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Biomedical subjects

Q Pan

Publications and source records attributed to Q Pan.

At least 55 records · Page 3Linked to original sources
PubMed2000

Effects of angiotensin II receptor blockade on hepatic fibrosis in rats.

OBJECTIVE: To investigate the effects of angiotensin II type 1 receptor blockade, losartan, on serum levels of components of extracellular matrix in experimental fibrotic rats. METHODS: Fifty male Spague-Dawley rats were separated into five groups (control, model, and 3 treatment groups). Excepting rats in control group, all rats were given subcutaneous injection of 40% carbon tetrachloride (once every 3 days for 6 weeks). Rats in 3 treatment groups were also given losartan of 10mg/kg, 5mg/kg, 2.5mg/kg daily for 6 weeks via gastrogavage, respectively. At the end of sixth week, all rats were sacrificed. Radioimmunoassay was performed to determine the serum levels of hyaluronic acid (HA), Laminin (LN), procollagen type III (PCIII) and collagen type IV. Van Giesion collagen staining was used to evaluate the extracellular matrix of the liver tissue. RESULTS: Compared with model group, losartan significantly reduced the serum levels of HA [from (911.66 +/- 345.49)microg/L to (425.05 +/- 115.80)microg/L], LN [from (209.87 +/- 91.57)microg/L to (83.56 +/- 22.12)microg/L, PCIII [from (31.82 +/- 6.90)microg/L to (22.78 +/- 8.38)microg/L] and collagen IV [from (54.09 +/- 19.81)microg/L to (30.51 +/- 12.39)microg/L] (P<0.05) and greatly attenuated the degree of liver fibrosis (P<0.05). CONCLUSION: Losartan can markedly reduce the serum levels of LN, HA, PCIII and collagen type IV of fibrotic rats induced by CCl(4) and greatly attenuate the degree of liver fibrosis.

Angiotensin Receptor Antagonists↗
PubMed2000

[Mutations in the connexin 26 gene in patients with nonsyndromic hearing impairment].

OBJECTIVE: To determine the prevalence and characteristics of deafness-causing mutations in Connexin 26(Cx26, GJB2) gene in Chinese with nonsyndromic hearing impairment(NSHI). METHODS: Study subjects are all Chinese including 16 infants with sporadic congenital deaf-mutism, 39 patients with autosomal recessive hereditary hearing loss, 30 patients with autosomal dominant hereditary hearing loss and 100 normal adults. The subjects were screened for base variations by single-strand conformational polymorphism (SSCP) analysis of the amplified products of polymerase chain reaction (PCR). Those who were found have abnormal conformational band were sequenced. RESULTS: Five kinds of polymorphism were found in 15 cases of controls and six kinds of polymorphism in 10 patients. No mutation was found in Cx26 gene in Chinese with autosomal recessive NSHI. Heterozygous deletion AT at position 299-300 of Cx26 cDNA, which results in premature chain termination, was found in a pedigree with autosomal dominant hereditary nonsyndromic hearing loss. CONCLUSION: The prevalence of deafness-causing mutations in Cx26 gene in Chinese with autosomal recessive NSHI maybe is lower than that of other ethnic groups. Heterozygous deletion AT at position 299-300 of Cx26 cDNA can lead to autosomal dominant hereditary hearing loss (DFNA3).

Asian People↗
PubMed1999

[A comparative study of HLA-A locus in northern and southern Chinese by means of PCR/SSOP typing]

OBJECTIVE: To compare the HLA-A locus in a population selected from Beijing (northern group) with that in a population selected from Guangzhou (southern group). METHODS: HLA typing was performed by using PCR/SSOP method. A pair of primer and 54 probes were used. RESULTS: In 18 alleles identified, the differences in gene frequency between northern and southern Chinese were found. In northern group, A*0205, 0210 and 2901 were absent, and the frequencies of A*2601, 3001 and 3101 were higher than those of southern group; while in southern group, A*3103, 3201 and 6801 were absent, the frequencies of A*0203 and 1101 were higher than those of northern group; and in addition, six subtypes of A2 serological specificity, namely A*0201, 0203, 0205, 0206, 0207 and 0210, were found, in which A*0201 predominated. CONCLUSION: There are some differences in the genetic background of northern and southern Chinese. A2 subtypes have important implications for unrelated-donor transplantation.

