PubMed Health⌕ Search

Biomedical subjects

Y Ma

Publications and source records attributed to Y Ma.

At least 19 recordsLinked to original sources
PubMed1992

Developmental expression of brain beta-spectrin isoform messenger RNAs.

We have investigated the expression of brain beta SpIIa and beta SpIb (previously referred to as the beta-subunits of brain spectrin (240/235) and brain spectrin (240/235E), respectively) during mouse brain development. The 9 kb transcript which encodes beta SpIIa is present in fetal mouse brain tissue and increases to a maximal level in a 30-day-old mouse. There is a coordinate accumulation of the 7.8 kb alpha SpIIa mRNA (with beta SpIIa) during mouse brain development. The coordinate expression of alpha SpIIa and beta SpIIa at the mRNA and protein level allows formation of (alpha SpIIa/beta SpIIa)2 tetramers (brain spectrin(240/235)) early in premitotic neuronal development; and avoids turnover of unassembled alpha and beta-subunits. An 11 kb transcript which encodes beta SpIb is not produced in embryonic tissue, and is first seen in a 6-day-old mouse. The protein translation products beta SpIIa and beta SpIb have previously been demonstrated by our laboratory to first appear in fetal mouse brain tissue and at postnatal day 6-8, respectively [J. Neurosci., 7 (1987) 864-874]. The expression of beta SpIb mRNA on postnatal day 6-8, and the appearance of brain spectrin(240/235E) in postmitotic and postmigratory neurons of the cerebellum at this same time; suggests that brain spectrin(240/235E) is involved in differentiated functions of the neuron (formation of cell-cell contacts, formation of dendritic processes and postsynaptic contacts). Thus, the data from the present study demonstrates that the expression of these two neuronal beta-spectrin isoforms is regulated at the level of mRNA expression.

Animals↗
PubMed1992

Mapping of the epitope on lipoprotein lipase recognized by a monoclonal antibody (5D2) which inhibits lipase activity.

A monoclonal antibody, 5D2, which inhibits human lipoprotein lipase (hLPL) activity has been widely used for assessment of LPL immunoreactive mass in the clinical evaluation of patients [1] and for analysis of structure-function relationships of LPL [2,3]. We have mapped the epitope on LPL, recognized by the 5D2 antibody, within residues 396-405. Ala400 is the critical amino acid residue conferring epitope specificity. This knowledge confirms that the C-terminal domain of LPL plays a critical role in LPL activity and also provides important information for studies exploring the structure-function relationship of LPL using this antibody.

Amino Acid Sequence↗
PubMed1992

Indirect photometric detection of polyamines in biological samples separated by high-performance capillary electrophoresis.

A rapid separation of polyamines and some related amino acids in cultured tumor cells by high-performance capillary zone electrophoresis with indirect photometric detection is demonstrated. 60 cm x 75 microns I.D. fused-silica capillary was used for the separation and quinine sulfate was used as a background electrolyte (BGE). Several polyamines (putrescine, spermidine and spermine), amino acids (lysine, arginine, histidine) and simple cations (K+, Na+) were easily separated in less than 10 min. Using the indirect photometric detection method, femtomole amounts of polyamines extracted from the tumor cells were detected from nanoliter injection volumes, and the signal response was linear over two orders of magnitude.

Animals↗
PubMed1992

A missense mutation Pro157 Arg in lipoprotein lipase (LPLNijmegen) resulting in loss of catalytic activity.

Here we report on the molecular defect that leads to a deficiency of lipoprotein lipase (LPL) activity in a proband of Dutch descent. Southern-blot analysis of the LPL gene from the patient did not reveal any major DNA rearrangements. Sequencing of polymerase-chain-reaction-amplified DNA revealed that the proband is a homozygote for G725C, resulting in a substitution of Pro157 for Arg. This substitution alters a restriction site for PvuII, which allowed rapid identification of the mutant allele in family members. Site-directed mutagenesis and transient expression of the mutant LPL in COS cells produced an enzymatically inactive protein, establishing the functional significance of this mutation. This naturally occurring mutation which alters the Pro157 adjacent to Asp156 of the proposed catalytic triad, indicates that this region of the protein is indeed crucial for LPL catalytic activity.

