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Biomedical subjects

S P Hui

Publications and source records attributed to S P Hui.

15 recordsLinked to original sources
PubMed2006

New method of surgical repair for 360-degree cyclodialysis.

A 44-year-old man suffered traumatic 360-degree cyclodialysis in the left eye complicated by persistent hypotony, disc edema, maculopathy, and cataract. Treatment was removal of the cataract with phacoemulsification followed by insertion of a capsular tension ring with 2-point scleral suture fixation with polypropylene in the ciliary sulcus. A foldable acrylic posterior chamber intraocular lens was implanted in the capsular bag through the 4.1 mm corneal tunnel incision. The intraocular pressure responded well with resolution of hypotony, choroidal detachment, disc edema, and maculopathy. Ultrasound biomicroscopy showed complete closure of the cyclodialysis cleft.

Adult↗
PubMed2005

Relationship of gender, body mass index, and axial length with central retinal thickness using optical coherence tomography.

BACKGROUND: Optical coherence tomography (OCT) acquires cross-sectional retinal images with high resolution using low-coherence interferometry. Few studies have studied the effect of demographic data and ocular parameters that may affect central retinal thickness. In this study, these factors were used as parameters to analyse if any significant relationship exists with central retinal thickness. METHODS: Volunteers with a best-corrected visual acuity of 6/12 or better and no evidence of ocular abnormalities or interventions were recruited from October 2001 to March 2003. Body mass index (BMI), autorefraction, and keratometry recordings were measured, followed by applanation tonometry and A-scan ultrasonography. The central retinal thickness of the right eye was analysed using a scan length of 3 cm. Another 25 eyes were selected for interobserver reproducibility. RESULTS: In all, 117 normal subjects (60 male and 57 female subjects) were recruited. The mean thickness of the central retina with a diameter of 1 mm was 203+/-23 microm for male and 189+/-20 microm for female subjects. Age, intraocular pressure, and keratometric readings were not significantly correlated with central retinal thickness. Using multiple regression, gender, BMI, axial length, and signal-to-noise ratio (P<0.05) were significantly associated with the central retinal thickness. The intraclass correlation coefficient was 0.98 for interobserver reproducibility. CONCLUSION: OCT has a high interobserver reproducibility. The male gender, larger BMI, and longer axial length are associated with a significantly thicker central retina and these parameters should be considered for assessing retinal thickening and baseline comparisons in future studies.

Adolescent↗
PubMed2001

Metabolic changes in human CD36 deficiency displayed by glucose loading.

Previous in vitro studies have shown that CD36 participates in cellular fatty acid (FA) uptake. In vivo evidence for a physiologic role of CD36 in this process is poor and mostly obtained in animals. To examine the metabolic role of human CD36, we performed a glucose loading test for normals (n = 16) and subjects with CD36 deficiency, both Type I (n = 5) and Type II (n = 16). After 30 min, FA levels had fallen by 60.1% in normals but by only 31.7% in Type II deficiency (P <0.01 vs. normals) and 16.5% in Type I deficiency which remained significantly higher than the other two groups out to 2 h. Further, changes in triglyceride and glucose metabolism were observed in the both types of CD36 deficiency. Impaired fast FA clearance by muscle and consequently increased hepatic FA uptake seem to underlie these changes. We conclude that human CD36 deficiency causes systemic metabolic changes.

Adult↗
PubMed2000

Human CD36 deficiency is associated with elevation in low-density lipoprotein-cholesterol.

To find out whether CD36 plays a role in the human lipoprotein metabolism, we studied lipoprotein profiles in subjects with CD36 deficiency. Apparently healthy Japanese volunteers (n = 790) were classified by flow cytometry into three groups of normal (platelet and monocyte CD36+, n = 741, 93.8%), type-II deficiency (platelet CD36- and monocyte CD36+, n = 45, 5.7%), and type-I deficiency (platelet and monocyte CD36-, n = 4, 0.5%). At least one of reported mutations in the CD36 gene was found in all four subjects with type-I deficiency and in 23 of the 45 subjects with type II. Among 779 subjects (731 normals, 44 type II, and four type I) with serum triglyceride levels of <400 mg/dL, serum total cholesterol and low-density lipoprotein (LDL) cholesterol were significantly elevated in type-II deficiency (P = 0.0095 and 0.0382 versus normal, respectively, Scheffe's F-test), while differences were not significant in triglyceride and high-density lipoprotein-cholesterol. Similar tendency was observed in type-I deficiency, although the differences were not statistically significant because of small sample size. We conclude that CD36 deficiency elevates LDL cholesterol, indicating a contribution of CD36 to LDL metabolism.