Journal Article↗
PubMed1999

c-myc intron element-binding proteins are required for 1, 25-dihydroxyvitamin D3 regulation of c-myc during HL-60 cell differentiation and the involvement of HOXB4.

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) suppresses c-myc expression during differentiation of HL-60 cells along the monocytic pathway by blocking transcriptional elongation at the first exon/intron border of the c-myc gene. In the present study, the physiological relevance of three putative regulatory protein binding sites found within a 280-base pair region in intron 1 of the c-myc gene was explored. HL-60 promyelocytic leukemia cells were transiently transfected with three different c-myc promoter constructs cloned upstream of a chloramphenicol acetyltransferase (CAT) reporter gene. With the wild-type c-myc promoter construct (pMPCAT), which contains MIE1, MIE2, and MIE3 binding sites, 1,25-(OH)2D3 was able to decrease CAT activity by 45.4 +/- 7.9% (mean +/- S.E., n = 8). The ability of 1, 25-(OH)2D3 to inhibit CAT activity was significantly decreased to 18. 5 +/- 4.3% (59.3% reversal, p < 0.02) when examined with a MIE1 deletion construct (pMPCAT-MIE1). Moreover, 1,25-(OH)2D3 was completely ineffective at suppressing CAT activity in cells transfected with pMPCAT-287, a construct without MIE1, MIE2, and MIE3 binding sites (-6.5 +/- 10.9%, p < 0.002). MIE1- and MIE2-binding proteins induced by 1,25-(OH)2D3 had similar gel shift mobilities, while MIE3-binding proteins migrated differently. Furthermore, chelerythrine chloride, a selective protein kinase C (PKC) inhibitor, and a PKCbeta antisense oligonucleotide completely blocked the binding of nuclear proteins induced by 1,25-(OH)2D3 to MIE1, MIE2, and MIE3. A 1,25-(OH)2D3-inducible MIE1-binding protein was identified to be HOXB4. HOXB4 levels were significantly increased in response to 1,25-(OH)2D3. Taken together, these results indicate that HOXB4 is one of the nuclear phosphoproteins involved in c-myc transcription elongation block during HL-60 cell differentiation by 1,25-(OH)2D3.

Alkaloids↗
PubMed1999

Targeting of human switch recombination breakpoints: implications for the mechanism of mu-gamma isotype switching.

We recently characterized the allelic variants of the human Sgamma4 region which makes it possible to accurately identity and map Smu-Sgamma4 fragments from in vivo switched B cells. Twenty-six fragments were identified and a comparison was made with all previously published Smu-Sgamma sequences ( n = 82). Switch recombination outside the region flanking the Sgamma repeat sequence is a rare event in vivo and differences previously observed in patterns between in vitro and in vivo switched B cells appear to be artefactual and due to constraints of the methods used. Furthermore, internal deletions in the switch regions are common, but do not appear to be involved in isotype stabilization. A slight preference for switching to the B (SNIP) site was observed, suggesting a limited importance of both the B and A (SNAP) in the switching process. Mutations can be identified on either one or both sides of the switch junction, showing involvement of an error-prone process, and the pattern of mutations/substitutions at and around the junctions shows non-random nucleotide replacements by the enzyme(s) involved which may help in its future identification.

Alleles↗
PubMed1999

Tandem application of flow cytometry and polymerase chain reaction for comprehensive detection of minimal residual disease in childhood acute lymphoblastic leukemia.

