Color Doppler sonographic study of an iatrogenic fistula between the common carotid artery and internal jugular vein.
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Adult↗
Biomedical subjects
W H Lin
Publications and source records attributed to W H Lin.
Genetic analysis of the HPRT mutation of Lesch-Nyhan syndrome in a Chinese family.
BACKGROUND: The Lesch-Nyhan syndrome is an X-linked recessive inherited disease caused by a complete deficiency of hypoxanthine guanine phosphoribosyl-transferase (HPRT) activity. Many different mutations throughout the HPRT coding region of Lesch-Nyhan patients have been described, including single base substitutions, partial or entire gene deletions, gene insertions or endoduplication of exons. However, study of gene mutation in Chinese patients has rarely been reported in Taiwan. METHODS: Polymerase chain reaction (PCR) and nucleotide sequence analysis were used to identify the location and the nature of the mutation at the HPRT locus in two brothers affected with Lesch-Nyhan syndrome. The HPRT cDNA, amplified from total RNA of patient's peripheral blood by reverse transcription-polymerase chain reaction, was cloned into a pGEM-3Zf(-) vector and then sequenced. Family study involved initial screening using single-strand conformation polymorphism, and further confirmation by direct sequencing of the exon encompassing the mutation. RESULTS: The mutation identified in these two affected siblings was a single nucleotide substitution, from cytosine to guanine, in exon 3 of the HPRT coding region. This transversion putatively caused a single amino acid substitution from phenylalanine to leucine at codon 74 in the translated protein. This base change was further confirmed by direct sequencing of both the HPRT cDNA fragment and the exon 3 of HPRT gene amplified from genomic DNA. The family study revealed that the patient's mother was a heterozygous carrier, and the mutation seemed to have occurred de novo in a germinal cell from one of the maternal grandparents. CONCLUSIONS: This is the first family study on Chinese patients with Lesch-Nyhan syndrome identified by molecular analysis in Taiwan. The mutation described herein is a novel substitution which occurs in a suggested "hotspot" of mutation (exon 3) of the HPRT gene. The application of molecular analysis of HPRT-gene allows not only DNA diagnosis by directly detecting the mutant alleles, but also prenatal diagnosis and carrier identification within individual families affected by Lesch-Nyhan syndrome.
Base Sequence↗
Effect of manganese on tyrosylprotein sulfotransferase activity in PC12 cells.
Recent studies in our laboratory have revealed that Mn2+ is capable of promoting cell spreading and neurite outgrowth in PC12 cells, a process which is dependent on Mn2+ stimulation of the interaction between extracellular matrix (ECM) components and their corresponding integrin receptors. Since the major ECM proteins implicated in the Mn(2+)-induced morphogenesis, fibronectin and vitronectin, are both tyrosine sulfated, it was of interest to determine whether Mn2+ can regulate the activity of the enzyme responsible for tyrosine sulfation, tyrosylprotein sulfotransferase (TPST). Results of the present studies demonstrated that Mn2+ can suppress TPST activity in PC12 cells in both a time and concentration-dependent manner at concentrations of Mn2+ (0.1 to 1 mM) that promote morphological changes in PC12 cells. Since uptake of Mn2+ may occur via the Ca2+ channel, LaCl3, an inhibitor of Ca2+ transport, was examined and found not to prevent the suppression of TPST activity induced by Mn2+, suggesting that Mn2+ may function at an extracellular site. Suppression of TPST activity occurred with cells plated in serum-free medium on a substrata consisting of either serum or polylysine, suggesting that attachment to extracellular matrix was not an absolute requirement for regulation of activity. Consistent with this is the fact that an RGD-containing pentapeptide did not prevent suppression of TPST activity. Results from the present study demonstrated that Mn2+ is capable of promoting the suppression of TPST activity in PC12 cells at concentrations that have been shown to induce cell spreading and neurite outgrowth. However, unlike the Mn(2+)-induced morphological changes, the presence of ECM proteins is not an absolute requirement for suppression of TPST activity.