CD36 Antigens↗
PubMed2000

Phenotype-genotype correlation in CD36 deficiency types I and II.

CD36 deficiency was studied with attention to the phenotype-genotype relationship. The diagnosis of CD36 deficiency was made when CD36 was negative on platelets (type II) or on both platelets and monocytes (type I). Among 827 apparently healthy Japanese volunteers, the type I and II deficiencies were found in 8 (1.0%) and 48 (5.8%), respectively. The T for C substitution at nt478 for Pro90Ser and the insertion of A at nt 1159 constituted the major causes of type I and II deficiencies. The dinucleotide deletion at nt539 had a minor role. In two family studies, we found a previously unreported polymorphic site in the 5'-proximal flanking region and the 3'-untranslated region. Including these new polymorphisms, DNA sequence other than the three known mutations affecting CD36 expression was not observed in the CD36 gene, calling into question the previous hypothesis that a platelet-specific silent allele exists near or at the CD36 gene.

Alleles↗
PubMed1999

Conjunctival melanotic lesions in Chinese: comparison with Caucasian series.

Conjunctival melanotic lesions in Chinese were studied and compared with those of Caucasians. These lesions were diagnosed in Chinese patients over a two-year period. They were excised under the clinical diagnoses of nevi, primary acquired melanosis (PAM) and malignant melanoma. For the cases included, the histology slides and clinical information were reviewed. Eighteen cases of nevi and nine non-nevoid lesions were identified. Among the non-nevoid lesions, there were eight cases of basal cell hyperpigmentation (one congenital, five acquired, two unknown) and one malignant melanoma. Benign or atypical melanocytic hyperplasias (MH) were not seen. This pattern is very different from that of Caucasian series. Acquired hyperpigmentation is almost only seen in Chinese and seldom in Caucasians. On the other hand, atypical MH is only seen in Caucasians, and not in Chinese. We conclude that conjunctival hyperpigmentation is associated with ethnicity and does not progress to MH, whether benign or atypical. It should be recognised as a distinct entity of no malignant potential that is part of the PAM clinical spectrum.

Adolescent↗
PubMed1997

Effects of triamcinolone on brain and cerebrospinal fluid apolipoprotein E levels in rats.

The effects of the short term administration of triamcinolone (0.5 mg per 100 g body weight, 5 days) on apolipoprotein E and A-I concentrations in cerebrospinal fluid (CSF), brain extract and serum were studied in male Wistar rats using enzyme immunoassays. ApoE was significantly increased by triamcinolone in apoE-rich HDL1 in serum; 40+/-13 (mean+/-SD) vs. 68+/-23 mg/dl (15 saline-treated rats vs. 11 triamcinolone-treated rats)(P<0.01), which was paralleled by an increase in serum apoA-I (76+/-21 vs. 184+/-24 mg/dl), while serum lipids also increased significantly. No significant difference was observed in the apoE concentrations in CSF (296+/-170 vs. 269+/-67 microg/dl) or brain extract (5.0+/-1.6 vs. 5.7+/-1.8 microg/g wet weight). The apoA-I concentrations found in CSF and brain extract were much lower than those for apoE and were not appreciably affected by triamcinolone: 7.7+/-5.5 vs. 4.5+/-3.1 microg/dl for CSF and <0.5 vs. <0.5 microg/g wet weight for brain extract. The apo E metabolism in the rat central nervous system appears to be refractory to the short term administration of triamcinolone and to changes in the serum lipoprotein metabolism. ApoA-I appears unlikely to play a significant role in the rat central nervous system.

