLUSIONS: The HLA haplotype DRB1*15-DPB1*05 can be a susceptibility gene marker for the development of TDI-induced asthma among the exposed workers in the Korean population.

Effects of salicylic-lactic acid conditioner on the shear bond strength of brackets and enamel surfaces.

The purpose of this study was to evaluate the effects of salicylic-lactic (SL) acid conditioner on the shear bond strength of brackets. Fluoride releasing (Light-bond) and non-fluoride releasing (Enlight) composite adhesives were used after conditioning with 0.22% salicylic + 9% lactic acid or 34% phosphoric acid. Composite adhesives were light cured with either a halogen light curing (HLC) unit for 30-50 s or a plasma arc curing (PAC) unit for 4 s. The shear bond strength was measured with an Instron. Failure modes of debonded brackets were identified based on adhesive remnants on the bracket and tooth. Salicylic-lactic acid conditioning was found to provide adequate shear bond strength. Groups conditioned with SL acid were debonded mainly at the enamel-resin interface and comparatively clean enamel surface after debonding was observed than those conditioned with phosphoric acid. Using confocal laser scanning microscopic examinations, it was found that demineralization patterns between SL acid and phosphoric acid conditioned groups were not different when the same adhesive was used. The SL acid conditioner did not reduce the demineralization. Light-bond adhesive showed less demineralization than Enlight adhesive. The PAC unit can be recommended as an alterative to the HLC unit because it significantly reduces the irradiation time.

Difference in the colour and colour change of dental resin composites by the background.

The objective of this study was to evaluate the difference in the colour and colour change of dental resin composites over commonly used two backgrounds. Colour of five uncured and cured resin composites before and after polishing with 600-, 1000- or 1500-grit SiC paper was measured according to the CIELAB colour scale relative to the illuminant D65 over a white background (WB; reflectance = 91.57%) and a light trap (LT; reflectance = 0.01%) on a reflection spectrophotometer with the SCE geometry. Colour difference (DeltaE*ab) by the background, and by the specimen conditions over each of two backgrounds was calculated. DeltaE*ab values between the same specimen by the background were 2.38-11.60. DeltaE*ab values by the specimen condition were varied by the background, and DeltaE*ab between cured/polished specimens over WB were significantly higher than those over LT (P < 0.05) except a few cases. Background influenced three-colour coordinates of CIE L*, a*, and b* values differently depending on the material and the specimen condition. Background significantly influenced the colour coordinates and colour difference by the specimen conditions. As the light trap can eliminate the influence of variations at the background, measured colour over the light trap can be the colour of material itself. Correlation between the measured colour and varied shades of background should be further studied.

Epstein-Barr virus-associated lymphoproliferative lesions presenting as a hydroa vacciniforme-like eruption: an analysis of six cases.

BACKGROUND: There are many reports of patients with a severe hydroa vacciniforme (HV)-like eruption in which cutaneous lesions occur in both sun-exposed and non-exposed areas, unlike in true HV. Several patients have died from a malignant haematological neoplasm. In most cases, a latent Epstein-Barr virus (EBV) infection has been detected in the skin lesions. OBJECTIVES: To describe the clinical and laboratory features of six additional patients with an EBV-associated HV-like eruption. METHODS: The clinical, histological and immunohistochemical features were reviewed. T-cell receptor gamma gene rearrangements were studied using polymerase chain reaction (PCR) and heteroduplex analysis. In-situ hybridization was performed to detect mRNA for EBV in skin biopsy specimens. PCR was performed to screen for EBV infection in the skin lesions of three patients and blood of two patients. Photoprovocation with repeated ultraviolet (UV) A exposure was performed in three patients. RESULTS: The severity of the skin lesions and the clinical course varied among the patients. Skin lesions were induced by repeated UVA exposure in three patients and a latent EBV infection was demonstrated in the photoprovoked lesions. CONCLUSIONS: Three different clinical courses were found in six patients with an HV-like eruption associated with chronic EBV infection: (i) spontaneous remission; (ii) clearing after photoprotection; and (iii) continuous recurrence irrespective of sun exposure. It is possible that there are two patterns of HV-like eruption associated with chronic EBV infection. One is characterized by recurrent necrotic papulovesicles of the face and the other by nodules and facial swelling. It was demonstrated that the skin lesions could be triggered by repeated UVA exposure in the patients showing recurrent necrotic papulovesicles of the face.

Effect of plasma arc curing on polymerization shrinkage of orthodontic adhesive resins.

The purpose of this study was to evaluate the polymerization shrinkage of three orthodontic adhesive resins when polymerized with a high-energy plasma arc light (1340 mW cm(-2)) and a conventional halogen light (500 mW cm(-2)), and to correlate the polymerization shrinkage with the degree of conversion. To equalize the total light energy delivered to the adhesive resin, irradiation time was varied between 3 or 6 s for a plasma arc-curing unit, and 8 or 16 s for a halogen light-curing unit. The polymerization shrinkage of adhesive resins during the light-curing process was measured using a computer-controlled mercury dilatometer and the degree of conversion was measured using Fourier transform infrared spectroscopy. A plasma arccuring unit produced significantly lower polymerization shrinkage than a halogen light-curing unit when the equivalent total light energy was irradiated to the orthodontic adhesive resins (P < 0.05). The magnitude of polymerization shrinkage was significantly different depending on the kind of adhesive resins (P < 0.05), but there was no significant correlation between the filler fraction and the polymerization shrinkage (r2 = 0.039). There was strong correlation (r2 = 0.787) between the polymerization shrinkage and the degree of conversion with a halogen light-curing unit, but poor correlation (r2 = 0.377) was observed with a plasma arc-curing unit.