2-Chloroadenosine↗
In vivo function of surfactants containing phosphatidylcholine analogs.
Increased phospholipase A2 activity demonstrated in some forms of lung injury may contribute to surfactant dysfunction. Phospholipase A2-resistant analogs of dipalmitoylphosphatidylcholine (DPPC) with surfactant properties might therefore be useful lipid components of treatment surfactants for certain lung injuries. The in vivo function of surfactants containing DPPC or the phospholipase-resistant analogs dihexadecylphosphatidylcholine (DEPC) or dihexadecylphosphonotidylcholine (DEPnC), with or without surfactant proteins B and C (SP-B+C), was thus evaluated in preterm rabbits (27 days' gestation). Rabbits randomly received one of seven surfactants (DPPC, DEPC, DEPnC, DPPC+SP-B+C, DEPC+SP-B+C, DEPnC+SP-B+C, or lipid extract surfactant [LES]) or 0.45% NaCl (control) and were ventilated for 30 min. Lipid-only surfactants decreased ventilatory pressures (peak inspiratory pressures minus positive end-expiratory pressure) relative to control (p < 0.05). Addition of SP-B+C further decreased ventilatory pressures to levels similar to LES (p < 0.01 versus control, lipid-only surfactants). Lung dynamic compliances and postventilation pressure-volume curves improved in the following order: LES, SP-B+C lipid surfactants > lipid-only surfactants > control (p < 0.05). All surfactant preparations decreased intravascular 125I-albumin recoveries in the lungs relative to control (p < 0.01 for all surfactants versus control). These results indicate that DEPC and DEPnC were as effective as DPPC as lipid components of synthetic surfactants. And like DPPC, the analogs interacted with isolated SP-B+C and improved in vivo function to levels comparable to LES.
Animals↗
Effect of caffeine on the levels of brain serotonin and catecholamine in the genetically obese mice.
BACKGROUND: Most obesities are known low in sympathetic activity, and brain neurotransmitters may play roles in the defective exhibitions of obesity. Caffeine, a stimulant, which can prompt lipolysis, has been applied on the therapy of obesity. Although the interactive combinations between caffeine and certain neurotransmitters has been appreciated recently, but its regulatory mechanisms are still obscure. This study investigated the effect of caffeine on the body fat deposition, and its interactions with brain serotonin and catecholamine in the genetically obese (ob/ob) mice. METHODS: At 12-week of age, obese mice and their lean counterparts (+/?) were administered with caffeine (4 mg/d) in water for 4 weeks. The brain neurotransmitters levels and body fat content were measured. RESULTS: The obese mice without caffeine treatment had lower brain norepinephrine and epinephrine levels than the lean controls. And there had no difference between obese and lean mice in brain levels of serotonin, tryptophan, and 5-hydroxyindoleacetic acid. Caffeine treatment showed no effect on the food intake, but decreased the body fat content significantly in obese mice. Mice with caffeine treatment showed increase of the levels of brain neurotransmitters in both phenotypes; this effect was more predominant in obese mice. CONCLUSIONS: This study indicated that the effect of caffeine to decrease body fat deposition in the obese mice might be associated with the recovered increases of sympathetic activity.
Adipose Tissue↗
Manganese induces spreading and process outgrowth in rat pheochromocytoma (PC12) cells.
