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Biomedical subjects

N Zhong

Publications and source records attributed to N Zhong.

At least 91 records · Page 5Linked to original sources
PubMed1997

[Effects of selective attention on distortion product otoacoustic emissions].

To investigate the effects of upper central nervous system on cochlear micromechanics, distortion product otoacoustic emissions (DPOAE) with and without a visual attention task were studied in 16 young subjects with normal hearing. The results showed that the DPOAE (2f1-f2) amplitude were reduced, and significantly decreased in 1 kHz and 2 kHz of F2. In the underlying mechanism of the effects, it is possible that the upper central nervous system facilitate the olivocochlear efferent system and then modulate the cochlear functions. It is suggested that the whole efferent system (from cerebral cortex to olivocochlear bundle) would be of great importance for cochlear function.

Adult↗
PubMed1997

[The effect of GM-CSF on endothelin-1 and endothelin converting enzyme gene expression in human airway smooth muscle cells with or without theophylline incubation].

OBJECTIVE: To explore the role of airway smooth muscle cells (ASMC) stimulated by inflammatory factors in the development of asthma and bronchial hyperresponsiveness (BHR) and the possible mechanism of low dose theophylline in the treatment of airway inflammation, the effects of GM-CSF on endothelin-1 and endothelin converting enzyme (ECE) gene expression in human ASMC and theophylline on their expressions were investigated. METHOD: The cultured human ASMCs were treated with GM-CSF (1,000 micrograms/ml), GM-CSF plus theophylline (125 ng/ml) respectively for 8 hours. Endothelin-1 and ECE gene expresion were measured by RT-PCR. RESULT: There was no ET-1 gene expression in control group, but strong expression in GM-CSF treated group; theophylline entirely inhibited GM-CSF induced ET-1 gene expression in the ASMC; no significant difference of ECE gene expression was found in three groups. CONCLUSION: GM-CSF causes a strong ET-1 gene expression but not ECE gene expression in cultured human airway smooth muscle cells; theophyllin inhibites this abnormal expression which may be one of the anti-inflammatory mechanisms of low dose theophylline in the management of chronic airway inflammation.

Aspartic Acid Endopeptidases↗
PubMed1997

[Chronic airway inflammation and atopic features in cough variant asthma].

OBJECTIVE: To elucidate the chronic airway inflammation and atopic features in 17 patients with cough variant asthma (CVA). METHODS: (1) Allergen skin prick test, and the atopy index (AI) calculation. (2) Fiberoptic bronchoscopy, inflammatory score of airway membrane under bronchoscopy. (3) Biopsy of the airway membrane and calculation of the eosinophil infiltration. (4) Bronchoalveolar lavage, classification of various cells in the BALF. (5) House dust mite and rabbit antihuman IgE induced histamine release from mast cell. The results were compared with those in 9 patients with typical asthma (Group 8) and 7 normal subjects (Group C). RESULTS: The number of EOS and mast cells in BALF and the AI of CVA group were found higher than in control group. CONCLUSION: (1) Similar to typical asthma, IgE dependent type I allergic reaction plays an important role in the pathogenesis of CVA. (2) Chronic inflammation including eosinophil infiltration was shown in airway membrane in CVA. (3) Bronchial hyperresponsiveness and chronic inflammation of the airway membrane in CVA are less severe than those in typical asthma. (4) In patients who are in difficulty of making a diagnose of CVA clinically. BAL and biopsy of the bronchial membrane will help to make a definite diagnosis.

Adult↗
PubMed1997

[Audiologic measure in Ménière's disease].

To determine some audiologic phenomena of Ménière's disease before and after ingestion of dehydration agent and evaluate its diagnostic value, 48 ears of Ménière's disease, 40 ears of other vertigo disease and 40 normal ears were investigated. The measures were undertaken before and after glycerol or urea ingestion, which included threshold of pure tone audiometry, peak static acoustic admittance (Ya) and conductance(Ga) at probetone signal of 678 Hz, peak compensate static admittance(delta Y) and conductance(delta G) at resonance frequency, -SP/AP, and width of SP-N1 in ECochG. Results showed that abnormal rates of glycerol group and urea group were similar, and there was no significant statistical difference. So these two groups were combined together as one in statistics. The rate of totally abnormal ears were 17/32 in seven measures. Abnormal rates of dehydration test were: pure audiometry 66.67%, Ga 62.50%, -SP/AP 52.08%, width of SP-AP N1 66.67%. chi 2 test showed no significance statistical difference among these results. It indicated that these measures had same diagnostic value for the Ménière's disease. The shift value of G a and delta G of dehydration test might be as the objective diagnostic methods of Ménière's disease.