Animals↗
PubMed1997

Quantitative and compositional changes in high density lipoprotein subclasses in patients with various genotypes of cholesteryl ester transfer protein deficiency.

High density lipoprotein (HDL) with and without apolipoprotein (apo) E was quantified and characterized in subjects with three genotypes of cholesteryl ester transfer protein (CETP) deficiency: the nonsense mutation in intron 14 (10 homozygotes and 5 heterozygotes); the missense mutation in the exon 15 (3 homozygotes and 9 heterozygotes); and the Int14A/D442G in 6 compound heterozygotes. ApoE-poor and apoE-rich HDL-cholesterol levels were elevated significantly in all genotypic groups with the decrease in CETP activity, indicating that both types of HDL-cholesterol can be a substrate for CETP. However, an unchanged or only slightly increased serum apoA-II level in each genotype indicated that the HDL particles with apoA-II are relatively resistant to CETP-mediated lipid transfer. Serum apoE-rich HDL level was considerably higher in the Int14A homozygotes than in the compound heterozygotes, in spite of similar apoE-poor HDL-cholesterol levels, which may indicate that apoE-rich HDL is a better substrate for CETP than apoE-poor HDL. Although the apoE-rich and apoE-poor HDL subclasses were similar in the accumulation of cholesteryl ester and depletion of triglyceride, the accumulation of free cholesterol was unique to apoE-rich HDL, indicating inhibited cholesterol esterification on this lipoprotein. Clinical laboratories should be aware of the discrepancy in HDL-cholesterol measurements that comes from the different recoveries of apoE-rich HDL using commercial reagents. In conclusion, CETP deficiency causes considerable quantitative and compositional changes in HDL subclasses, reflecting a significant physiological role for CETP in HDL metabolism.

Adult↗
PubMed1997

[Frequency and effect on plasma lipoprotein metabolism of a mutation in the cholesteryl ester transfer protein gene in the Chinese].

The aspartate to glycine substitution at codon 442 (D442G) in the cholesteryl ester transfer protein (CETP) gene is a common mutation in Japan and is thought to be a factor that elevates the serum high-density lipoprotein (HDL)-cholesterol level in the general Japanese population. In the present study, we investigated the frequency of the D442G mutation in the Chinese subjects living in Beijing. We also studied the effects of the mutation on plasma lipoprotein metabolism in the same population and compared it with that in the Japanese Diagnosis of D442G mutation was established by polymerase chain reaction followed by restriction digestion. Among 379 subjects studied, 16 were found heterozygous thereto (allelic frequency = 2.1%). Unexpectedly, the D442G mutation was not associated with elevated HDL-cholesterol levels in the Chinese. Instead, in comparison to the unaffected, significantly decreased low-density lipoprotein (LDL)-cholesterol and total cholesterol levels were observed in the heterozygotes. These results were discrepant from those obtained in Japan: Japanese D442G heterozygotes had elevated HDL-cholesterol levels with unchanged LDL-cholesterol and total cholesterol levels. The divergence in the effect of D442G mutation on plasma lipoprotein metabolism appears to be related to the significantly low CETP activities in the Chinese affected and unaffected. Although the difference between Japan and China in nutritional conditions is supposed to contribute to the divergence, the precise mechanism remains to be determined.

Apolipoproteins↗
PubMed1996

Native lipoproteins inhibit platelet activation induced by oxidized lipoproteins.

Copper-catalyzed oxidation of low-density lipoproteins (LDL) (0.8 g protein/l LDL, 20 mumol/l CuSo4, 37 degrees C) resulted in the formation of thiobarbituric reactive substances that was substantially completed at 24 hrs whereas their formation from high-density lipoproteins (HDL) plateaued at only 25% of that amount after 8 hrs. The oxidized lipoproteins induced aggregation and increases in [Ca2+]i in washed platelets, but not in platelet-rich plasma, and these activating effects were not inhibited by aspirin or EGTA but were inhibited by both of the native lipoproteins. These results show that oxidized HDL, like oxidized LDL, have platelet activating ability and suggest that the native lipoproteins may play a crucial role in preventing the oxidized lipoprotein-mediated platelet activation.