Mn2+ has been shown to promote cell-substrate adhesion and cell spreading in many cell culture systems. In this study, we present data demonstrating that Mn2+ not only promotes spreading, but also induces process outgrowth in rat pheochromocytoma (PC12) cells. In the presence of 1.0 mM MnCl2, cell spreading was apparent by 6 hr, and nearly 50% of the exposed cells extended neurite-like processes. These morphological effects of Mn2+ were both time- and dose-dependent. In the presence of cycloheximide, a protein synthesis inhibitor, both Mn(2+)-induced spreading and neurite outgrowth were prevented, indicating that de novo protein synthesis is required for the effects of Mn2+ to take place. Of the other divalent cations tested, Mg2+, Cd2+, Cu2+, Ni2+, and Zn2+ were ineffective, and only Co2+ partially mimicked the effects of Mn2+. Although Mn(2+)-induced cell adhesion and spreading have been extensively studied, this is the first report that this divalent cation can cause neurite outgrowth. The neurite outgrowth-promoting effects of Mn2+ were distinct from those of nerve growth factor in that the response to Mn2+ was considerably more rapid, but apparently lacked the ability to sustain continuous outgrowth and networking of neurites. Mn2+ also induced the levels of GAP-43 and peripherin, two proteins associated with neuronal differentiation of PC-12 cells. In cells grown in serum-free defined medium, Mn2+ was capable of promoting neurite outgrowth when the cells were plated on surfaces pretreated with normal growth medium, vitronectin, or fibronectin, while it failed to cause these morphological changes in cells plated on untreated or poly-D-lysine-coated substrata. Similarly, Mn2+ also promoted neurite outgrowth from rat sympathetic neurons attached to laminin-treated substrate, but had no effect on neurons maintained on substrate with polylysine only. The pentapeptide Gly-Arg-Gly-Asp-Ser nearly completely prevented the morphological effects of Mn2+ on PC12 cells. These findings are consistent with a hypothesis that Mn(2+)-mediated alteration of an RGD-dependent extracellular matrix-integrin interaction is responsible for the neuritogenic effects.
Amino Acid Sequence↗
[Epidemiological study of gestational diabetes mellitus in Taipei and factors effecting blood glucose].
The prevalence of non-insulin-dependent diabetes mellitus has increased significantly in the last decade. Meanwhile, it has been found that patients with gestational diabetes have a greater chance of developing diabetes than normal subjects. This study was designed to survey the prevalence of GDM in metropolitan Taipei. A screening test with 50 g of glucose was performed on pregnant patients between 24 and 28 weeks of gestation, and a blood sample was collected one hour after ingestion. The subjects with a plasma glucose level over 130 g/dL were scheduled for a standard 75 g oral glucose tolerance test for diagnosis. Altogether, 872 pregnant women participated in the study. According to the WHO criteria which were published in 1985, a total of 224 (25.7%) subjects had a positive screening test. Thirty-seven (4.2%) subjects had impaired glucose tolerance (IGT) and five (0.6%) subjects were found to have GDM after the 75 g OGTT. Comparisons of the glucose levels of women of different ages (< 30 and > or = 30), BMI (< or = 24 and > 24), and parity (0 and > or = 1) demonstrated that women over 30, with a BMI over 24, or a parity over 1 had a significantly higher plasma glucose level than their counterparts in the screening test. Even after BMI-adjustment, the difference was still significant for the age and parity comparisons.
Adult↗
[Studies on the chemical constituents of Fritillaria taipaiensis L].
A new C-nor-D-homo-steroidal alkaloid named taipaienine, together with five known alkaloids namely chuanbeinone, imperialine, verticinone, perimissine and isoverticine were isolated from the bulbs of Fritillaria taipaiensis L. var. ningxiaensis Y. et W.. The unusual structure of taipaienine was a first sample with a hydroxyl group substituted at C-25 of (22)R-trans quinolizidine moiety with orientation of nitrogen lone pair. Their structures were determined by various spectral analyses.
Alkaloids↗
[Effects of fasting and diet resupplementation on the variation of blood zinc, copper, calcium and magnesium levels in two laboratory rodents: DBA/2 mouse and SD rat].