Adult↗
PubMed1992

Molecular genetics of human lipoprotein lipase deficiency.

Lipoprotein lipase (LPL) hydrolysis the triglyceride core of circulating chylomicrons and very-low-density lipoprotein, and modulates the levels and lipid composition of low and high density lipoproteins. Worldwide, more than 20 mutations in the LPL gene have been identified in patients with familial LPL deficiency. Most of these mutations are clustered in the region encoded by exons 4, 5 and 6 which forms the proposed catalytic domain of LPL. In French Canadians who have the highest reported frequency for LPL deficiency, three common mutations in the LPL gene have been identified which account for approximately 97% of mutant genes in this group. Simple DNA-based tests for the detection of all these mutations have been developed for the screening for carriers of LPL deficiency. This will facilitate further studies of phenotypic expression in heterozygous carriers and assessment of the risk of atherosclerosis in these individuals.

Arteriosclerosis↗
PubMed1992

Developments in the dynamical theory of high energy electron reflection.

High energy electron reflection (HEER) is an important technique in surface science and uses the information carried by high energy electrons reflected from surfaces to study surface structures and surface electronic states. With the development of reflection high energy electron diffraction (RHEED), high energy electron microscopy (REM), and high energy electron energy loss spectroscopy (EEL) in surface science, the usefulness of HEER has been widely recognized and demonstrated. However, a stationary dynamical solution for an arbitrary surface for HEER has not been obtained yet. In this paper, some developments in understanding the dynamical theory of HEER, particularly in recent years, are reviewed: 1. The introduction of the concept of current flow for a semi-infinite crystal model has removed the confusion around the wave points in the "band gap." 2. The consistency between the Bloch wave and multislice in the Bragg case has verified the validity of the argument of current flow and led to the emergence of the BMCR method (Bloch wave + Multislice Combined for Reflection). 3. The failure of the Bloch Wave-Only solution (the BWO solution) on Au (110) surfaces in the Bragg case revealed by the BMCR method implies that previous BWO calculations in the Bragg case might be at fault. 4. The 2-D dependence of the electron wave fields and Picard iteration-like character of multislice calculation in the Bragg case has led to the emergence of an Edge Patching method in Multislice-mode-Only (the EPMO method). The new method yields an infinitely convergent stationary dynamical solution for an arbitrary surface.

Crystallization↗
PubMed1992

Phenotypic heterogeneity associated with defective apolipoprotein B-100 and occurrence of the familial hypercholesterolemia phenotype in the absence of an LDL-receptor defect within a Canadian kindred.

Of 163 individuals with a diagnosis of heterozygous familial hypercholesterolemia (FH), only one subject was found to be positive for familial defective apo B-100 (FDB). The eight-member kindred ascertained through this subject who presented with both a clinical phenotype of FH and the FDB apo B-100 (Arg3500----Gln) mutation was studied. Plasma lipid and lipoprotein profiles, apo E phenotypes, apo B gene markers at the 3' hypervariable region and LDL-receptor haplotypes (ApaLI, PvuII, NcoI), were determined, together with LDL-receptor activity on freshly isolated blood lymphocytes. The FDB mutation, present in four relatives, was associated with three different phenotypes: FH and severe hypercholesterolemia, moderate hypercholesterolemia and normolipidemia. The FH phenotype occurred in the absence of any functional LDL-receptor defect. In homozygotes for the absence of the PvuII cutting site who had the apo B mutation, LDL-cholesterol levels were low in the presence of the apo E3/2 phenotype and high in the presence of the apo E4/4 phenotype. None of the major known environmental influences accounted for the wide range of variation in LDL-cholesterol among the affected members. Further observations in the spouse and offspring of the normolipidemic FDB subject confirmed the association of apo E4, the FDB mutation and the PvuII(-/-) genotype with high cholesterol levels. It is concluded that the phenotypic expression of the FDB mutation may vary widely as a function of the genetic environment within a family.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Characteristics of toxin-neutralization by anti-tetanus human monoclonal antibodies directed against the three functional domains [A], [B] and [C] of the tetanus toxin molecule and a reliable method for evaluating the protective effects of monoclonal antibodies.

