272 research outputs found

    New Method of Avoiding Underestimation of Caries Incidence and Its Association with Possible Risk Factors in Japanese University Students: A Prospective Cohort Study

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    The objective of this three-year prospective cohort study was to investigate the association between a new definition of an increase in dental caries and risk factors in Japanese young adults. Data of Okayama University students who volunteered to undergo oral examinations and answer questionnaires in 2015 and 2018 were analyzed. The status of filled teeth and the status of occlusal/proximal surfaces of filled or decayed teeth were recorded. An increase in dental caries was defined as a change in the status of filled teeth and/or an increase in dental caries of occlusal and proximal surfaces. A total of 393 participants (18.2 +/- 0.8 years) were analyzed. First and second molars showed a high prevalence of dental caries. Of the participants, 144 (36.6%) showed an increase in dental caries. In all the participants and in the females, the decayed, missing, and filled teeth (DMFT) score and history of orthodontic treatment at baseline were significantly associated with an increase in dental caries (p = 2) at baseline were significantly associated with an increase in dental caries (p = 0.04). The DMFT score and history of orthodontic treatment at baseline can be risk factors for an increase in dental caries using the new definition in young adults

    Study of Pine Needle (Pinus thunbergii) as an Indicator of Atmospheric Heavy Metal Particles

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    神戸大学Scedule:17-18 March 2003, Vemue: Kanazawa, Japan, Kanazawa Citymonde Hotel, Project Leader : Hayakawa, Kazuichi, Symposium Secretariat: XO kamata, Naoto, Edited by:Kamata, Naoto

    Necessity for Reassessment of Patients with Serogroup 2 Hepatitis C Virus (HCV) and Undetectable Serum HCV RNA

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    We encountered a patient positive for anti-hepatitis C virus (HCV) whose serum HCV RNA was undetectable with the Roche AmpliPrep/Cobas TaqMan HCV assay (CAP/CTM) version 1 but showed a high viral load with the Abbott RealTime HCV assay (ART). Discrepancies in the detectability of serum HCV RNA were investigated among 891 consecutive patients who were positive for anti-HCV. Specific nucleotide variations causing the undetectability of HCV RNA were determined and confirmed by synthesizing RNA coding those variations. Serum samples with the discrepancies were also reassessed by CAP/CTM version 2. Among the 891 anti-HCV-positive patients, 4 patients had serum HCV RNA levels that were undetectable by CAP/CTM version 1 despite having levels of > 5 log IU/ml that were detected by ART. All four patients had HCV genotype 2a and high titers of anti-HCV. Sequencing of the HCV 5' noncoding regions revealed 2 common variations, A at nucleotide (nt) 145 and T at nt 151. Synthesized RNAs of the HCV 5' noncoding region with standard (NCR145G151C) and variant nucleotides at nt 145 and nt 151 were quantified with CAP/CTM. RNAs of NCR145G151C and NCR145G151T were quantifiable with CAP/CTM version 1, while those of NCR145A151T and NCR145A151C went undetected. The substitution from G to A at nt 145 specifically conferred this undetectability, while this undetectability was reverted in synthesized HCV RNA with correction of this variation. Reassessment of these samples by CAP/CTM version 2 resulted in similar levels of HCV RNA being detected by ART. We conclude that HCV patients with undetectable HCV RNA by CAP/CTM version 1 should be reassessed for viral quantification

    Functional promoter upstream p53 regulatory sequence of IGFBP3 that is silenced by tumor specific methylation

