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Biomedical subjects

L Ma

Publications and source records attributed to L Ma.

At least 379 records · Page 21Linked to original sources
PubMed1997

Ig S gamma-specific DNA binding protein SNAP is related to the helix-loop-helix transcription factor E47.

SNAP, a DNA-binding protein, is specific for the S gamma switch regions. Two E-2 box consensus binding motifs are located within the SNAP recognition site. Direct- and competition-binding analyses demonstrate that a truncated form of the E47 transcription factor, E47S, is capable of specific interactions with the SNAP binding motif. The methylation interference pattern for E47S binding on the pl.S gamma 3.A.1 probe was similar to that previously obtained for SNAP binding activity and was also related to that found for E47S on the microE5 probe. The interaction of purified E47S with the SNAP recognition motif was cooperative and formed complexes which migrated more slowly than the E47S homodimer complex. SNAP is distinguished from full-length E47 homodimers, found in BCF-1, by its migration position in the gel shift assay, differences in the competition-binding results and its unique reactivity with anti-E47 antibodies. SNAP is related to E47 as judged by a similar methylation interference pattern on S gamma 3 A site DNA and by its reactivity with anti-E47 mAb. The anti-E47 antibodies block SNAP binding to its cognate site, whereas anti-E47 antibodies supershift E47 homodimers bound to the microE5 recognition site. Thus, SNAP may be a hetero-oligomeric species containing E47 or highly related proteins.

Animals↗
PubMed1997

Effect of 17-beta estradiol in the rabbit: endothelium-dependent and -independent mechanisms of vascular relaxation.

Short-term estrogen administration has been independently proposed to produce arterial vasodilation by both an indirect mechanism and a direct mechanism (inhibition of calcium entry though the L-type calcium channel). The proposed contributions of such diverse mechanisms to the vascular actions of 17beta-estradiol were examined in perfused hearts and in aortic ring sections isolated from female rabbits. In isolated rabbit hearts retrogradely perfused with Tyrode's solution, concentration-response curves to 17beta-estradiol (10(-9)-10(-5) M) were performed under control conditions and during perfusion with Bay K8644 (10(-7) M). 17beta-Estradiol produced a concentration-dependent decrease in coronary vascular resistance proportional to nitric oxide (NO) release in the presence and absence of Bay K8644. The addition of N(G)-nitro-L-arginine methyl ester (L-NAME; 10(-4) M) to the perfusate (a) completely inhibited NO formation, (b) produced a 2.3-fold and 1.55-fold rightward shift in the concentration-response curve to 17beta-estradiol for Bay K8644 treated and control hearts, respectively, and (c) failed to prevent coronary artery vasodilation. In isolated aortic rings contracted with Bay K8644, 17beta-estradiol (10(-5) M) relaxed both intact (58%) and denuded (54%) aortic rings. L-NAME (10(-4) M) completely blocked NO release in intact rings but did not prevent relaxation in denuded aortic rings. The data demonstrate (a) an endothelium-dependent relaxation by 17beta-estradiol, coincident with NO formation and suppressed by L-NAME, and (b) a direct relaxation of aortic and coronary smooth muscle independent of NO formation at higher 17beta-estradiol concentrations.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Mandibular reconstruction in children with obstructive sleep apnea due to micrognathia.

Obstructive sleep apnea in children with micrognathia may be severe enough to necessitate permanent airway maintenance. Affected children form a small, but important, group of patients because early reconstructive surgery to the mandible may permit decannulation. A policy of early and aggressive surgical management has been pursued for the past 15 years, and an audit of outcome was undertaken to confirm whether or not this policy has been justified. The records of 25 patients so treated between 1980 and 1994 were analyzed by an independent clinician. Decannulation was achieved in 20 of the children (80 percent). The conditions that were most amenable to successful treatment (100 percent) were hemifacial microsomia, temporomandibular ankylosis, and the Pierre Robin sequence. The outcome for children with Treacher Collins syndrome and Nager syndrome was less successful (75 and 60 percent, respectively). The worst outcome occurred in a mixed group of three children with other syndromes, two of whom failed decannulation. Surgery was most successful when carried out before the age of 2 years (87 percent) and after the age of 4 years (90 percent).

Adolescent↗
PubMed1997

Human TAP1 polymorphisms detected by denaturing gradient gel electrophoresis.

