Pinning down the thickness of twin walls.
Explore the source record for details and available documents.
Comment↗
Biomedical subjects
W T Lee
Publications and source records attributed to W T Lee.
Familial risk of allergic rhinitis and atopic dermatitis among Chinese families in Singapore.
INTRODUCTION: This study aims to determine the familial risk of atopic dermatitis (AD) and allergic rhinitis (AR) in Chinese children. MATERIALS AND METHODS: A cross-sectional study was conducted in a housing estate in Singapore. Data was collected using an interviewer-administered questionnaire. Participants included 257 Chinese families. Prevalence rate ratios (PRRs) and 95% confidence interval (CI) were calculated. RESULTS: For AD in all children, an increasing trend was found with PRRs of 1.9 (95% CI, 0.3 to 11.8) and 1.5 (95% CI, 0.4 to 5.5) for only father and only mother affected, respectively, to 2.3 (95% CI, 0.4 to 13.7) for both parents affected. In AR, a PRR of 2.7 (95% CI, 1.8 to 3.9) and 2.2 (95% CI, 1.5 to 3.2) for only father and only mother affected, respectively, and 4.5 (95% CI, 3.3 to 6.1) for both affected was found. The PRR (2.2; 95% CI, 1.4 to 3.7) of the first child developing AR when paternal or maternal history was positive was similar. This rose to 3.4 (95% CI, 2.2 to 5.1) when both parents also had AR. The PRR of the second child developing AR was 3.9 (95% CI, 1.7 to 8.9) when the first child alone was positive for AR and 7.0 (95% CI, 3.5 to 13.9) when both parents and the eldest child had AR. CONCLUSION: A positive family history increases the risk of developing AD and AR with increasing risk dependent on number of relatives affected. The second child's risk of AR is also associated with AR in the first child, suggesting mechanisms of incomplete penetrance.
China↗
MEG localization of rolandic spikes with respect to SI and SII cortices in benign rolandic epilepsy.
The purpose of this study was to study the relationship between interictal spike sources and somatosensory cortices in benign rolandic epilepsy of childhood (BREC) using a whole-scalp neuromagnetometer. We recorded spontaneous magnetoencephalography (MEG) and EEG signals and cortical somatosensory-evoked magnetic fields (SEFs) to electric stimulation of the median nerve in 9 children with BREC. Interictal rolandic discharges (RDs) and SEFs were analyzed by equivalent current dipole (ECD) modeling. Based on the orientation and locations of corresponding ECDs, we compared generators of RDs with primary (SI) and second somatosensory cortices (SII). Our results showed that RDs and SII responses had similar ECD orientation on the magnetic field maps. The ECDs of RDs were localized 15.3 +/- 1.9 and 12.2 +/- 2.8 mm anterior to SI and SII, respectively. The spatial distance on average from the location of RDs to SII (21.9 +/- 1.6 mm) cortex was significantly shorter than to SI cortex (29.7 +/- 1.7 mm) (P<0.01, Wilcoxon signed-rank test). In conclusion, the cortical generators for RDs in patients with BREC are localized in the precentral motor cortex, closer to hand SII than to SI cortex.
Child↗
The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload.