The effects of fasting and diet resupplementation on the variation of certain blood metals were studied in DBA/2 mice and SD rats. Metal concentrations in serum and erythrocyte were determined by atomic absorption spectrometer. Blood zinc levels were decreased and varied within sampling time from 0800 to 1200 AM, and the other blood metals concentrations were no change when animals had no fasting. After overnight fasting, blood zinc levels both in serum and erythrocyte, and erythrocyte magnesium concentration were decreased significantly. Fasting did not alter the sampling time-related variation on serum zinc levels, but would increase the erythrocyte zinc levels in opposite when in comparison with non-fasting. When animals resupplied with diet after fasting, blood zinc increased smoothly, and blood copper, calcium and magnesium would exhibit a lower concentration at the sampling time of 1400 and 1600, respectively. The species and sex did not affect the variation of blood metals levels in this study. This study showed that food intake and absorptive equilibrium of body metals had effects on the variation of blood metals concentration. Endocrine and nutrient factors also might indirectly affect this variation. So, it is suggested that a standard and compatible concern on the sampling time, animals breeding and selection should be noticed when conducting the relevant metals studies with biological samples in order to prohibit any mistakes on the explanatory results.
Animals↗
[Studies on the chemical constituents of Croomia japonica Miq].
A new steroid alkaloid, namely croomionidine (II), together with four known compounds pachysamine A(I), croomine (III), didehydrocroomine (IV) and beta-sitosterol were isolated from the roots of Croomia japonica Miq. Their structures were identified by IR, MS, 1H NMR, 13C NMR and chemical conversion.
Drugs, Chinese Herbal↗
[Alterations of zinc levels in patients with thyroid disorders].
It is known that patients with hyperthyroidism have a lower zinc content in their erythrocytes, and that this decrement returns to normal after treatment with anti-thyroid drugs. This study was designed to investigate the alteration of body zinc levels in thyroid disorder. Two groups of out-patients associated with hyperthyroidism or hypothyroidism, and a group of normal healthy controls were collected. Zinc contents in the blood, hair and 24-hour urine samples were determined by a flame atomic absorption spectrometer. The results showed that patients with hyperthyroidism had a lower erythrocyte zinc level and an increased urinary zinc excretion (p < 0.05). The hypothyroidism had a higher hair zinc content and a decrement in urinary zinc excretion (p < 0.05). Body zinc levels, excluding the plasma zinc, held a certain correlation to the plasma thyroid hormones levels. The urinary zinc levels showed a more parallel variation in the thyroid disorders (p < 0.05). This data indicates that the alteration of urinary zinc levels might be a useful index for thyroid disorder evaluation. Body zinc could also play a physiological role in the metabolic regulation(s) of a thyroid disorder.
Adult↗
[The evaluation of blood perfusion of lower extremities in patients with NIDDM by 133Xe muscle clearance test: a preliminary report].
In this study, we collected twenty NIDDM patients with impaired sensation and clinically suspected angiopathy over both lower extremities. All the patients underwent testing by means of the ultrasonic Doppler technique and were separated into two groups, group 1 with impaired blood flow, and group 2 with no significant impairment of blood flow. Ten normal persons were also included in this study (group 3). The results of the 133Xe muscle clearance test showed that the Q value of group 1 was 0.85 +/- 0.24 [mean +/- SE, ml (100g tissue min-1)], 1.05 +/- 0.31 in group 2 and 1.78 +/- 0.23 in group 3 of normal controls. After statistical analysis, there were significant differences in groups 1 and 2 relative to group 3 (p < 0.05), respectively. This preliminary result indicates that the 133Xe muscle clearance test may be an effective and convenient method to evaluate angiopathy of lower extremities in patients with NIDDM.
Adult↗
Recognition of substrates by tyrosylprotein sulfotransferase. Determination of affinity by acidic amino acids near the target sites.