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    BACKGROUND: Insulin-like growth factor binding protein (IGFBP)-3 functions as a carrier of insulin-like growth factors (IGFs) in circulation and a mediator of the growth suppression signal in cells. There are two reported p53 regulatory regions in the IGFBP3 gene; one upstream of the promoter and one intronic. We previously reported a hot spot of promoter hypermethylation of IGFBP-3 in human hepatocellular carcinomas and derivative cell lines. As the hot spot locates at the putative upstream p53 consensus sequences, these p53 consensus sequences are really functional is a question to be answered. METHODS: In this study, we examined the p53 consensus sequences upstream of the IGFBP-3 promoter for the p53 induced expression of IGFBP-3. Deletion, mutagenesis, and methylation constructs of IGFBP-3 promoter were assessed in the human hepatoblastoma cell line HepG2 for promoter activity. RESULTS: Deletions and mutations of these sequences completely abolished the expression of IGFBP-3 in the presence of p53 overexpression. In vitro methylation of these p53 consensus sequences also suppressed IGFBP-3 expression. In contrast, the expression of IGFBP-3 was not affected in the absence of p53 overexpression. Further, we observed by electrophoresis mobility shift assay that p53 binding to the promoter region was diminished when methylated. CONCLUSION: From these observations, we conclude that four out of eleven p53 consensus sequences upstream of the IGFBP-3 promoter are essential for the p53 induced expression of IGFBP-3, and hypermethylation of these sequences selectively suppresses p53 induced IGFBP-3 expression in HepG2 cells

    Simple surrogate index of the fibrosis stage in chronic hepatitis C patients using platelet count and serum albumin level.

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    This study was conducted to develop a simple surrogate index comprised of routinely available laboratory tests to reflect the histological fibrosis stage. Clinical characteristics and laboratory data from 368 and 249 consecutive patients with chronic hepatitis C, a training cohort and a validation cohort, respectively, were retrospectively evaluated. Platelet (Plt) count and albumin (Alb) level contributed to the discrimination of the respective fibrosis stages. We derived the fi brosis index (FI), FI = 8.0-0.01 x Plt (10 multiply 3/microliter) - Alb (g/dl), from a multiple regression model. FI significantly correlated with the histological fibrosis stage in both the initial and validation cohort at p=0.691 and p=0.661, respectively (Spearman's rank correlation coefficient, p&#60;0.0001). The sensitivity and positive predictive value of FI at a cutoff value &#60; 2.10 for predicting fibrosis stage F0-1 were 66.8% and 78.8% in the initial cohort and 68.5% and 63.6% in the validation cohort, respectively. Corresponding values of FI at a cutoff value &#62;- 3.30 for the prediction of F4 were 67.7% and 75.0% in the initial cohort and 70.8% and 81.0% in the validation cohort. The fibrosis index comprised of platelet count and albumin level reflected the histological fibrosis stage in patients with chronic hepatitis C.</p

    Increased serum HO-1 in hemophagocytic syndrome and adult-onset Still's disease: use in the differential diagnosis of hyperferritinemia

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    Heme oxygenase-1 (HO-1), an inducible heme-degrading enzyme, is expressed by macrophages and endothelial cells in response to various stresses. Because ferritin synthesis is stimulated by Fe(2+), which is a product of heme degradation, we examined the relation between HO-1 and ferritin levels in the serum of patients with hemophagocytic syndrome (HPS), adult-onset Still's disease (ASD), and other diseases that may cause hyperferritinemia. Seven patients with HPS, 10 with ASD, 73 with other rheumatic diseases, 20 with liver diseases, 10 recipients of repeated blood transfusion because of hematological disorders, and 22 healthy volunteers were enrolled. Serum HO-1 and ferritin levels were determined by ELISA. Expression of HO-1 mRNA and protein by peripheral blood mononuclear cells (PBMCs) was determined by real-time PCR and immunocytochemical techniques, respectively. Serum levels of HO-1 were significantly higher in patients with active HPS and ASD than in the other groups (P < 0.01). HO-1 levels were not elevated in patients with other causes of hyperferritinemia but were moderately elevated in patients with dermatomyositis/polymyositis. Among patients with HPS and ASD, serum HO-1 levels correlated closely with serum ferritin levels, and the levels of both returned to normal after therapy had induced remission. Increased expression of HO-1 mRNA was confirmed in PBMCs from some patients with HPS and ASD. Hyperferritinemia correlated closely with increased serum HO-1 in patients with HPS and ASD but not other conditions, indicating that measurement of serum HO-1 and ferritin levels would be useful in the differential diagnosis of hyperferritinemia and perhaps also in monitoring disease activity in HPS and ASD

    Pregabalin- and azithromycin-induced rhabdomyolysis with purpura: An unrecognized interaction: A case report