Presentation of endogenous peptides by major histocompatibility complex class I (MHC) molecules is controlled, in part, by the Tap1 and Tap2 genes in the MHC class II region that encode a heterodimeric peptide transporter. Polymorphisms of human Tap1 in normal individuals have now been investigated systematically by denaturing gradient gel electrophoresis (DGGE) analysis of fragments of genomic DNA generated by the polymerase chain reaction. Polymorphisms identified by distinctive DGGE band patterns were confirmed by DNA sequencing. In addition to four previously described polymorphisms in the open reading frame, DGGE detected three new polymorphisms: a G-->T substitution in the promoter region, a 10-bp insert in intron 9, and a G-->T substitution 80-bp downstream of the translation termination codon.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Screening of the TAP1 gene by denaturing gradient gel electrophoresis in insulin-dependent diabetes mellitus: detection and comparison of new polymorphisms between patients and controls.

New protective or disease-associated polymorphisms in the TAP1 gene were sought in insulin-dependent diabetes mellitus (IDDM) patients with the use of denaturing gradient gel electrophoresis (DGGE) screening of genomic DNA. The TAP1 gene is located in the human leukocyte antigen (HLA) class II region of the genome and encodes components of a peptide transporter essential for antigen presentation by HLA class I molecules. Fragments of TAP1 corresponding to the 5' promoter, each of the 11 exons (with portions of adjacent intronic regions) and the 3' flanking region were amplified by the polymerase chain reaction and then subjected to DGGE. DNA fragments of TAP1 yielded DGGE bands with patterns whose frequencies differed between IDDM patients and controls. Specific DGGE band patterns with fragments corresponding to the promoter, exons or introns 3, 6, 7, 8, 9 or 10 of TAP1 were detected exclusively in either patients or controls. Sequencing of TAP1 fragments encompassing exon 7 gave rise to a DGGE band pattern exclusively observed in an IDDM patient and sequencing revealed a previously unidentified polymorphisms at codon 518 (GTC-->ATC, Val-->Ile). Another unique polymorphism uncovered by DGGE revealed by sequencing a polymorphism in intron 2 in a diabetic patient. The genotypes of additional HLA class II matched patients and controls were determined with regard to five exonic and one intronic TAP1 polymorphism. A 10 base pair intronic insertion in intron 9 was exclusively identified in controls and missing from patients (P = 0.017). Further large population-based studies may reveal whether these newly identified at risk or protective TAP1 variants confer markers of statistical risk in diverse population groups.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Retardation of pain development: a case of recovery from congenital insensitivity to pain.

Congenital analgesia is a rare genetic disorder. We report here that a 12-year-old boy was able to recover from congenital insensitivity to pain. Neurological examinations revealed that there was a 'stocking' distribution of pain decrement on the lower extremities under the patient's knee joints. Magnetic Resonance Imaging (MRI) of his brain showed gyrus thinning with sulcus widening at both sides of the parietal lobe. Southern blot hybridization probed with cDNAs of various opioid receptors did not detect any significant abnormality. Our results suggest that this rare case may not be genetically determined.

Arthropathy, Neurogenic↗
PubMed1997

Quality assurance for dynamic multileaf collimator modulated fields using a fast beam imaging system.

A quality assurance procedure was developed for x-ray beam intensity modulated conformal radiotherapy (IMCRT) using dynamic multileaf collimators (MLC). The procedure verifies a prescribed intensity modulated x-ray beam pattern in the beam eye's view (BEV) before the treatment procedure is applied to a patient. It verifies that (a) the leaf sequencing computer files were transferred correctly to the linac control computer; (b) the treatment can be correctly executed without machine faults. A fast beam imaging system (BIS) consisting of a Gd2O2S scintillation screen, a charge-coupled device (CCD) camera, and a portable personal computer (Wellhöfer Dosimetrie, Schwarzenbruck, Germany) was commissioned for this purpose. Measurements for the BIS performance are presented in this work. Reference images were derived from MLC leaf sequencing files that were used to drive a dynamic MLC system (Varian Oncology Systems, Palo Alto, CA). A correlation method was developed to compare the BIS measurements with the calculated reference images. A correlation coefficient calculated using 26 correct intensity modulated fields was shown to be a reliable threshold to identify inaccurate treatment delivery files. The study has demonstrated the feasibility of using the BIS and the correlation method to carry out on-line quality assurance tasks for IMCRT treatment fields in the BEV.

Biophysical Phenomena↗
PubMed1997

Activation of N-methyl-D-aspartate receptor attenuates acute responsiveness of delta-opioid receptors.