Previous studies showed that 3-nitropropionic acid, an irreversible inhibitor of succinate dehydrogenase, produced neuronal death secondary to perturbed intracellular calcium homeostasis. However, the response of intramitochondrial calcium ([Ca(2+)](m)) to 3-nitropropionic acid remains unknown. In this study, we investigated the roles of and relationships among [Ca(2+)](m) overload, mitochondrial reactive oxygen species, and mitochondrial membrane depolarization in 3-nitropropionic acid-induced neuronal death. Following 1 mM 3-nitropropionic acid treatment on primary rat neuronal cultures, there was a gradual increase of [Ca(2+)](m) beginning at 2-4 h post 3-nitropropionic acid application, and a twofold increase of mitochondrial reactive oxygen species at 4 h. These were followed by mitochondrial membrane depolarization at 6-8 h post-treatment. By inhibiting [Ca(2+)](m) uptake, Ruthenium Red attenuated the production of reactive oxygen species, and prevented the 3-nitropropionic acid-induced mitochondrial membrane depolarization and 70% of apoptotic neuronal death (P<0.001). Inhibition of caspase activation attenuated the elevation of [Ca(2+)](m) (P<0.001), indicating that caspase activation plays a role in the elevation of [Ca(2+)](m). MK-801, an antagonist of N-methyl-D-aspartate (NMDA) glutamate receptors, prevented 3-nitropropionic acid-induced [Ca(2+)](m) elevation, caspase-3 activation, mitochondrial depolarization, and neuronal death. We conclude that the activation of NMDA glutamate receptor contributes to mitochondrial alterations induced by 3-nitropropionic acid. Inhibition of its activation and [Ca(2+)](m) overload with subsequent mitochondrial membrane depolarization can therefore attenuate the neuronal death induced by 3-nitropropionic acid.
Animals↗
The catalytic incineration of (CH3)2S and its mixture with CH(3)SH over a Pt/Al(2)O(3) catalyst.
Catalytic incineration is one of the cost-effective technologies to solve the troublesome volatile organic compounds (VOCs). However, some sulfur containing VOCs, such as dimethyl sulfide, may deactivate the Pt catalyst that is commonly used in the catalytic incineration process. This paper provides information on the poisoning effect of (CH3)2S. The catalytic incineration of (CH3)2S, typically emitted from the petrochemical industry, over a Pt/Al(2)O(3) fixed bed catalytic reactor was studied. The effects of operating parameters including inlet temperature, space velocity, (CH3)2S concentration, O2 concentration and catalyst size were characterized. Catalytic incineration on a mixture of (CH3)2S with CH(3)SH was also tested. The results show that the conversions of (CH3)2S increase as the inlet temperature increases and the space velocity decreases. The higher the (CH3)2S concentration is, the lower its conversion is. The O2 concentration has a positive effect on the conversion of (CH3)2S. (CH3)2S has a poisoning effect on the Pt/Al(2)O(3) catalyst, especially at lower temperatures. The conversion of (CH3)2S is significantly suppressed by the existence of CH(3)SH.
Air Pollution↗
IFN-gamma production by Th1 cells generated from naive CD4+ T cells exposed to norepinephrine.
During activation in vivo, naive CD4(+) T cells are exposed to various endogenous ligands, such as cytokines and the neurotransmitter norepinephrine (NE). To determine whether NE affects naive T cell differentiation, we used naive CD4(+) T cells sort-purified from either BALB/c or DO11.10 TCR-transgenic mouse spleens and activated these cells with either anti-CD3/anti-CD28 mAbs or APC and OVA(323-329) peptide, respectively, under Th1-promoting conditions. RT-PCR and functional assays using selective adrenergic receptor (AR) subtype antagonists showed that naive CD4(+) T cells expressed only the beta 2AR subtype to bind NE and that stimulation of this receptor generated Th1 cells that produced 2- to 4-fold more IFN-gamma. This increase was due to more IFN-gamma produced per cell upon restimulation instead of more IFN-gamma-secreting cells, as determined by IFN-gamma-specific immunofluorescence and enzyme-linked immunospot. In contrast, Th1 cell differentiation was unaffected when naive T cells were exposed to NE and activated either in the presence of a neutralizing anti-IL-12 mAb or by APC from IL-12-deficient mice. Moreover, the addition of IL-12 to the IL-12-deficient APC cultures restored the ability of NE to increase Th1 differentiation. Taken together, these results indicate that a possible link may exist between the signaling pathways used by NE and IL-12 to increase naive CD4(+) T cell differentiation to a Th1 cell.
Animals↗
Coronary artery fistulas: long-term results of surgical correction.
