[Analysis of the malaria surveillance in Fujian Province in the past 20 years].
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Animals↗
Biomedical subjects
L S Li
Publications and source records attributed to L S Li.
[The development of a multifunctional molecular electrophoretograms processing system].
This paper presents to you the principles, composition and features of the multifunctional molecular electrophoretograms processing system.
Computer Systems↗
A case-controlled MRI/MRA study of neurovascular contact in hemifacial spasm.
BACKGROUND: Neurovascular contact (NVC) with the root exit zone (REZ) of the ipsilateral facial nerve is associated with hemifacial spasm (HFS), but unresolved issues remain. OBJECTIVES: To 1) determine the frequency of symptomatic and nonsymptomatic NVC, 2) determine the features of NVC associated with HFS, and 3) correlate severity of HFS to these features. METHODS: Two independent, blinded, prospective assessments of high-resolution MR and MR angiography (MRA) images were performed on Chinese cases (HFS: n = 44; age-matched control subjects: n = 20). RESULTS: Over 88% of 44 symptomatic sides in patients with HFS had NVC of the ipsilateral facial nerve. At least 80% of symptomatic sides involved NVC at the anterior aspect of the REZ [REZ(ant.)]. Although NVC was observed in approximately half of nonsymptomatic sides, at least 70% of them were not at REZ(ant.). NVC at the cisternal and intracanalicular portions of the facial nerve were not associated with HFS. Half of our patients with HFS had bilateral NVC, but none had bilateral symptoms. Most of our MR/MRA images showed that the size and position of the arterial branches of the vertebrobasilar system were markedly asymmetric. Of patients with bilateral NVC, over 83% had asymmetric NVC sites. The anterior inferior cerebellar artery was the most common vessel involved in NVC, but was not significantly associated with HFS. Most of the NVC involved one vessel at one contact point with no indentation. The development of HFS was significantly associated with nerve indentation in NVC. The development and severity of HFS were not associated with multiple contact points in NVC. No significant interobserver variability existed between the blinded assessments. CONCLUSIONS: MRI/MR angiography are accurate, fast, and safe in characterizing neurovascular contact (NVC) at the brainstem. The site of NVC and ipsilateral facial nerve indentation in NVC are significant determinants for the development of hemifacial spasm (HFS). The lack of bilateral NVC at the anterior aspect of the root exit zone of the facial nerve could explain in part the lack of bilateral symptoms. The development and severity of HFS are not associated with a specific blood vessel or multiple contact points in NVC.
Adult↗
Corticotropin releasing factor and substance P mediate the nucleus amygdaloideus centralis-nucleus ventromedialis-nucleus dorsomedialis pressor system.
Prolonged emotional stress is an important factor in the development of neurogenic hypertension, but its mechanism is still unclear. The purpose of the present study is to analyze the possible neural basis of hypertension induced by prolonged emotional stress. In the brain many nuclei are involved in emotional reaction, stress or defense response; among them the nucleus amygdaloideus centralis (AC) is the most important one which widely connects with other nuclei controlling emotion and stress, such as nucleus ventromedialis (NVM), nucleus dorsomedialis (NDM), nucleus paraventricularis (NPV) etc. These nuclei contain corticotropin releasing factor (CRF)- and substance P (SP)-immunoreactive cell bodies, nerve terminals and corresponding receptors. Our previous and present studies showed that microinjection of CRF or SP into these nuclei induced pressor responses. These data imply that excitation of the AC can activate many nuclei controlling emotion and stress via CRF and SP, and excessive activities of these nuclei may be the neural basis of hypertension induced by prolonged emotional stress. The present study revealed that (1) the AC pressor response to glutamate (Glu) could be reduced by preinjection of CRF antagonist (alpha-Helical CRF[9-41] or SP antagonist ([D-Pro(2), D-Phe(7), D-Trp(9)]-substance P) into bilateral NVM, (2) the NVM pressor response to Glu were decreased by pretreatment of the NDM with CRF- or SP-antagonist, (3) the AC-, NVM- or NDM-pressor responses were all attenuated by preinjection of CRF- or SP-antagonist into bilateral NPV or rostral ventrolateral medulla (RVL). The results indicate that excitation of the AC can indirectly activate the NPV and RVL to evoke pressor response via the NVM-NDM, CRF and SP are transmitters in each connection of this pathway; this is one component of the mechanism underlying the AC pressor response. Taken together with the findings of our previous studies, it provides neurophysiological basis for the above-mentioned implications.
Amygdala↗
Cloning and characterization of a bifunctional RelA/SpoT homologue from Mycobacterium tuberculosis.