Children with acute lymphoblastic leukemia (ALL) with > or = 0.01% leukemic cells in the bone marrow after remission induction are at a greater risk of relapse. The most promising methods of detecting minimal residual disease (MRD) are flow cytometric identification of leukemia-associated immunophenotypes and polymerase chain reaction (PCR) amplification of antigen-receptor genes. However, neither assay can be applied to all patients. Moreover, both assays carry the risk of false-negative findings due to clonal evolution. The simultaneous use of both assays might resolve these problems, but the correlation between the methods is unknown. We studied serial dilutions of normal and leukemic cells by flow cytometry and PCR amplification of IgH genes and found the two methods highly sensitive (one leukemic cell among 10(4) or more normal cells), accurate (r2 was 0.999 for flow cytometry and 0.960 for PCR by regression analysis) and concordant (r2 = 0.962). We then examined 62 bone marrow samples collected from children with ALL in clinical remission. In 12 samples, both techniques detected MRD levels > or = 1 in 10(4). The percentages of leukemic cells measured by the two methods correlated well (r2 = 0.978). Of the remaining 50 samples, 48 had MRD levels < 1 in 10(4). In only two samples results were discordant: 2 in 10(4) and 5 in 10(4) leukemic cells by PCR but < 1 in 10(4) by flow cytometry. We conclude that immunologic and molecular techniques can be used in tandem for universal monitoring of MRD in childhood ALL.

Child↗
PubMed1999

[A comparative study of HLA-A locus in northern and southern Chinese bymeans of PCR/SSOP typing].

OBJECTIVE: To compare the HLA-A locus in a population selected from Beijing (northern group) with that in a population selected from Guangzhou (southern group). METHODS: HLA typing was performed by using PCR/SSOP method. A pair of primer and 54 probes were used. RESULTS: In 18 alleles identified, the differences in gene frequency between northern and southern Chinese were found. In northern group, A*0205, 0210 and 2901 were absent, and the frequencies of A*2601, 3001 and 3101 were higher than those of southern group; while in southern group, A*3103, 3201 and 6801 were absent, the frequencies of A*0203 and 1101 were higher than those of northern group; and in addition, six subtypes of A2 serological specificity, namely A*0201, 0203, 0205, 0206, 0207 and 0210, were found, in which A*0201 predominated. CONCLUSION: There are some differences in the genetic background of northern and southern Chinese. A2 subtypes have important implications for unrelated-donor transplantation.

Alleles↗
PubMed1999

[Angiotensin 1-converting enzyme gene insertion/deletion polymorphism in patients with coronary artery disease and essential hypertension and its nucleotide sequence].

OBJECTIVE: To determine angiotensin 1-coverting enzyme(ACE) gene insertion/deletion(I/D) polymorphism distributions in patients with coronary artery disease(CAD) and essential hypertension(EH),and to detect its nucleotide sequence. METHODS: ACE genotypes of 137 patients with CDA, 42 patients with EH and 63 healthy people were detected by PCR methods. At the same time, nucleotide sequences of D and I allele were determined by fluorescein labeling automatic sequencing method. RESULTS: the frequency of DD genotype in CAD group was significantly higher than that in control group (0.45 and 0.21,P < 0.01), but there was no significant difference of ACE geneI/D polymorphism distribution between EH and control group. The lengths of D and I alleles are 191bp and 479bp separately and their nucleotide sequences are somewhat different with the results of foreign countries. CONCLUSION: ACE gene I/D polymorphism is an independent risk factor of CAD, but it has no relationship with EH. A 288bp insertion segment results in the I/D polymorphism of ACE gene.

Adult↗
PubMed1999

[CAG trinucleotide mutation detection in patients with hereditary spinocerebellar ataxia].

OBJECTIVE: To assess the frequency of the SCA1, SCA2,SCA3/MJD, SCA6, SCA7 and DRPLA CAG trinucleotide repeat expansions(CAG)n among individuals diagnosed with hereditary spinocerebellar ataxia(SCA) from Chinese families. METHODS: The SCA1, SCA2, SCA3/MJD, SCA6, SCA7 and DRPLA(CAG)n mutations were detected by polymerase chain reaction (PCR), denaturing polyacrylamide gel electrophoresis and silver staining technique in 167 patients with autosomal dominant SCA from 85 Chinese families and 37 sporadic SCA patients. RESULTS: Among 85 families, four families(4.70%) had seven SCA1 patients with the CAG repeat expanded to 53 to 62 repeats, five (5.88%) had twelve SCA2 patients with the CAG repeat expanded to 43 to 47 repeats, and 41 (48.23%) had 83 SCA3/MJD patients with the CAG repeat expanded to 68 to 83 repeats. Analysis of the mutation in these families showed a strong negative correlation between the size of the expanded CAG repeat and the age of disease onset. None of the SCA patients were positive for SCA6, SCA7, or DRPLA. Nor was any of the sporadic SCA patients positive for the CAG repeat expansion in the SCA1, SCA2, SCA3/MJD, SCA6, SCA7, or DRPLA gene. CONCLUSION: The frequency of SCA3/MJD is substantially higher than that of SCA1 and SCA2 in the autosomal dominant SCA from Chinese families. Chinese SCA3/MJD patients are non-Portuguese. Clinical expressions of the various SCAs overlap one another and hence can make the phenotype-based diagnostic classification inaccurate in many instances. It is important for SCA clinical studies to make an SCA gene diagnosis and genotype analysis.