BACKGROUND: Opinions vary as to whether operation should be offered patients with coronary artery fistula, particularly to those who are asymptomatic. Published studies lacked long-term follow-up data. METHODS: We studied 41 patients with coronary artery fistula operated in our unit in the past 30 years with restudies including coronary angiograms in those who agreed to the investigation. RESULTS: There was no operative mortality and operative morbidity was low. The mean duration of follow-up was 9.1 years and 96.9% of the patients were asymptomatic. Twenty-one patients had a coronary angiogram. The native coronary artery either remained dilated and tortuous, or more frequently had thromboses with a short proximal stump. (None of these patients had evidence of myocardial ischemia.) Four patients had demonstrable recurrence fistula but without hemodynamic disturbance. CONCLUSIONS: We advocate operation for all patients with coronary artery fistulas and demonstrable shunting in view of minimal operative risks. Small asymptomatic fistulas without demonstrable shunting should be left alone. The relatively high incidence of residual or recurrent fistula makes long-term follow-up mandatory.
Adolescent↗
Early epileptic encephalopathy with suppression burst electroencephalographic pattern--an analysis of eight Taiwanese patients.
Early epileptic encephalopathy with suppression burst (SB) comprises two distinct epileptic syndromes, early infantile epileptic encephalopathy (EIEE) and early myoclonic encephalopathy (EME). We reviewed etiologies, neurological outcome and clinico-electroencephalographic features of EIEE and EME. Chart records of early epileptic encephalopathy with SB from January 1997 to December 2000 were reviewed. These cases fulfilled the diagnostic criteria of EIEE and EME. Totally eight patients (four females, four males) were enrolled. They consisted of three cases of EIEE and five cases of EME. The follow-up periods ranged from 6 to 30 months. For EIEE, two cases had migrational disorders, and one was cryptogenic; for EME, three cases had non-ketotic hyperglycinemia (NKH), one was pyridoxine dependency and one was cryptogenic. The main initial seizure patterns were tonic spasms in EIEE, and were erratic myoclonus in EME. The age of seizure onset ranged from 26 h to 5 days after birth for EIEE, and 2 h to 7 days of life for EME. The SB pattern in the electroencephalography (EEG) was noted mainly during sleep state in EME, but in both awake and sleep states in EIEE. Asymmetric SB pattern and background activities in EEG were found in migrational disorders. The EEG in all cases of EIEE changed to hypsarrhythmia at 4-6 months of age. In EME, only the EEG in cases of NKH evolved to hypsarrhythmia. Response to anti-convulsants was generally poor. All had severe psychomotor retardation. Although EIEE and EME share several common features, differences in terms of seizure seminology and evolution, EEG patterns and etiologies still exist.
Anticonvulsants↗
Selective and biphasic effect of the membrane lipid peroxidation product 4-hydroxy-2,3-nonenal on N-methyl-D-aspartate channels.
Increased oxyradical production and membrane lipid peroxidation occur in neurons under physiological conditions and in neurodegenerative disorders. Lipid peroxidation can alter synaptic plasticity and may increase the vulnerability of neurons to excitotoxicity, but the underlying mechanisms are unknown. We report that 4-hydroxy-2,3-nonenal (4HN), an aldehyde product of lipid peroxidation, exerts a biphasic effect on NMDA-induced current in cultured rat hippocampal neurons with current being increased during the first 2 h and decreased after 6 h. Similarly, 4HN causes an early increase and a delayed decrease in NMDA-induced elevation of intracellular Ca2+ levels. In contrast, 4HN affects neither the ion current nor the Ca2+ response to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA). The initial enhancement of NMDA-induced current is associated with increased phosphorylation of the NR1 receptor subunit, whereas the delayed suppression of current is associated with cellular ATP depletion and mitochondrial membrane depolarization. Cell death induced by 4HN is attenuated by an NMDA receptor antagonist, but not by an AMPA receptor antagonist. A secreted form of amyloid precursor protein, previously shown to protect neurons against oxidative and excitotoxic insults, prevented each of the effects of 4HN including the early and late changes in NMDA current, delayed ATP depletion, and cell death. These findings show that the membrane lipid peroxidation product 4HN can modulate NMDA channel activity, suggesting a role for this aldehyde in physiological and pathophysiological responses of neurons to oxidative stress.