The sulfation of proteins by tyrosylprotein sulfotransferase (TPST) is highly site-specific. In this study, we examined the sequence specificity of the target site for TPST by determining the kinetics of rat liver TPST with peptides related to the sequence of the C4 component of complement. The data obtained from this study demonstrate that selective elimination of negative charges from the -5 to +5 region of the acceptor tyrosine, either by removal or by isosteric substitution or the acidic amino acids in the region, produced a substantial change in the Km value, with relatively little effect on Vmax. Substitutions at -1 and +1 positions increase the Km value by 22- and 4-fold, respectively, whereas removal of the acidic amino acids from the -5, -4, or +4 positions increased the Km values by a factor of 2-4. The effect of elimination of an acidic amino acid on the Km value was constant and specific for its particular position in relation to tyrosine, and the effect of modification of more than one amino acid was multiplicative. This study provides evidence that: 1) acidic residues near tyrosines promote sulfation by increasing the affinity of enzyme-substrate binding and have little effect on catalytic rate; 2) the contribution of each acidic residue to affinity for TPST is independent and varies according to position relative to the acceptor tyrosine; and 3) the enzyme interacts with a segment of at least 4-5 residues on each side of the tyrosine, with the residues on the -1 and +1 positions being the most important determinants. In general, residues on the NH2-terminal side of the tyrosine have a greater effect on affinity for TPST.
Amino Acid Sequence↗
Thyrotoxicosis accompanied with periodic seizure attacks a case report and review of literature.
A 58-year-old female was admitted and discovered to be a victim of thyrotoxicosis. She had experience periodic seizure attacks for 14 months. These seizures disappeared when function of the thyroid returned to normal. We performed many studies to search for the cause of the seizures. No epileptic focus could be detected from an EEG or a MRI of the brain. There was no abnormal laboratory data such as: hypoglycemia, hypoxemia, serum electrolyte imbalance, or an acid-base imbalance. No evidence of CNS infection was noted. She had good response to antithyroid treatment. We therefore suggest, that the seizure attacks may be related to thyrotoxicosis. In reviewing the literature, we found that only 13 cases of thyrotoxicosis with seizures have been reported since 1956 [1-9].
Female↗
[Investigation of the profile of selected trace metals in genetically obese (ob/ob) and lean (+/?) mice].
Trace metals are known to have important effects on the activity of metalloenzymes and insulin secretion and to be involved in the etiology of various diseases. This study was designed to investigate the distribution and concentration of selected trace metals in the tissues of genetically obese mice, which were known to have hyperinsulinemia. Different phenotypes (ob/ob; +/?) and sexes of 4, 8, 12 week-old mice were killed by decapitation. Metal levels (Zn, Cu, Cd, Cr) in the brain, liver, serum, hair and carcass were determined by an atomic absorption spectrometer. The results showed that obese mice had lower concentrations of zinc in the serum, hair, liver and carcass than lean controls (p less than 0.05), but there was no difference in the brain. Obese mice also had a low carcass cadmium concentration (p less than 0.01), which depended on the sex-age interaction. When expressed in terms of total content, obese mice had higher total liver zinc and carcass chromium contents (p less than 0.05). Obese mice had a higher total carcass copper content at 8 weeks of age. Serum and carcass zinc were showed to be inversely related to body fat in obese mice. The results indicate that zinc may play a special role in thermoregulation and fat metabolism in the liver of obese mice. The tissue distribution and absorption of zinc may have an important correlation in the development of obesity. The roles of copper, cadmium and chromium are still obscure, the related regulations are still open for further questions.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Relationship between brain serotonin and calmodulin in young, genetically obese (ob/ob) mice.
The possible relationships between altered brain serotonin and calmodulin contents on the development of obesity were studied. Eight groups of mice separated by differences in phenotype, sex and age were used in this study. The brain contents of tryptophan, serotonin, 5-hydroxyindoleacetic acid (5-HIAA) and calmodulin were assayed. The contents of brain tryptophan showed no significant differences in any of the mice. The amount of brain serotonin in obese mice was 82% higher than that in their lean counterparts at four weeks of age, but only 11% higher at eight weeks of age. Regardless of age and sex, brain serotonin was positively correlated to the brain calmodulin in the lean mice (r = 0.559, p < 0.01), yet this was not found in obese mice. There was a strong positive correlation between serotonin and 5-HIAA in all mice (r = 0.679, p < 0.001). The elevated amount of serotonin in the brain of four-week-old obese mice is suggested to have important effects on thermoregulation in young genetically obese mice. The results also suggest that abnormal brain serotonin synthesis in obese mouse regulated by calmodulin might interact with certain factors, such as calcium ions, to complete the activation of serotonin-synthesized enzymes in the development of obesity.