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    AbstractIntroductionRhabdomyolysis associated with the use of pregabalin or azithromycin has been demonstrated to be a rare but potentially life-threatening adverse event. Here, we report an extremely rare case of rhabdomyolysis with purpura in a patient who had used pregabalin and azithromycin.Presentation of caseWe present the case of a 75-year-old woman with a history of fibromyalgia who was admitted with mild limb weakness and lower abdominal purpura. She was prescribed pregabalin (75mg, twice daily) for almost 3 months to treat chronic back pain. Her medical history revealed that 3days before admission, she began experiencing acute bronchitis and was treated with a single dose of azithromycin (500mg). She had developed rapid onset severe myalgia, mild whole body edema, muscle weakness leading to gait instability, abdominal purpura and tender purpura on the lower extremities. Laboratory values included a white blood cell count of 25,400/mL and a creatinine phosphokinase (CPK) concentration of 1250 IU/L. Based on these findings and the patient’s clinical history, a diagnosis of pregabalin- and azithromycin-induced rhabdomyolysis was made.DiscussionThe long-term use of pregabalin and the initiation azithromycin therapy followed by a rapid onset of rhabdomyolysis is indicative of a drug interaction between pregabalin and azithromycin.ConclusionWe report an extremely rare case of rhabdomyolysis with purpura caused by a drug interaction between pregabalin and azithromycin. However, the mechanisms of the interactions between azithromycin on the pregabalin are still unknown

    Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients

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    <p>Abstract</p> <p>Background</p> <p>Hepatitis B virus (HBV) is a major cause of hepatocarcinogenesis.</p> <p>To identify mutations relevant to hepatocellular carcinoma (HCC) development, we compared the full genome sequences of HBV from the sera of patients with and without HCC.</p> <p>Methods</p> <p>We compared the full genome sequences of HBV isolates from 37 HCC patients (HCC group 1) and 38 patients without HCC (non-HCC group 1). We also investigated part of the core promoter region sequences from 40 HCC patients (HCC group 2) and 68 patients without HCC. Of the 68 patients who initially did not have HCC, 52 patients remained HCC-free during the follow-up period (non-HCC group 2), and 16 patients eventually developed HCC (pre-HCC group 2). Serum samples collected from patients were subjected to PCR, and the HBV DNA was directly sequenced.</p> <p>Results</p> <p>All patients had genotype C. A comparison of the nucleotide sequences of the HBV genome between HCC group 1 and non-HCC group 1 revealed that the prevalence of G1613A and C1653T mutations in the core promoter region was significantly higher in the HCC group. These mutations tended to occur simultaneously in HCC patients. Multivariate analysis with group 2 revealed that the presence of HCC was associated with aging and the double mutation. Future emergence of HCC was associated with aging and the presence of a single G1613A mutation.</p> <p>Conclusions</p> <p>G1613A and C1653T double mutations were frequently found in patients with HCC. A single G1613A mutation was associated with future emergence of HCC. These mutations may serve as useful markers in predicting HCC development.</p

    Effects of self-efficacy on oral health behaviours and gingival health in university students aged 18- or 19-years-old

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    Aim Although self-efficacy is known to affect various health-related practises, few studies have clearly examined how self-efficacy correlates with oral health behaviors or the oral health condition. We examined the relationship between gingivitis, oral health behaviors and self-efficacy in university students. Material & Methods A total of 2,111 students (1,197 males, 914 females) aged 18 and 19 years were examined. The degree of gingivitis was expressed as the percentage of bleeding on probing (%BOP). Additional information was collected via a questionnaire regarding oral health behaviors (daily frequency of tooth-brushing, use of dental floss and regular check-up). Self-efficacy was assessed using the Self-Efficacy Scale for Self-care (SESS). Path analysis was used to test pathways from self-efficacy to oral health behaviors and %BOP. Results In the final structural model, self-efficacies were related to each other, and they affected oral health behaviors. Good oral health behaviors reduced dental plaque and calculus, and lower levels of dental plaque and calculus resulted in lower %BOP. Conclusion Higher self-efficacy correlated with better oral health behaviours and gingival health in university students. Improving self-efficacy may be beneficial for maintaining good gingival health in university students. To prevent gingivitis, the approach of enhancing self-efficacy in university students would be useful
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