Five anti-tetanus human monoclonal antibodies (MAbs) produced by hybrid cell lines we established previously were characterized. Their abilities to neutralize tetanus toxin in vitro and to protect mice against challenge with toxin were studied by observing the changes in the progress of symptoms in mice. Immunostaining showed that MAbs MAb-G4 and G2 recognized the N-terminal domain, [A] and the C-terminal domain, [C] of the tetanus toxin molecule, respectively, while MAbs MAb-G1, G3 and G6 recognized its middle domain, [B]. Enzyme-linked immunosorbent assay showed that the binding affinity of MAb-G3 was 2.9 x 10(10) M-1 and those of the other MAbs were as high as approximately 10(11) M-1. In in vitro neutralization experiments, at sufficient doses all the MAbs as single reagents protected mice completely against the effect of tetanus toxin. However, at lower doses than those sufficient to rescue mice, the kinetic patterns of progress of symptoms with the individual MAbs differed with each other and, except for MAb-G4, were different from that of anti-tetanus human polyclonal antibody. They suppressed the development and/or slowed the rate of progress of symptoms for over 96 h and delayed death of the mice. We propose that the comparison of the minimum survival dose with that of human polyclonal antibody of known international units is a reliable method for estimating the actual protective activity of a MAb. Intravenous (IV) injection of doses of individual MAbs or their mixtures at over 0.03 IU per mouse protected mice from subsequent challenge with 20 MLD of tetanus toxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

A missense mutation (Asp250----Asn) in exon 6 of the human lipoprotein lipase gene causes chylomicronemia in patients of different ancestries.

We have previously reported two common lipoprotein lipase (LPL) gene mutations underlying LPL deficiency in the majority of 37 French Canadians (Monsalve et al., 1990. J. Clin. Invest. 86: 728-734; Ma et al., 1991. N. Engl. J. Med. 324: 1761-1766). By examining the 10 coding exons of the LPL gene in another French Canadian patient, we have identified a third missense mutation that is found in two of the three remaining patients for whom mutations are undefined. This is a G to A transition in exon 6 that results in a substitution of asparagine for aspartic acid at residue 250. Using in vitro site-directed mutagenesis, we have confirmed that this mutation causes a catalytically defective LPL protein. In addition, the Asp250----Asn mutation was also found on the same haplotype in an LPL-deficient patient of Dutch ancestry, suggesting a common origin. This mutation alters a TaqI restriction site in exon 6 and will allow for rapid screening in patients with LPL deficiency.

Amino Acid Sequence↗
PubMed1992

Concentration-dependent regulation of neuronal gene expression by nerve growth factor.

NGF is a neurotrophic protein that promotes the survival, growth, and differentiation of developing sympathetic neurons. To directly determine the effects of different concentrations of NGF on neuronal gene expression, we examined mRNAs encoding the p75 low-affinity NGF (LNGF) receptor, T alpha 1 alpha-tubulin (T alpha 1), and tyrosine hydroxylase (TH) in pure cultures of rat sympathetic neurons from postnatal day 1 superior cervical ganglia. Studies of the timecourse of gene expression during 2 wk in culture indicated that a 5-d incubation period would be optimal for the concentration-effect studies. Analysis of RNA isolated from neurons cultured in 2-200 ng/ml 2.5S NGF for 5 d revealed that, as the NGF concentration increased, neurons expressed correspondingly increased levels of all three mRNAs. Both LNGF receptor and TH mRNAs increased seven-fold, and T alpha 1 mRNA increased four-fold in neurons cultured in 200 versus 10 ng/ml NGF. In contrast, T26 alpha-tubulin mRNA, which is constitutively expressed, did not alter as a function of NGF concentration. When neurons were initially cultured in 10 ng/ml NGF for 5 d, and then 200 ng/ml NGF was added, LNGF receptor, T alpha 1, and TH mRNAs all increased within 48 h. The timecourse of induction differed: T alpha 1 mRNA was maximal by 5 h, whereas LNGF receptor and TH mRNAs first began to increase at 12 h after the NGF increase. These experiments show that NGF regulates expression of a subset of mRNAs important to neuronal growth and differentiation over a broad concentration range, suggesting that the effects of NGF may be mediated by more than just a single receptor operating at one fixed affinity. These results also suggest a mechanism for coupling neuronal synthesis of axonal proteins to increases in size of the innervated target territory during growth of the organism.