Adenosine Triphosphate↗
The kinetics of catalytic incineration of C2H5SH and (CH3)2S2 over a Pt/Al2O3 catalyst.
Catalytic incineration is one of the cost-effective technologies to solve the troublesome VOCs. However, some sulfur containing VOCs, such as ethyl mercaptan and dimethyl disulfide, may deactivate the Pt catalyst that is commonly used in the catalytic incineration process. The catalytic incineration of these compounds over a Pt/Al2O3 catalyst was carried out in a bench scale catalytic incinerator. Three kinetic models, such as power-rate law, Mars and Van Krevelen model, and Langmuir-Hinshelwood model were used to analyze the results. A differential reactor design was used for best fit of kinetic models in this study. The results show that the Langmuir-Hinshelwood model is feasible to describe the catalytic incineration of both C2H5SH and (CH3)2S2. This suggests that the chemical adsorption of O2 molecule is important in the process of catalytic incineration of C2H5SH and (CH3)2S2.
Adsorption↗
Studies on the changes of c-fos protein in spinal cord and neurotransmitter in dorsal root ganglion of the rat with an experimental peripheral neuropathy.
Animal models for human chronic pain syndromes have been developed and widely used for pain research. One of these neuropathic pain models by Kim and Chung (1992) has many advantages for operation and pain elicitation. In this neuropathic model we have examined the c-fos protein, substance P, CGRP immunoreactivity in dorsal root ganglia and dorsal horn. 50 Sprague-Dawley rats were used for this study. L5 and L6 spinal nerves were ligated tightly to produce the neuropathic pain model. After 2, 4, 8, 16, and 24 hours and 1 week of surgery, rats were anesthetized and sacrificed by perfusion. After confirmation of the roots transected by the surgery, the L5 and L6 dorsal root ganglions and spinal cord were removed and processed for immunohistochemistry. All tissue sections were immunohistochemically stained for substance P, CGRP and c-fos using the peroxidase-antiperoxidase (PAP) method. The number of immunostained substance P and CGRP dorsal root ganglion cells and c-fos immunoreactive dorsal horn cells were counted and analyzed statistically with Mann-Whitney U test. The results are as follows. The number of c-fos protein immunoreactive neurons in the superficial layer of dorsal horn were increased markedly 2 hours after operation, and gradually decreased to normal level 1 week after operation. The number of c-fos protein immunoreactive neurons in the deep layer of the dorsal horn gradually increased to a peak 24 hours after operation, then decreased to the normal level 1 week after operation. The number of substance P and CGRP immunoreactive L5 and L6 dorsal root ganglion neurons were decreased markedly 1 week after the pain model operation. In conclusion, after neuropathic pain model operation, c-fos proteins were immediately expressed in the superficial layer of spinal dorsal horn, thereafter c-fos proteins in the deep layer of spinal dorsal horn were expressed. CGRP and substance P immunoreactive neurons in DRG were decreased markedly 1 week after neuropathic pain model operation. These decrements do not coincide with the other chronic pain models, which show great increases in these pain transmitting substances. Therefore, the relationship between pain and c-fos, SP and CGRP should be investigated further.
Animals↗
Human papilloma virus type 16 E7 genes protect astrocytes against apoptotic and necrotic death induced by hydrogen peroxide.
Hydrogen peroxide is considered to be a dose- and time-dependent mediator in apoptotic and necrotic death. In this study, we examined the signaling of the E6 and E7 proteins with respect to apoptosis or necrosis after H2O2 injury using an in vitro model with overexpressed E6 or E7 genes. For this purpose, the E6 and E7 gene expressing astrocytes were exposed to 10 micromole and 200 micromole H2O2 solutions. Twenty- four hours after treatment with the lower dosage(10 micromole H2O2), control, E6-expressing cells suffered about 45% injury and LXSN-expressing cells decreased by 67% as assessed by LDH release. However, E7-expressing cells showed less injury, resulting in 20-30% of LDH release. Astrocytes expressing E6, E7, LXSN and mock-infected cells showed a typical apoptotic death pattern on the DNA gel after treatment with a low-dose of H2O2 (10 micromole), however they died from necrotic death after a high-dose (200 micromole) H2O2. Overexpression of HPV-E7 genes protected the cells from apoptotic death after a low-dose of H2O2 and from necrotic death after a high-dose of H2O2, while the overexpression of E6 genes from the necrotic death. E7 expressing astrocytes showed higher catalase activity and the levels of E2F protein surged more than 100-folds compared with the control astrocytes. We believe that the activity of E7 protein to protect astrocytes from H2O2 injury was at least partly due to increased catalase, a scavenger protein.
