Neurocutaneous melanosis and negative fluorodeoxyglucose positron emission tomography

Neurocutaneous melanosis is a rare condition characterized by cutaneous melanocytic naevi and the presence of melanocytes in the leptomeninges. It is commonly associated with malignant melanoma formation in the central nervous system (CNS) with poor prognosis. Herewe report a 13-year-old boy with neurocutaneous melanosis who presented with seizure with diffuse CNS malignant melanoma, as demonstrated by magnetic resonance imaging (MRI). 18F-fluorodeoxyglucose positron emission tomography (PET) was carried out, but was unable to detect the CNS involvement. So far, this is the first report involving the use of PET in neurocutaneous melanosis and we suggest that MRI is more sensitive than PET with 18F-fluorodeoxyglucose in such conditions. © 2010 The Authors. Journal compilation © 2010 College of Surgeons of Hong Kong.postprin

Editorial: Advanced methods for public transport system management

published_or_final_versionSpringer Open Choice, 01 Dec 201

Diagnosed duration of type-2 diabetes mellitus and periodontitis

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Liver Enzymes and Risk of Ischemic Heart Disease and Type 2 Diabetes Mellitus: A Mendelian Randomization Study

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Nucleotide precursors prevent folic acid-resistant neural tube defects in the mouse

Closure of the neural tube during embryogenesis is a crucial step in development of the central nervous system. Failure of this process results in neural tube defects, including spina bifida and anencephaly, which are among the most common birth defects worldwide. Maternal use of folic acid supplements reduces risk of neural tube defects but a proportion of cases are not preventable. Folic acid is thought to act through folate one-carbon metabolism, which transfers one-carbon units for methylation reactions and nucleotide biosynthesis. Hence suboptimal performance of the intervening reactions could limit the efficacy of folic acid. We hypothesized that direct supplementation with nucleotides, downstream of folate metabolism, has the potential to support neural tube closure. Therefore, in a mouse model that exhibits folic acid-resistant neural tube defects, we tested the effect of specific combinations of pyrimidine and purine nucleotide precursors and observed a significant protective effect. Labelling in whole embryo culture showed that nucleotides are taken up by the neurulating embryo and incorporated into genomic DNA. Furthermore, the mitotic index was elevated in neural folds and hindgut of treated embryos, consistent with a proposed mechanism of neural tube defect prevention through stimulation of cellular proliferation. These findings may provide an impetus for future investigations of supplemental nucleotides as a means to prevent a greater proportion of human neural tube defects than can be achieved by folic acid alone

Formate supplementation enhances folate-dependent nucleotide biosynthesis and prevents spina bifida in a mouse model of folic acid-resistant neural tube defects

The curly tail mouse provides a model for neural tube defects (spina bifida and exencephaly) that are resistant to prevention by folic acid. The major ct gene, responsible for spina bifida, corresponds to a hypomorphic allele of grainyhead-like 3 (Grhl3) but the frequency of NTDs is strongly influenced by modifiers in the genetic background. Moreover, exencephaly in the curly tail strain is not prevented by reinstatement of Grhl3 expression. In the current study we found that expression of Mthfd1L, encoding a key component of mitochondrial folate one-carbon metabolism (FOCM), is significantly reduced in ct/ct embryos compared to a partially congenic wild-type strain. This expression change is not attributable to regulation by Grhl3 or the genetic background at the Mthfd1L locus. Mitochondrial FOCM provides one-carbon units as formate for FOCM reactions in the cytosol. We found that maternal supplementation with formate prevented NTDs in curly tail embryos and also resulted in increased litter size. Analysis of the folate profile of neurulation-stage embryos showed that formate supplementation resulted in an increased proportion of formyl-THF and THF but a reduction in proportion of 5-methyl THF. In contrast, THF decreased and 5-methyl THF was relatively more abundant in the liver of supplemented dams than in controls. In embryos cultured through the period of spinal neurulation, incorporation of labelled thymidine and adenine into genomic DNA was suppressed by supplemental formate, suggesting that de novo folate-dependent biosynthesis of nucleotides (thymidylate and purines) was enhanced. We hypothesise that reduced Mthfd1L expression may contribute to susceptibility to NTDs in the curly tail strain and that formate acts as a one-carbon donor to prevent NTDs

One-stage debridement versus conventional therapy in type-2 diabetic periodontitis patients

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Simple Non-laboratory- and Laboratory-based Risk Assessment Algorithms and Nomogram for Detecting Undiagnosed Diabetes Mellitus

Background: To develop a simple nomogram which can be used to predict the risk of diabetes mellitus (DM) in asymptomatic non-diabetic general population based on non-laboratory-based and laboratory-based risk algorithms. Methods: Anthropometric data, plasma fasting glucose, full lipid profile, exercise habit and family history of DM were collected from Chinese non-diabetic subjects aged 18-70. Logistic regression analysis was performed on the data of a random sample of 2518 subjects to construct non-laboratory-based and laboratory-based risk assessment algorithms for the detection of undiagnosed DM; both algorithms were validated on the data of the remaining sample (n=839). Hosmer-Lemeshow χ2 statistic and area under the receiver-operating characteristic curve (AUC) were employed to assess the calibration and discrimination of the different DM risk algorithms. Results: Of 3357 subjects recruited, 271 (8.1%) had undiagnosed DM defined by fasting glucose≥7.0mmol/L or 2-hour post-load plasma glucose≥11.1mmol/L after oral glucose tolerance test. The non-laboratory-based risk algorithm, with score ranging from 0 to 33, included age, body mass index, family history of DM, regular exercise and uncontrolled blood pressure; the laboratory-based risk algorithm, with score ranging from 0 to 37, added triglyceride level to the risk factors. Both algorithms demonstrated acceptable calibration (Hosmer-Lemeshow test: P=0.229 and P=0.483, respectively) and discrimination (AUC: 0.709 and 0.711, respectively) for the detection of undiagnosed DM. The optimal cutoff point on the receiver-operating characteristic curve was 18 for the detection of undiagnosed DM in both algorithms. Conclusions: Simple-to-use nomogram for detecting undiagnosed DM has been developed using the validated non-laboratory-based and laboratory-based risk algorithms.postprin

Use of biologics for inflammatory bowel disease in Hong Kong: consensus statement

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Diabetes incidence and prevalence in Hong Kong, China during 2006-2014

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