Animals↗
PubMed1992

Demonstration of a B-lymphocyte mitogen produced by the Lyme disease pathogen, Borrelia burgdorferi.

Lyme disease refers to the multisymptomatic illness in humans which results from infection with the tick-borne spirochete Borrelia burgdorferi. The white-footed mouse is the major reservoir for B. burgdorferi and, upon infection, certain inbred mice develop symptoms similar to those reported in human disease. Sonicated preparations of washed spirochetes were found to have potent mitogenic activity when cultured with lymphocytes from naive C57BL/6, C3H/HeJ, or BALB/c mice. The activity of the B. burgdorferi sonicate was approximately fourfold greater than that of a similarly prepared Escherichia coli sonicate. Polymyxin B efficiently inhibited the mitogenic activity of the E. coli sonicate but only slightly inhibited that of the B. burgdorferi sonicate, suggesting that a lipid A-containing lipopolysaccharide was not responsible for the B. burgdorferi activity. Kinetic analysis indicated peak proliferation at 2 to 3 days of culturing, suggesting polyclonal activation. B- and T-lymphocyte depletion experiments indicated that the major cell type responding to the B. burgdorferi mitogen was the B lymphocyte. This mitogen stimulated murine B cells not only to proliferate but also to differentiate into antibody-secreting cells, as demonstrated by the production of immunoglobulin by stimulated splenocytes. Furthermore, the sonicated preparation stimulated the B-cell tumor line CH12.LX to secrete immunoglobulin in the absence of accessory cells. B. burgdorferi also stimulated interleukin-6 production in splenocyte cultures. The observation that B. burgdorferi can stimulate activation of and immunoglobulin production by normal B lymphocytes may directly reflect on the development of arthritis associated with persistent infection by this organism.

Animals↗
PubMed1992

Evidence for B-lymphocyte mitogen activity in Borrelia burgdorferi-infected mice.

Borrelia burgdorferi produces a mitogen for murine B lymphocytes which can be measured in vitro by polyclonal stimulation of proliferation and immunoglobulin production (R. Schoenfeld, B. Araneo, Y. Ma, L. Yang, and J. J. Weis, Infect. Immun. 60:455-464, 1992). Sonicated B. burgdorferi cells also stimulated IL-6 production by splenocyte cultures. We have used the murine model for Lyme disease described by Barthold et al. (S. W. Barthold, D. S. Beck, G. M. Hansen, G. A. Terwilliger, and K. D. Moody, J. Infect. Dis. 162:133-138, 1990) to determine whether the B. burgdorferi B-cell mitogen is expressed during active infection. To correlate arthritic changes with immune events, we have studied two strains of mice injected with B. burgdorferi; one of them, C3H/HeJ, developed severe disease, and the other, BALB/c, developed only mild disease. C3H/HeJ mice displayed a persistent 10-fold increase in circulating immunoglobulin G (IgG) levels, a 2-fold increase in IgM levels, and a 15-fold increase in peripheral lymph node B-cell numbers, providing evidence of mitogenic activity. Infected BALB/c mice also had evidence for mitogen activity, since the IgG level in serum increased three- to fourfold. The bulk of the increase in circulating IgG levels was not directed against B. burgdorferi antigens, supporting the occurrence of polyclonal B-cell activation. Analysis of IgG isotypes pointed out a contrast between C3H/HeJ and BALB/c mice in that levels of all isotypes were elevated somewhat in both strains of infected mice but IgG2a levels were much more dramatically increased in the C3H/HeJ mice (28-fold) than in the BALB/c mice (4-fold). In this study, interleukin-6 levels were found to be persistently elevated in the serum of infected C3H/HeJ mice. Interestingly, interleukin-6 levels in serum were much lower in the infected BALB/c mice. These findings indicate that the B. burgdorferi mitogen is active in infected animals and may contribute to the inflammatory and immune response to infection.