Aspirin↗
PubMed1995

Evaluation of G-to-A substitution in the apolipoprotein A-I gene promoter as a determinant of high-density lipoprotein cholesterol level in subjects with and without cholesteryl ester transfer protein deficiency.

The effect of a polymorphism, guanine (G) to adenine (A) substitution in the promoter of apolipoprotein A-I gene at a position 78 bp upstream of the transcription initiation site, on the serum high-density lipoprotein (HDL)-cholesterol level was studied in 168 Japanese subjects with HDL-cholesterol levels ranging from 26 to 171 mg/dl. Considering the significant effect of cholesteryl ester transfer protein (CETP) on the HDL-cholesterol level and the common occurrence of its deficiency, we performed statistical analyses separately for two groups: one without CETP deficiency (n = 126) and the other with CETP deficiency (n = 42). In the group without CETP deficiency, in which the numbers of G/G, G/A, and A/A genotypes were 92 (73.0%), 28 (22.2%), and 6 (4.8%), respectively, the frequency of the A allele in the subjects with HDL-cholesterol levels of > or = 70 mg/dl did not differ from subjects with HDL-cholesterol levels of < or = 69 mg/dl, irrespective of gender: 0.154 and 0.145 in males, and 0.182 and 0.174 in females, respectively, for the > or = 70 mg/dl and < or = 69 mg/dl groups. Additionally, the HDL-cholesterol levels for the subjects with the G/G genotype did not differ from those for the subjects with the A allele: 64 +/- 22, 58 +/- 14, 77 +/- 14 and 62 +/- 16 mg/dl, respectively, for the G/G, G/A, A/A, and G/A + A/A in males, and 72 +/- 18, 74 +/- 24, 63 +/- 4, and 73 +/- 23 mg/dl in females. For the group with CETP deficiency, in which the numbers of G/G and G/A + A/A genotypes were 25 (59.5%) and 17 (40.5%), the HDL-cholesterol levels also did not differ: 98 +/- 24 mg/dl and 99 +/- 30 mg/dl, respectively, for the G/G and G/A + A/A genotypes. Thus, there is no evidence that the polymorphism has any effect on serum HDL-cholesterol levels regardless of CETP status. We conclude that the G-to-A substitution in the promoter of apolipoprotein A-I gene does not significantly alter serum HDL-cholesterol level.

Adult↗
PubMed1979

Nitrogen control of Salmonella typhimurium: co-regulation of synthesis of glutamine synthetase and amino acid transport systems.

Nitrogen control in Salmonella typhimurium is not limited to glutamine synthetase but affects, in addition, transport systems for histidine, glutamine, lysine-arginine-ornithine, and glutamate-aspartate. Synthesis of both glutamine synthetase and transport proteins is elevated by limitation of nitrogen in the growth medium or as a result of nitrogen (N)-regulatory mutations. Increases in the amounts of these proteins were demonstrated by direct measurements of their activities, by immunological techniques, and by visual inspection of cell fractions after gel electrophoresis. The N-regulatory mutations are closely linked on the chromosome to the structural gene for glutamine synthetase, glnA: we discuss the possibility that they lie in a regulatory gene, glnR, which is distinct from glnA. Increases in amino acid transport in N-regulatory mutant strains were indicated by increased activity in direct transport assays, improved growth on substrates of the transport systems, and increased sensitivity to inhibitory analogs that are trnasported by these systems. Mutations to loss of function of individual transport components (hisJ, hisP, glnH, argT) were introduced into N-regulatory mutant strains to determine the roles of these components in the phenotype and transport behavior of the strains. The structural gene for the periplasmic glutamine-binding protein, glnH, was identified, as was a gene argT that probably encodes the structure of the lysine-arginine-ornithine-binding protein. Genes encoding the structures of the histidine- and glutamine-binding proteins are not linked to glnA or to each other by P22-mediated transduction; thus, nitrogen control is exerted on several unlinked genes.

Amino Acids↗