Animals↗
2-Chloroadenosine decreases tyrosylprotein sulfotransferase activity in the Golgi apparatus in PC12 cells. Evidence for a novel receptor.
In the present studies, we investigated the activity of tyrosylprotein sulfotransferase (TPST) in the Golgi apparatus of PC12 cells and the regulation of this enzyme by 2-chloroadenosine, an adenosine receptor agonist. Studies employing continuous sucrose gradient and trypsinization of the membranes demonstrate that TPST is located on the luminal side of Golgi apparatus in PC12 cells. Treatment of PC12 cells with 2-chloroadenosine results in a dose-dependent decrease of TPST activity which is observable as early as 3 h after initiation of treatment, maximizes at 24-48 h with continuous exposure, and is readily reversible upon removal of the drug. While forskolin, an agent that directly increases intracellular cAMP, has no effect on TPST activity, 2-chloroadenosine equally suppressed the enzyme activity in both the wild type and a protein kinase A-deficient mutant strain of PC12 cells, indicating that such regulation of TPST activity by 2-chloroadenosine was independent of cAMP-dependent protein phosphorylation. This effect of 2-chloroadenosine can be potentiated by an adenosine uptake blocker dipyridamole but cannot be elicited by other adenosine A1 or A2 receptor agonists, further suggesting that TPST activity in PC12 cells is regulated by 2-chloroadenosine via a novel membrane receptor. Incubation of the cells with cyclo heximide, a protein synthesis inhibitor, also led to a time- and dose-dependent suppression of TPST activity. At concentrations of cycloheximide that produced maximal inhibition (approximately 50%), cotreatment with 2-chloroadenosine did not lead to a further decrease of the TPST activity. These results suggest that the sensitivity of TPST activity to be controlled by protein synthesis provides a mechanism for regulation of its activity by 2-chloroadenosine.
2-Chloroadenosine↗
Chemical synthesis and surface activity of lung surfactant phospholipid analogs. II. Racemic N-substituted diether phosphonolipids.
A series of racemic 16:0 disaturated N-substituted diether phosphonolipid analogs of glycerophospholipids have been synthesized and purified. Isosteric methylene substitution at three of the four ester sites (carboxyl, phosphate) of conventional glycerophospholipids enhanced the hydrophobicity of analog compounds compared with dipalmitoyl phosphatidylcholine (DPPC), the major glycerophospholipid component of lung surfactant. Further substitutions at the nitrogen headgroup also contributed to hydrophobicity/hydrophilicity characteristics, as well as allowing graded variations in headgroup size among the members of the diether phosphonolipid analog series. Interfacial property studies showed that these compounds had significant differences in surface activity characteristics compared with DPPC, including increased adsorption and respreading facility, plus an enhanced ability to generate low surface tension (less than 1 to 4 mN/m) on an oscillating bubble apparatus at 37 degrees C. In addition, pressure-volume mechanical studies in surfactant-deficient excised rat lungs showed that the diether phosphonate analog of DPPC could partially restore pressure-volume characteristics toward normal, both as a pure component and in binary mixtures with palmitoyl-oleoyl phosphatidylglycerol. These findings suggest that selected analog compounds, synthesized with relatively small structural modifications from biologic glycerophospholipids, may have eventual applications as components of synthetic exogenous lung surfactants. Of more immediate importance, analog molecules with defined structural variations are convenient molecular probes for developing structure-surface activity correlates for phospholipid-like surfactants and for investigating the specificity of interactions between glycerophospholipids and other compounds such as proteins.
1,2-Dipalmitoylphosphatidylcholine↗