Coadministration of antagonists of N-methyl-D-aspartate (NMDA) receptor and opioids has been shown to prevent development of opiate tolerance in animal and clinical studies, but its cellular and molecular mechanisms are not understood. In this study, the effect of NMDA on delta-opioid receptor (DOR)-mediated signal transduction was investigated in neuroblastoma x glioma NG108-15 cells that functionally express both DOR and NMDA receptors. Acute incubation of NG108-15 cells with NMDA, a specific agonist of NMDA receptor, significantly attenuated the ability of DOR agonist [D-Pen2, D-Pen5]-enkephalin (DPDPE) to inhibit forskolin-stimulated cAMP production. The attenuation caused by NMDA was dose-dependent, and the EC50 of DPDPE increased 100-fold (from 4.6 nM to 500 nM) after NMDA treatment. The NMDA effect on responsiveness of delta-opioid receptors to DPDPE could be blocked by ketamine, a NMDA receptor-specific antagonist. This NMDA attenuation effect on DOR activity was also observed in neuronal primary cell cultures from fetal mouse brain but not in the Chinese hamster ovary cell line stably transfected with DOR alone. Interestingly, NMDA pretreatment reduced the cellular response to epinephrine but not to that of prostaglandin E1 in NG108-15 cells, which suggests differential modulation of NMDA on different G protein-coupled receptors. Pretreatment of NG108-15 cells with ketamine along with DPDPE greatly attenuated DPDPE-induced acute desensitization of DOR. Furthermore, the specific inhibitors of protein kinase C, either chelerythrine chloride or Go 6979, effectively blocked the NMDA effect, which indicates the involvement of protein kinase C in the process. In conclusion, the activation of NMDA receptors can attenuate acute responsiveness of DOR in neuronal cells, whereas its blockage leads to reduction of DOR desensitization. These results have thus provided an insight into cross-talk between NMDA and opioid signal transduction.

Analgesics↗
PubMed1997

Immunodiagnosis of alveolar echinococcosis by enzyme-linked immunosorbent assay using a partially purified Em18/16 enriched fraction.

An improved enzyme-linked immunosorbent assay (ELISA) system using partially purified Eml8/16 enriched fraction (PP-Em18/16) prepared by isoelectric focusing was evaluated for serodiagnosis of alveolar echinococcosis (AE). The PP-Em18/16-ELISA was compared with Em2plus-ELISA by using sera from AE and cystic echinococcosis (CE) patients in China, where both AE and CE are endemic; sera from CE patients in Australia, where only CE exists; and sera from patients with cysticercosis, paragonimiasis, or sparganosis in Korea, where no indigenous AE or CE exists. We used Em2plus-ELISA as a standard ELISA and found 24.6% (17 of 69 specimens) cross-reactivity with sera from CE. Furthermore, some of the sera from paragonimiasis, sparganosis, and cysticercosis patients were also cross-reactive in the Em2plus-ELISA. When we tested for similar cross-reactivity in the same sera from CE patients by PP-Em18/16-ELISA (23.2%, 16 of 69), it became evident that the specificity of the PP-Em18/16-ELISA was better than that of the Em2plus-ELISA, since no sera from patients with the examined parasitic diseases except CE showed cross-reactivity. Some CE patients from China showed exceptionally high levels of antibody in comparison with those of CE patients from Australia, where no AE occurs. It is speculated that these patients with strongly positive cases of CE from China may have been exposed to both species of Echinococcus.

Animals↗
PubMed1997

Cholesteryl ester transfer protein activity enhances plasma cholesteryl ester formation. Studies in CETP transgenic mice and human genetic CETP deficiency.

The plasma cholesteryl ester transfer protein (CETP) promotes the removal of HDL cholesteryl esters and is thought to stimulate reverse cholesterol transport (RCT). However, mechanisms by which CETP may stimulate RCT are poorly understood. Thus, we examined the relationship between plasma CETP expression and plasma cholesteryl ester formation in CETP transgenic (Tg) mice, hamsters, and human subjects with genetic CETP deficiency. Incubation of CETP Tg mouse plasma showed a 20% to 40% increase in plasma cholesterol esterification rate (CER, P < .05) compared with control mice. Injection of a neutralizing CETP monoclonal antibody (MAb) (TP2) into natural flanking region CETP Tg mice resulted in an increase in plasma free cholesterol (FC) concentration, FC/CE ratio, FC/phosphatidylcholine ratio, and hepatic CETP mRNA. In hamsters, CETP inhibition also resulted in an increase in plasma FC/phosphatidylcholine ratio and increased CETP mRNA in adipose tissue. In humans with two common CETP gene mutations (an intron 14 splicing defect and a D442G missense mutation), mean plasma CERs were 39 and 60, respectively, compared with 89 nmol x mL-1 x h-1 in normal subjects. By contrast, lecithin:cholesterol acyltransferase (LCAT) mass was normal in CETP-deficient subjects. MAb neutralization of CETP activity in incubated human plasma did not alter the LCAT reaction, even after supplementation with discoidal HDL and VLDL. Thus, genetic alterations in CETP levels lead to secondary changes in the plasma LCAT reaction, possibly because of remodeling of HDL by CETP acting in concert with other factors in vivo. In human genetic CETP deficiency, a moderate impairment in the plasma LCAT reaction may contribute to a defect in RCT, providing a potential mechanism to explain the recently observed excess of coronary heart disease in these subjects.