Animals↗
Immunogenicity of a foreign peptide expressed within a capsid protein of an attenuated coxsackievirus.
The immunogenicity of soluble peptides can be improved by expression within recombinant microorganisms. The immunogenicity of a peptide expressed within a capsid protein of an attenuated coxsackievirus B4 was evaluated. The insertion site was chosen based on its antigenic structure. A foreign peptide was inserted into a region of the VP1 capsid protein that was identified as a T helper cell epitope. A recombinant virus containing ten amino acids of ovalbumin sequence was genetically stable and retained the biological and physical characteristics of the parental virus. The recombinant was able to elicit a T helper cell response against ovalbumin sequences. This study shows, for the first time, that coxsackievirus can be used as an expression vector and that insertion of heterologous peptides into an immunogenic region is a viable strategy for inducing T helper cell responses against foreign sequences. The implications of this work are that the attenuated coxsackievirus variant may be useful as a vaccine vector for expressing T helper cell epitopes that are important in inducing protective immunity.
Amino Acid Sequence↗
Pepsin-mediated processing of the cytoplasmic histone H2A to strong antimicrobial peptide buforin I.
The intestinal epithelium forms a first line of innate host defense by secretion of proteins with antimicrobial activity against microbial infection. Despite the extensive studies on the antimicrobial host defense in many gastrointestinal tracts, little is known about the antimicrobial defense system of the stomach. The potent antimicrobial peptide buforin I, consisting of 39 aa, was isolated recently from the stomach tissue of an Asian toad, Bufo bufo gargarizans. In this study we examined the mechanism of buforin I production in toad stomach tissue. Buforin I is produced by the action of pepsin isozymes, named pepsin Ca and Cb, cleaving the Tyr39-Ala40 bond of histone H2A. Immunohistochemical analysis revealed that buforin I is present extracellularly on the mucosal surface, and unacetylated histone H2A, a precursor of buforin I, is localized in the cytoplasm of gastric gland cells. Furthermore, Western blot analysis showed that buforin I is also present in the gastric fluids, and immunoelectron microscopy detected localization of the unacetylated histone H2A in the cytoplasmic granules of gastric gland cells. The distinct subcellular distribution of the unacetylated histone H2A and the detection of the unacetylated buforin I both on the mucosal surface and in the lumen suggest that buforin I is produced from the cytoplasmic unacetylated histone H2A secreted into the gastric lumen and subsequently processed by pepsins. Our results indicate that buforin I along with pepsins in the vertebrate stomach may contribute to the innate host defense of the stomach against invading microorganisms.
Amino Acid Sequence↗
Neonatal administration of IL-12 enhances the protective efficacy of antiviral vaccines.
Neonates are highly susceptible to infectious agents and are known to display polarized expression of Th2-like cytokines and Abs. This neonatal immune bias has important implications for the development of vaccine strategies, particularly against viral infections. We now report that coadministration of IL-12 and an influenza subunit vaccine at birth enhances the protective efficacy of antiviral vaccination. Immunization and treatment with IL-12 within 24 h of birth resulted in elevated expression of IFN-gamma, IL-10, and IL-15 mRNA in the spleens of newborn mice compared with animals exposed to vaccine only. In addition, these animals showed dramatic increases in IFN-gamma-, IL-2-, and IL-4-secreting cells, and in IgG2a Ab levels upon adult challenge compared with mice primed with vaccine alone. Most importantly, animals vaccinated and simultaneously treated with IL-12 at birth displayed enhanced survival after lethal challenge with infectious influenza virus as adults compared with infected animals that had been primed with vaccine alone. This augmented protection required B cells and could be transferred to naive mice by immune serum. Collectively, these results provide evidence that administration of IL-12 to neonates induces a Th1-like response in newborns and elicits protective antiviral immune memory.