A 2.2kb relA/spoT homologue was isolated from Mycobacterium tuberculosis (Mtb) genomic DNA by PCR-amplification. The Mtb gene encodes a protein of 738 amino acid residues, and is flanked upstream by an ORF that is highly similar to the apt gene, and downstream by an ORF that is highly similar to the cypH gene. This dual function Mtb homologue belongs to the relA/spoT family of genes that mediate the stringent response by regulating the synthesis and degradation of guanosine 3',5'-bis(diphosphate) (ppGpp) and pppGpp. In vitro biochemical data indicate that purified RelMtb is a ribosome- and tRNA-independent ATP:GTP/GDP/ITP 3'-pyrophosphoryltransferase. Additionally, purified RelMtb is an Mn2+-dependent, ribosome and tRNA-independent, (p)ppGpp 3'-pyrophosphohydrolase. These reactions were also assessed in vivo in E. coli deleted in both the relA and spoT genes, which generates a (p)ppGpp0 phenotype. RelMtb can suppress this phenotype and can generate more (p)ppGpp than relA in the wild type E. coli control.
Amino Acid Sequence↗
A rat genetic linkage map including 67 new microsatellite markers.
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Animals↗
Inhibition of rat parotid ecto-ATPase activity.
The inhibitory profile of several known and suspected ecto-ATPase inhibitors was compared on ecto-ATPase activity in rat parotid plasma membranes. Those chemicals with high IC50 (above 130 microM) were the nucleotides alpha,beta-methylene ATP, beta,gamma-methylene ATP, 2-methylthio ATP, inosine triphosphate, 5'-p-fluorosulphonylbenzoyladenosine, the sulphonates, 1-amino-2-naphthol-4-sulphonic acid, Coomassie brilliant blue G, and the stilbene disulphonates, DIDS and SITS. Those agents with low IC50 were: Coomassie brilliant blue R (114 microM), ATPgammaS (49 microM), suramin (72 microM) and Reactive blue 2 (28 microM). The last three inhibitors have similar potencies as inhibitors of ATP hydrolysis by whole parotid acinar cells. ARL67156, a selective inhibitor of ecto-ATPase, had an IC50 of approx. 120 microM. Suramin displayed non-competitive inhibition of ecto-ATPase whereas the inhibitory effects of ATPgammaS and Reactive blue 2 were curvilinear on Dixon plots. These results define the effects of various agents on ecto-ATPase in an exocrine tissue that has been shown to respond to extracellular ATP.
Adenosine Triphosphatases↗
Cytochrome P4502D6 (debrisoquine 4-hydroxylase) and Parkinson's disease in Chinese and Caucasians.
Four polymorphic sites (C/T188, C/T2938, G/C4268, G/A1934) in the cytochrome P4502D6 (debrisoquine 4-hydroxylase) gene were investigated for their association with sporadic Parkinson's disease (PD). Three mutant alleles (C/T188, C/T2938 and G/C4268) result in amino acid changes which could alter the substrate specificity or alter its ability to metabolize their substrates; the fourth (G/A1934) causes a loss of enzyme activity. The study was carried out in two ethnically homogenous populations: Chinese (123 PD patients, 124 controls); and Caucasian (95 PD patients, 62 controls). Haplotype status, which took into account amino acid changes at three polymorphic sites, was deduced from genotyping results in order to investigate whether substrate specificity was important rather than loss of enzyme activity. There was no gender difference in the distribution of the alleles in either race. There was, however, significant association among the three polymorphic sites (C/T188, C/T2938, G/C4268) in both ethnic groups. T/T188:C/C2938:C/C4268 is the most common genotype in the Chinese population, in contrast to C/C188:C/T2938:C/G4268 (followed by C/C188:C/C2938:G/G4268) in Caucasians. All 69 of the sub-group of Chinese patients tested were homozygous for the wild-type allele at the G/A1934 polymorphic site. Neither the CYP2D6 allele nor haplotype was associated with PD in either ethnic group.
Aged↗
Glucose transporter (GLUT1) allele (XbaI-) associated with nephropathy in non-insulin-dependent diabetes mellitus.