Acoustic Impedance Tests↗
PubMed1997

[Extraction, purification and ascertainment of anti-hepatoma active principles for targeted preparation of radix Aconiti Kusnezoffii].

The extraction, purification, pharmacological experiments and chemical analysis of anti-hepatoma active principles of Radix Aconiti Kusnezoffii have been studied. The results show that the medicinal material Radix Aconiti Kusnezoffii is efficacious in inhibiting hepatoma, and the active principles are mainly made up of poisonous ester alkaloids. The liver targeting delivery system will be the first choice for its anti-hepatoma preparation, and the effective component AY3a is fit for the preparation of targeted microspheres.

Aconitum↗
PubMed1997

Atypical late infantile and juvenile forms of neuronal ceroid lipofuscinosis and their diagnostic difficulties.

We have collected 122 late-infantile neuronal ceroid lipofuscinosis (LINCL, CLN2) and 191 juvenile NCL (JNCL, CLN3) cases, diagnosed on the basis of age-at-onset, clinical symptomatology, and pathological findings and representing the most common forms of NCL in the United States, and Europe. However, careful analysis of available data revealed that about 80% of cases show typical and 20% show atypical clinical course and/or pathological findings and thus, may represent variants of LINCL and JNCL, respectively. Recent progress in the biochemistry and molecular genetics of NCL inclined us to reevaluate these atypical NCL cases. The gene responsible for LINCL has not yet been identified, except for the Finnish variant. Accumulation of subunit c of mitochondrial ATP synthase, to curvilinear profiles, is found in LINCL cases. A novel variant of LINCL, with predominantly granular profiles in the lysosomal storage, as well as normal excretion of subunit c in urine samples, was found in five cases. When the palmitoyle-protein thioesterase (PPT) was studied in these five cases, it was found that the level was deficient, suggesting that they are not LINCL, but the infantile form of neuronal ceroid lipofuscinosis (INCL). Using molecular genetic techniques in the typical JNCL cases, common 1.02 kb deletion to CLN3 was found in 23/27 (homozygotes) and in one allele 4/27 (heterozygotes) in affected pedigrees. In atypical JNCL pedigrees, it was found in 5/16 heterozygotes, while in 1/5 pedigrees, a novel mutation of one atypical JNCL where a single amino acid substitution at 295 E-->K was found in one allele. None of the atypical JNCL cases was homozygote. In atypical JNCL cases where mutation in CLN3 has not been identified (11/16 probands), several possibilities may exist. The phenotype may be caused by a yet undefined mutation in CLN3 or may be due to phenotypically overlapping with other forms of NCL. Pheno/genotypic correlation and the diagnostic difficulties are discussed.

Adolescent↗
PubMed1997

[Study of optimal parameters and normal values for auditory P300].

Study of optimum seeking method with orthogonal test for auditory P300 measuring was carried out in healthy adolescents. The result showed that the optimal conbination of parameters was as follows: stimulus sound was Logon, recording electrode site Cz, analysis time 750 ms, average 100, stimulus rate 1 c/s, target stimulus (TS) probability 10%, bandpass filter 1-50 Hz, non-target stimulus (NTS) freqency 1 kHz, target stimulus (TS) frequency 2 kHz, stimuli intensities 110 dB peSPL. The normal values of auditory P300, obtained from 30 healthy adolescents, including latencies and amplitudes, were measured under optimal parameters. P300 latency was about 310 ms, RT about 258 ms, these two values present a significant linear correlation.

Adolescent↗
PubMed1996

Fragile X "gray zone" alleles: AGG patterns, expansion risks, and associated haplotypes.