Animals↗
PubMed1992

[Observation on the effectiveness of repellent coating against mosquitoes].

The present paper reports on the effectiveness of a repellent coating for the first time. The repellent coating was made by combining DETA (N,N-diethyl-meta-toluamide) with slow-releasing reagent. With this coating employed in the laboratory against Aedes aegypti, the rate of blood-sucking was 3.9-9.5% and the rate of protection was 88.9-95.3% for 1-720 days. During 1-77 days' field trial, the RPI (Relative Population Index) was 0-8.98% in the day-time and 0.74-17.15 during the night-time against Anopheles sinensis, Culex pipiens pallens and Culex tritaeniorhynchus. It is concluded that the repellent coating is effective against mosquitoes, safe and prolongs the protection time following exposure to mosquitoes.

Aedes↗
PubMed1992

[Balloon pulmonary valvuloplasty after initial pulmonary valvotomy for pulmonary atresia with intact ventricular septum].

Seven patients with pulmonary atresia and intact ventricular septum have undergone closed pulmonary valvotomy on the early neonatal period (2-6 days) with satisfactory results. Follow-up catheterization showed significant residual pulmonary valve stenosis requiring a second operation. Percutaneous balloon dilatation of the pulmonary valve was successful in 6 cases with the mean right ventricular systolic pressure reduced from 6.8 to 4.9 kPa (50.8 to 37 mmHg) and the mean transvalvular gradient dropped from 5.7 to 2.1 kPa (4.28 to 15.8 mmHg). One case failed and required surgical treatment. The results showed that balloon valvuloplasty could be applied instead of surgery for treatment of selected cases of pulmonary atresia with intact ventricular septum after an initial pulmonary valvotomy.

Catheterization↗
PubMed1991

A mutation in the human lipoprotein lipase gene as the most common cause of familial chylomicronemia in French Canadians.

BACKGROUND: Lipoprotein lipase hydrolyzes the triglyceride core of chylomicrons and very-low-density lipoproteins and has a crucial role in regulating plasma lipoprotein levels. Deficiencies of lipoprotein lipase activity lead to aberrations in lipoprotein levels. Worldwide, the frequency of lipoprotein lipase deficiency is highest among French Canadians. We sought to determine the molecular basis of the disorder in this population. METHODS: The entire coding sequence of the lipoprotein lipase gene from one French Canadian patient was amplified by the polymerase chain reaction and sequenced. Exon 5 from 36 other French Canadian patients was amplified and analyzed by dot blot hybridization with allele-specific oligonucleotides. RESULTS: Sequence analysis revealed a missense substitution of leucine (CTG) for proline (CCG) at residue 207 in exon 5. This mutation was found on 54 of the 74 mutant alleles (73 percent) in the patients. Studies of site-directed in vitro mutagenesis have confirmed that this mutation generates inactive lipoprotein lipase and is the cause of lipoprotein lipase deficiency. CONCLUSIONS: We have identified a missense mutation at residue 207 of the lipoprotein lipase gene that is the most common cause of lipoprotein lipase deficiency in French Canadians. This mutation can be easily detected by dot blot analysis, providing opportunity for definitive DNA diagnosis of the disorder and identification of heterozygous carriers.

Base Sequence↗