BACKGROUND: Although multiple factors contribute to the initiation and progression of diabetic nephropathy (DN), hyperglycemia and genetic predisposition are two major components implicated in the development of DN. Several pieces of experimental evidence suggest that glucose transporter (GLUT1) activity is an important modulator for the cell hypertrophy and extracellular matrix formation of glomerular mesangial cells. METHODS: To evaluate the role of the GLUT1 gene mutation in the development of DN in Chinese patients with non-insulin-dependent diabetes mellitus (NIDDM), the polymorphic XbaI site of GLUT1 gene was analyzed by polymerase chain reaction in 124 normal subjects and 131 patients with NIDDM, among whom 64 were complicated with DN. DN was defined as persistent albuminuria with or without impaired renal function with no known cause of renal disease other than diabetes. RESULTS: The frequencies of XbaI (+/-) genotype (75 vs. 44%, P < 0.01) and XbaI (-) allele (44 vs. 29%, P < 0.05) were significantly higher in NIDDM patients with DN than those without nephropathy. There were no significant differences for GLUT1 genotype and allele frequency between NIDDM patients without nephropathy and normal subjects. The presence of the XbaI (-) allele appeared to have a strong association with the development of DN. The odds ratio was 1.915, and the 95% confidence interval was 1.044 to 3.514. In addition, no strong association was found between GLUT1 gene polymorphism and retinopathy in NIDDM patients. CONCLUSION: Our results indicate that the XbaI (-) allele of the GLUT1 gene might be a genetic marker of NIDDM with DN, and this genetic susceptibility is independent of its retinopathy in Chinese subjects.
Adult↗
Role of corticotropin-releasing factor and substance P in pressor responses of nuclei controlling emotion and stress.
The wide distribution of corticotropin-releasing factor (CRF) and substance P (SP)-immunoreactive cell bodies, nerve terminals and corresponding receptors in pressor nuclei controlling emotion and stress implies that CRF and SP may play important roles in pressor responses of these nuclei; hence CRF or SP was microinjected into these nuclei respectively in Wistar male rats anesthetized with urethane to test this possibility. Microinjection of CRF into nucleus amygdaloideus centralis, nucleus paraventricularis, nucleus ventromedialis, lateral hypothalamus-perifornical region, periaqueductal gray matter, nucleus parabrachialis, locus coeruleus or rostral ventrolateral medulla respectively could evoke pressor responses (but CRF injection into nucleus dorsomedialis could not elicit significant pressor responses). Injection of substance P into all the above nuclei could also elicit hypertensive responses of different magnitudes, whereas normal saline injection into these nuclei had no effect. These results indicate that both CRF and SP in the above mentioned nuclei may play important roles in hypertension induced by prolonged emotional stress.
Animals↗
Chimeric small subunit inhibitors of mammalian ribonucleotide reductase: a dual function for the R2 C-terminus?
Here we report on the formation and activity of complexes between the large subunit (mR1) dimer of mouse ribonucleotide reductase (mRR) and small subunit chimeric dimers (cR2) derived from Escherichia coli and mouse small subunits. cR2 subunits were constructed by substituting mouse C-terminal gene sequences, coding for either 7 or 33 amino acid residues, for the corresponding E.coli R2 (eR2) sequences, with the remainder of the gene corresponding to eR2. The purified cR2s contained the micro-oxo bridged diferric center and tyrosine radical necessary for reductase activity, although the radical signal was broadened compared with wild-type eR2. Neither chimera formed an active complex with mR1, but each was a competitive inhibitor, with respect to mR2, of mRR activity. The inhibition constants for both chimeras were similar, and were sevenfold higher than the dissociation constant of mR2 dimer to mR1 dimer (0.24 +/- 0.02 microM). Analysis of inhibition data showed that chimeric R2 subunits bind to mammalian R1 with a 1:1 (R1:R2) stoichiometry and permit the inference that both C-termini in a cR2 dimer bind to the two sites per mR1 dimer. The lack of enzymatic activity in the mR1-cR2 complex is attributed to perturbation or elimination of interactions linking the tyrosine radical/dinuclear iron center and the C-terminus within R2.
Amino Acid Sequence↗
[Immobilization of N-acetyl-1,6-diaminohexane(NADAH) on diol-silica and study of mechanism of NADAH and hexamethylene bisacetamide(HMBA) inducing tumor cells differentiation].
A method for separating NADAH and its immobilization onto diol-silica have been developed. HMBA and its meabolite NADAH were used as the inducers for many types of tumor cells' differentiation. The inducing mechanism of HMBA is not clear yet. Experiments show that HMBA and NADAH have a relatively strong hydrophobic reaction and hardly ion-exchange with some DNA and some proteins of the cytosolic fraction of HL-60 human acute progranulocytic leukemia cells, BIU-87 human bladder carcinoma cells and the human erythrocyte membrane, when utilizing immobilization of NADAH. The retention time of the proteins and DNA was longer than that of the phosphatides. These results show that the adsorption of HMBA and NADAH with some proteins and DNA is higher than that with the phosphatides. The expected receptor binding biospecifically with HMBA has not been found.