Adjuvants, Immunologic↗
Temporal changes of cerebral metabolites and striatal lesions in acute 3-nitropropionic acid intoxication in the rat.
To investigate the mechanisms of neuronal death in neurodegeneration, in vivo localized proton magnetic resonance spectroscopy ((1)H-MRS) and diffusion-weighted MRI (DWI) were used to evaluate temporal changes in rat striata after administration of 3-nitropropionic acid. It was found that N-acetylaspartate (NAA) reduction, with nearly simultaneous evidence of striatal lesions in DWI, was preceded by a significant and progressive increase of acetate. Shortly before the NAA levels decreased to the lowest point, acetate levels peaked and began to gradually decline toward the control levels. These results suggest that acetate increase may arise from fatty acid degradation, inhibition of succinate dehydrogenase and possible NAA hydrolysis. The elevated acetate may provide a source of acetyl group for membrane repair during excitotoxic brain injury. Magn Reson Med 44:29-34, 2000.
Acetates↗
Cytokine production by naive and primary effector CD4+ T cells exposed to norepinephrine.
We recently showed that clones of Th1 cells, but not Th2 cells, expressed a functional beta-2-adrenergic receptor (beta2AR) and that either norepinephrine or the beta2AR agonist terbutaline stimulated this receptor to modulate the level of Th1 cytokines produced. In the present study, we show that norepinephrine and terbutaline stimulate the beta2AR to decrease the level of IL-2 produced by freshly isolated murine splenic naive CD4+ T cells from either Balb/C or DO11.10 transgenic mice and activated polyclonally with anti-CD3 and anti-CD28 mAbs. In contrast, the level of cytokines produced by primary effector Th1 and Th2 cells were unaffected when norepinephrine, terbutaline, or cAMP analogs were added at the time of restimulation. These results suggest that a diversity exists among CD4+ T-cell subsets with respect to the level of adrenergic receptor expression, responsiveness to cAMP, stage of cell differentiation, or a combination of the above.
Adrenergic beta-Agonists↗
Neuroprotective effect of lamotrigine and MK-801 on rat brain lesions induced by 3-nitropropionic acid: evaluation by magnetic resonance imaging and in vivo proton magnetic resonance spectroscopy.
Magnetic resonance imaging and in vivo proton magnetic resonance spectroscopy were used to evaluate the therapeutic effect of lamotrigine and MK-801 on rat brain lesions induced by 3-nitropropionic acid. Systemic administration of 3-nitropropionic acid (15 mg/kg per day) to two-month-old Sprague-Dawley rats (n = 10 for each group) for five consecutive days induced selective striatal and hippocampal lesions and specific behavioral change. Pretreatment with lamotrigine (10 mg/kg or 20 mg/kg per day) or MK-801 (2 mg/kg per day) attenuated the lesions and behavioral change. There were no significant differences in T2 values of the striatum and hippocampus among rats pretreated with MK-801, lamotrigine (20 mg/kg) and sham controls. Significant elevations of succinate/creatine and lactate/creatine ratios and decreases of N-acetylaspartate/creatine and choline/creatine ratios were observed after 3-nitropropionic acid injections (P < 0.001). The changes were nearly prevented after pretreatment with lamotrigine (20 mg/kg). However, the N-acetylaspartate/creatine in rats pretreated with lamotrigine (10 mg/kg) (P < 0.01) and MK-801 (P < 0.05) still showed significant reduction as compared with sham controls. Thus we conclude that both lamotrigine and MK-801 are effective in attenuation of brain lesions induced by 3-nitropropionic acid. A higher dose of lamotrigine provides a better neuroprotective effect than MK-801. With a better therapeutic effect and fewer side effects, lamotrigine is more promising for potential clinical application.
Animals↗