Animals↗
PubMed1997

Enhancement of membrane fluidity in cholesterol-poor endothelial cells pre-treated with simvastatin.

We examined the membrane fluidity of the cholesterol-poor bovine carotid artery endothelial cells (BAEC). Cholesterol-poor BAEC were obtained by treating the cells with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors under 10% low density lipoprotein (LDL)-deficient serum condition for 2 days. Simvastatin reduced the intracellular cholesterol content significantly at a concentration of 0.1 microgram/ml. The reduction in the cholesterol content was accompanied by the enhancement of the cell membrane fluidity which was measured by a photobleaching technique. Additional data suggested that the reduction in cholesterol content referred to the reduction in the proliferation of BAEC.

Animals↗
PubMed1997

Variation of antigenic proteins of eggs and developmental stages of Paragonimus westermani.

Diagnosis of early paragonimiasis is difficult because parasitological evidence is not easily obtained. Antibody tests have been proposed as a good substitute for classical diagnostic techniques. Using the crude extracts of Paragonimus westermani eggs, metacercariae, 4- and 7-week juveniles, and 16-week adults as antigens, we observed the early antibody responses. Sera were obtained from 4 experimental cats, fed 50 metacercariae each, at intervals until 13 weeks post-infection. Antibody (IgG) responses were identified by ELISA using extracts of 4-week juveniles, followed by those of 7- and 16-week worms. Antibody responses were minimal against the metacercarial extracts. Antibodies to P. westermani egg extracts were elevated after 10 weeks post-infection. In immunoblot analysis, more than nine protein bands in 4-week juveniles reacted with the early infection sera. Antigenic proteins in adult worms were different from those of juveniles. After four weeks of infection, 32 and 35 kDa bands in the adult extracts were increasingly reactive. Egg specific proteins at 28, 46 and 94 kDa were reactive only after 10 weeks. Antigenic components reacting to the early infection sera changed during the maturation stages of P. westermani; almost all juvenile antigens were replaced by adult antigen components.

Animals↗
PubMed1997

Antibody responses against Em18 and Em16 serodiagnostic markers in alveolar and cystic echinococcosis patients from northwest China.

Western blot analysis was carried out in order to evaluate new serodiagnostic markers, Em18 and Em16, for differentiation of alveolar echinococcosis (AE) from cystic echinococcosis (CE) using 36 serum samples from hydatid patients from Xinjiang, China, where AE and CE are both endemic and one double infection case has been reported. All AE cases except one (5/6) who exhibited a calcified lesion and a single case of double infection showed antibody responses against Em18 and Em16. Some of CE patient sera (6/22) showed antibody response against Em16 except one who showed that against Em18. Analyses of IgG subclass responses against Em18 and Em16 were carried out using all serum samples showing antibody responses against Em18 and/or Em16 (seven CE, five AE, and one AE + CE) and additional samples of three CE and 22 AE from Sichuan, China. IgG4 was the most predominant antibody subclass. Em18 and Em16 were recognized by both IgG4 and IgG1 (in most cases) or by either IgG4 or IgG1 (in minor cases) or by IgG3 (in very rare cases). Neither Em18 nor Em16 was recognized by IgG2 antibodies. The usefulness of Em18 and Em16 as potential new markers for serological differentiation of human AE and CE, respectively, is discussed.

Antibody Formation↗
PubMed1997

[Meningo-cerebral arteriovenous malformations].

22 patients with meningo-cerebral arteriovenous malformations, we treated in our hospital between 1990 and 1995. Clinical manifestations included headache, nausea, seizure, intracranial hemorrhage, and progressive hemispheric neurologic deficits. The niduses were extensive and had dual feeding from internal and external carotid arteries. All patients underwent endovascular treatment and 4 surgical operations. The curative effect was satisfactory. The clinical and angiographic characteristics were discussed.

Adolescent↗
PubMed1997

[Experimental comparison of two coxsackievirus B3 variants in murine myocardial cells].

There is lack of direct evidence whether the myocarditis can be induced by CVB3o. The two coxsackievirus B3 variants were used to infected murine myocardial cells. The results showed that: (1) In culture medium of murine myocardial cells infected with two variants, it did not show much differences in titers at 12 and 24 hours between CVB3o and CVB3m. (2) The two variants could all induce the death of myocardium, but with the elapse of time, the cell death rate of CVB3m infected cells was much higher than CVB3o. (3) CVB3o could not block the myocardial cells from infection by CVB3m. It is concluded that myocardial cells can be infected by CVB3o, but the degree of infection is lower than CVB3m.

Animals↗