Acetamides↗
Mortality attributable to cigarette smoking in China.
CONTEXT: The few published prospective studies of smoking and mortality in China have reported low relative risks, but the durations of follow-up were short. OBJECTIVE: To assess the mortality of ever- and never-smokers in a cohort after 20 years of follow-up. DESIGN, SETTING, AND SUBJECTS: A cohort analytic study in a machinery factory in Xi'an, China, involving 1696 people aged 35 years or older (1124 men and 572 women) examined in May 1976. MAIN OUTCOME MEASURES: All-cause and tobacco-associated mortality. RESULTS: A total of 56% of the men and 12% of the women were ever-smokers at baseline. Through August 31, 1996, 218 persons (173 men and 45 women) had died. The relative risks (95% confidence intervals [CIs]) for ever smoking (after adjusting for age, marital status, occupation, education, diastolic blood pressure, and triglyceride and cholesterol levels) for deaths resulting from all causes, all cancer, and coronary heart disease were, respectively, 2.42 (95% CI, 1.72-3.42), 2.50 (95% CI, 1.41-4.43), and 3.61 (95% CI, 1.35-9.67) in men and 2.32 (95% CI, 1.18-4.56), 1.98 (95% CI, 0.50-7.92), and 4.67 (95% CI, 0.78-27.8) in women. CONCLUSIONS: Previous prospective studies of smoking-related mortality in China tended to underestimate the risks, probably because of short durations of follow-up. We have demonstrated that smoking is a major cause of death in China, and the risks are similar to those seen in the United States and the United Kingdom. Thus, about half of the 300 million smokers in China will eventually die of smoking-related diseases if urgent tobacco-control measures are not instituted to prevent this growing epidemic.
Adult↗
G/A1947 polymorphism in catechol-O-methyltransferase (COMT) gene in Parkinson's disease.
High and low catechol-O-methyltransferase (COMT) activity is significantly determined by thermostability, which is caused by a valine/methionine108 polymorphism associated with polymorphic G/A1947 bases, in exon 4 of the COMT gene. Our allelic association study on this polymorphism did not find any statistically significant difference between our Chinese Parkinson's disease and that of control subjects. These results show that this polymorphism and hence the thermostability of COMT enzyme are not related to a risk of developing Parkinson's disease.
Aged↗
Physiological and genetic characterization of the Gly40Ser mutation in the glucagon receptor gene in the Sardinian population. The Sardinian Diabetes Genetic Study Group.
A Gly40Ser amino acid substitution in the glucagon receptor gene has been associated with non-insulin-dependent diabetes mellitus (NIDDM), but the questions raised about its physiological implications have not been resolved. The aim of this study was to determine the frequency of the Gly40Ser mutation in different regions of Sardinia and to investigate the physiological implications of the mutation in glucose and insulin homeostasis. We studied a population of 691 subjects selected on the basis of their Sardinian origin. Only heterozygous subjects were found, 21 of 574 (3.6%) in NIDDM patients and 5 of 117 in non-diabetic subjects (4.2%). In northern Sardinia 3.4% of the NIDDM patients were carriers of the Gly40Ser substitution, 1.4% in central Sardinia, while 7.6% carried the substitution in the Southern part. No significant differences were found between hypertensive and normotensive subjects with respect to the presence of Gly40Ser. Ten subjects with Gly40Ser were carefully matched for diabetic state, BMI, age, sex, and geographical origin with 10 patients with Gly40, and a glucagon infusion test was performed using 1, 3, 9 and 27 ng glucagon kg-1.min-1 for 30 min. Blood for determination of glucose, glucagon, and insulin concentrations was drawn at 15-min intervals from the Controlateral arm. Plasma glucagon increased dose-dependently during the infusion with no significant difference between the two groups. Carriers of Gly40Ser had a significantly lower (p < 0.02) increase in plasma glucose concentration in response to glucagon infusion compared to Gly40 homozygous subjects at all times, while the plasma insulin increase was not significantly different at any time. In conclusion, our results indicate that the Gly40Ser variation is not associated with NIDDM in the Sardinian population and that its frequency varies in different parts of Sardinia. Moreover in vivo Gly40Ser plays a physiological role in the glucose homeostasis under glucagon control both in NIDDM and non-diabetic subjects. This latter result suggests that this amino acid substitution in the glucagon receptor may lead to a decreased blood glucose concentration because of the reduced stimulation of liver glucose output via the glucagon receptor.