The risk for fragile X "gray-zone" alleles to expand appears to depend on the absence of stabilizing AGGs, which interrupt the CGG repeat region. To characterize such alleles better, we analyzed a series of 101 chromosomes with triplet repeat lengths ranging from 35 to 59 for variations in their AGG interspersion patterns. Among these, 11.9% had 3 AGGs, 59.3% had 2, 24.8% had 1, and 4.0% had 0. An inverse relationship between FMR1 repeat length and the number of interrupting AGGs was observed. Within the range of 35-44 repeats, 98.7% of alleles were found to have a pure CGG repeat length (PCGG) of less than 33. However, among alleles with 45-59 repeats, 50% were found to have 0 or 1 AGG and a PCGG of more than 33. Thus, gray-zone alleles with 45-59 repeats frequently have a long stretch of pure CGGs and thus are more likely to be unstably inherited than alleles with 35-44 repeats. We found length associations of PCGG with 2 flanking microsatellites, DXS548 and FRAXAC1: a PCGG < or = 20 was strongly associated with haplotype 20-19, whereas a PCGG > 20 was more strongly associated with the haplotype 25-21. This result could reflect a founder effect or a generalized instability of CGGs and microsatellites.

Alleles↗
PubMed1996

Reverse mutations in the fragile X syndrome.

Three females were identified who have apparent reversal of fragile X premutations. Based on haplotype analysis of nearby markers, they were found to have inherited a fragile X chromosome from their premutation carrier mothers, and yet had normal size FMR1 repeat alleles. The changes in repeat sizes from mother to daughter was 95 to 35 in the first, 145 to 43 in the second, and 82 to 33 in the third. In the first family, mutations of the nearby microsatellites FRAXAC2 and DXS548 were also observed. In the other two, only mutations involving the FMR1 repeats were found. We suggest differing mutational mechanisms such as gene conversion versus DNA replication slippage may underlie such reversions. We estimate that such revertants may occur among 1% or less of premutation carrier offspring. Our results indicate that women identified to be carriers by linkage should be retested by direct DNA analysis.

DNA Replication↗
PubMed1996

Tissue differences in fragile X mosaics: mosaicism in blood cells may differ greatly from skin.

The fragile X mutation is diagnosed from the structure of the FMR1 gene in blood cell DNA. An estimated 12 to 41% of affected males are mosaics who carry both a "full mutation" allele from which there is no gene expression and a "premutation" allele which has normal gene expression. We compared the DNA in blood cells and skin fibroblasts from four mosaic fragile X males to see if there was a difference in the relative amounts of premutation and full mutation alleles within the tissues of these individuals. Two of these males showed striking differences in the ratio of premutation to full mutation in different tissues while the other two showed only slight differences. These observations conform with the widely accepted hypothesis that the fragile X CGG repeat is unstable in somatic tissue during early embryogenesis. Accordingly, the mosaicism in brain and skin, which are both ectodermal in origin, may be similar to each other but different from blood which is not ectodermal in origin. Thus, the ratio of full mutation to premutation allele in skin fibroblasts might be a better indicator of psychological impairment than the ratio in blood cells.

Blood Cells↗
PubMed1996

A survey of FRAXE allele sizes in three populations.

FRAXE is a fragile site located at Xq27-8, which contains polymorphic triplet GCC repeats associated with a CpG island. Similar to FRAXA, expansion of the GCC repeats results in an abnormal methylation of the CpG island and is associated with a mild mental retardation syndrome (FRAXE-MR). We surveyed the GCC repeat alleles of FRAXE from 3 populations. A total of 665 X chromosomes including 416 from a New York Euro-American sample (259 normal and 157 with FRAXA mutations), 157 from a Chinese sample (144 normal and 13 FRAXA), and 92 from a Finnish sample (56 normal and 36 FRAXA) were analyzed by polymerase chain reaction. Twenty-seven alleles, ranging from 4 to 39 GCC repeats, were observed. The modal repeat number was 16 in the New York and Finnish samples and accounted for 24% of all the chromosomes tested (162/665). The modal repeat number in the Chinese sample was 18. A founder effect for FRAXA was suggested among the Finnish FRAXA samples in that 75% had the FRAXE 16 repeat allele versus only 30% of controls. Sequencing of the FRAXE region showed no imperfections within the GCC repeat region, such as those commonly seen in FRAXA. The smaller size and limited range of repeats and the lack of imperfections suggests the molecular mechanisms underlying FRAXE triplet mutations may be different from those underlying FRAXA.

Alleles↗
PubMed1996

Fragile X founder effects and new mutations in Finland.