Aged↗
Glucagon receptor Gly40Ser amino acid variant in Sardinian hypertensive non-insulin-dependent diabetic patients. Sardinian Diabetic Genetic Study Group (SDGSG).
A significantly different prevalence in the Gly40Ser variant of the glucagon receptor gene in a small group of essential hypertensive patients compared with normotensive probands was described in a Caucasian population. It has been postulated that this variant may exacerbate the antinatriuretic effect of high plasma insulin levels commonly seen in hypertensive subjects, leading to volume expansion and rise in blood pressure level. The aim of this study was to evaluate the prevalence of the Gly40Ser variant in a population of 404 non-insulin-dependent diabetic patients of Sardinian origin. No association of the Gly40Ser variant with hypertension was seen in this large population.
Adult↗
Interleukin-1 receptor antagonist allele: is it a genetic link between Henoch-Schönlein nephritis and IgA nephropathy?
Henoch-Schönlein purpura nephritis (HSPN) is a multi-organ systemic vasculitis, which shares many clinical, histological and immunological features with IgA nephropathy (IgAN). To address whether these two diseases have a common genetic background, the polymorphism of the variable number tandem repeat (VNTR) of IL-1 receptor antagonist (IL-1ra) gene has been analyzed using PCR in patients diagnosed with HSPN (N = 43) and IgAN (N = 97), together with normal controls (N = 98) and patients with acute post-infectious glomerulonephritis (APGN), under the concept that IL-1 might play an important role in mediating pathogenesis of vasculitis and glomerulonephritis. It was found that the allele frequency and carriage rate of the interleukin-1 receptor antagonist allele (IL1RN*2) of the IL-1ra gene increased significantly in HSPN patients as compared to IgAN (P < 0.01), APGN (P < 0.05) and normal subjects (P < 0.01). Interestingly, varied carriage rates of IL1RN*2 were found among various groups of IgAN patients presenting with different clinical manifestations. The carriage rate of IL1RN*2 was significantly higher in patients with recurrent gross hematuria than other groups of IgAN patients (P < 0.01). Furthermore, although the carriage rate of IL1RN*2 was higher in HSPN (46.5%) than average IgAN patients (26.8%; P < 0.01), there was no significant difference in the carriage rate of IL1RN*2 between HSPN and those IgAN patients with recurrent gross hematuria (42.8%l P > 0.05). It suggested that the IL1RN*2 allele might be a genetic marker shared by HSPN and a special group of IgAN patients with recurrent gross hematuria. Our preliminary observation provided a genetic evidence to support the hypothesis that HSPN and certain subgroup of IgAN are closely related diseases. Such an association of the gene polymorphism of IL-1ra between HSPN and IgAN with recurrent gross hematuria might serve as a key to explore their pathogenesis and eventually a specific intervention.
Adolescent↗
Characterization of two genes encoding the Mycobacterium tuberculosis ribonucleotide reductase small subunit.
Two nrdF genes, nrdF1 and nrdF2, encoding the small subunit (R2) of ribonucleotide reductase (RR) from Mycobacterium tuberculosis have 71% identity at the amino acid level and are both highly homologous with Salmonella typhimurium R2F. The calculated molecular masses of R2-1 and R2-2 are 36,588 (322 amino acids [aa]) and 36,957 (324 aa) Da, respectively. Western blot analysis of crude M. tuberculosis extracts indicates that both R2s are expressed in vivo. Recombinant R2-2 is enzymatically active when assayed with pure recombinant M. tuberculosis R1 subunit. Both ATP and dATP are activators for CDP reduction up to 2 and 1 mM, respectively. The gene encoding M. tuberculosis R2-1, nrdF1, is not linked to nrdF2, nor is either gene linked to the gene encoding the large subunit, M. tuberculosis nrdE. The gene encoding MTP64 was found downstream from nrdF1, and the gene encoding alcohol dehydrogenase was found downstream from nrdF2. A nrdA(Ts) strain of E. coli (E101) could be complemented by simultaneous transformation with M. tuberculosis nrdE and nrdF2. An M. tuberculosis nrdF2 variant in which the codon for the catalytically necessary tyrosine was replaced by the phenylalanine codon did not complement E101 when cotransformed with M. tuberculosis nrdE. Similarly, M. tuberculosis nrdF1 and nrdE did not complement E101. Activity of recombinant M. tuberculosis RR was inhibited by incubating the enzyme with a peptide corresponding to the 7 C-terminal amino acid residues of the R2-2 subunit. M. tuberculosis is a species in which a nrdEF system appears to encode the biologically active species of RR and also the only bacterial species identified so far in which class I RR subunits are not arranged on an operon.
Adenosine Triphosphate↗