The apparent associations between fragile X mutations and nearby microsatellites may reflect both founder effects and microsatellite instability. To gain further insight into their relative contributions, we typed a sample of 56 unrelated control and 37 fragile X chromosomes from an eastern Finnish population for FMR1 CGG repeat lengths, AGG interspersion patterns, DXS548, FRAXAC1, FRAXE and a new polymorphic locus, Alu-L. In the controls, the most common FMR1 allele was 30 repeats with a range of 20 to 47 and a calculated heterozygosity of 88%. A strong founder effect was observed for locus DXS548 with 95% of fragile X chromosomes having the 21 CA repeat (196 bp) allele compared to 17% of controls, while none of the fragile X but 69% of controls had the 20 repeat allele. Although the FRAXAC1 locus is much closer than DXS548 to FMR1 (7 kb vs. 150 kb), there was no significant difference between fragile X and control FRAXAC1 allele distributions. The FRAXE repeat, located 600 kb distal to FMR1, was found to show strong linkage disequilibrium as well. A newly defined polymorphism, Alu-L, located at approximately 40 kb distal to the FMR1 repeat, showed very low polymorphism in the Finnish samples. Analysis of the combined loci DXS548-FRAXAC1-FRAXE showed three founder haplotypes. Haplotype 21-19-16 was found on 27 (75%) of fragile X chromosomes but on none of controls. Three (8.4%) fragile X chromosomes had haplotypes 21-19-15, 21-19-20, and 21-19-25 differing from the common fragile X haplotype only in FRAXE. These could have arisen by recombination or from mutations of FRAXE. A second haplotype 21-18-17 was found in four (11.1%) fragile X chromosomes but only one (1.9%) control. This may represent a more recent founder mutation. A third haplotype 25-21-15, seen in two fragile X chromosomes (5.6%) and one (1.9%) control, was even less common and thus may represent an even more recent mutation or admixture of immigrant types. Analysis of the AGG interspersions within the FMR1 CGG repeat showed that 7/8 premutation chromosomes lacked an AGG whereas all controls had at least one AGG. This supports the hypothesis that the mutation of AGG to CGG leads to repeat instability and mutational expansion.

Finland↗
PubMed1996

Familial transmission of the FMR1 CGG repeat.

To better define the nature of FMR1 CGG-repeat expansions, changes in allele sizes for 191 families with fragile X and for 33 families with gray-zone repeats (40-60) were analyzed. Expansion of the fragile X chromosome to the full mutation was seen in 13.4% of offspring from premutation mothers with 56-59 repeats, 20.6% of those with 60-69 repeats, 57.8% of those with 70-79 repeats, 72.9% of those with 80-89 repeats, and 97.3% of those with 90-199 repeats. For premutation fathers, the majority (62%) of their daughters had a larger repeat number, while a few had either a smaller (22%) or the same (16%) repeat number, compared with their fathers' sizes. However, daughters with a smaller repeat number were observed only if their fathers had > or = 80 repeats. Fifteen (39.5%) of 38 such daughters carried a smaller repeat than did their fathers. We observed that a similar repeat number was inherited more often than expected by chance, among the members of a sibship segregating fragile X. This familial clustering, observed in the offspring of both males and females with a premutation, implies there may be an additional factor, independent of parental repeat size, that influences CGG-repeat instability. Instability in gray-zone allele transmissions was observed in 25% of alleles with 50-60 CGGs but in <8% of those with 40-49 CGGs. Examination of gray-zone allele organization revealed that long tracts of pure CGGs (>34) are not always unstably transmitted. These results raise new questions regarding the familial factors that may determine transmission expansions.

Alleles↗
PubMed1996

[The correlation of auditory brainstem response and transcranial Doppler on the vertebrobasilar transient ischemic vertigo].

To investigate the correlation of brainstem response (ABR) and transcranial doppler examination (TCD) on the vertebrobasilar transient ischemic vertigo (VBTIV), 24 patients (48 ears) with VBTIV and 12 patients (24 ears) with non-VBTIV were studied. The results showed that the incidence of abnormality of ABR in VBTIV group was 58.3%, TCD 54.2%, there being no significant difference by Chi-square test; while in non-VBTIV group ABR 8.3%, TCD 45.8%. Both ABR and TCD were abnormal in VBTIV 19/48, non-VBTIV 0/24 and normal VBTIV 13/48, non-VBTIV 11/24. The ratio of there cases (normal and abnormal) as a whole was VBTIV 66.7%, non-VBTIV 45.8%. It indicates that ABR with high stimulus rates combined with TCD and clinical signs can make the diagnosis of VBTIV. The results of TCD alone can't be a considerable diagnostic basis for VBTIV.

Evoked Potentials, Auditory, Brain Stem↗