Adult↗
PubMed1999

[Molecular cloning of one splicing form of human M6b cDNA].

X-linked, early onset Pelizaeus-Merzbacher disease (PMD) and part of X-linked spastic paraplegia are caused by mutation of proteolipid protein. M6b (U45955) partially cloned by Olinsky was considered as a member of PLP gene family. One novel fragment about 300 bp partially overlapped but differed in 5'part with U45955 was obtained by nested PCR. Assembly of the novel sequence with U45955 make a 1.642kb cDNA sequence with an open reading frame encoding 265 amino acids, which was verified by sequence of PCR products from brain cDNA library. The cDNA (termed M6ba) and its deduced peptide sequence showed significant similarity to murine M6b gene and protein (91.2% and 93.4% respectively). Northern blot, PCR amplification in cDNA library and EST analysis indicated that human M6b gene has at least three splicing forms. M6ba also showed significant similarity to PLP gene, they encode strongly hydrophobic protein and all their hydrophobic region are highly conserved. Gene structure analysis showed that the coding region of M6ba was composed of seven exons.

Amino Acid Sequence↗
PubMed1999

[Molecular clonging of the human dimethyglycine dehydrogenase-like gene (DMGDHL1) from the sarcosinemia critical region at 9q34].

Through the analysis of EST database, we obtained one human EST (GenBank: H28856) which showed significant similarity with the partial coding sequence of rat dimethylglycine dehydrogenase gene. This EST was mapped to 9q34 due to 95.6% identity with one genomic sequence (GenBank: AC002295). A pair of primers (HRP-1/HRP-2) designed on the sequence of the EST were coupled with the primers (lambda gt10-5/lambda gt10-3) on the vector flanking cloning site respectively to amplify the 5' and 3' cDNA beyond the EST. New primers designed based on novel cDNA sequence overlapped with the sequence within EST H28856 were used for amplification with lambda gt10-5 and lambda gt10-3 by the similar way as above untill a complete ORF was obtained. Finally, a 1,970 bp sequence (termed as dimethylglycine dehydrogenase like gene isoform I, DMGDHL1a) containing a 1,428 bp complete coding sequence from the live cDNA library and 1,475 bp sequence (isoform II, termed as DMGDHL1b) containing a 1,296 bp complete coding sequence from the fetas live cDNA library were obtained. Fourteen exons were identified in isoform I and the first nine exons of isoform II which shared with isoform I could be determined too. The last 105 bp cDNA sequence of isoform II could not be found in the public database, indicating a very large intron (> 123 kb) existed between exon 9 and exon 10 of isoform II. DMGDHL1 showed highly homology on both cDNA and amino acid level with rat dimethylglycine dehydrogenase (60% identity in 135 bp and 35% identity in 436 residues respectively). It was reported that human sarcosinemia gene was mapped at 9q34. Therefore it could be a good candidate gene for the sarcosinemia.

Amino Acid Sequence↗
PubMed1999

Identification of mutation in a candidate gene for hereditary multiple exostoses type II.

OBJECTIVES: To identify possible mutations in our previously cloned candidate gene for hereditary multiple exostoses type II (EXT2) in affected members of EXT families so as to confirm that it is the disease-causing gene. METHODS: The mutation was detected first by single strand conformational polymorphism (SSCP) of all coding exons of the candidate gene and then by sequencing analysis. RESULTS: After analyzing 37 patients from 20 Chinese EXT families by SSCP and DNA sequencing analysis, one 2-bp insertion mutation was identified in this candidate gene in affected members of an EXT family. This mutation resulted in the frameshift and generated a truncated gene product consisting of 105 amino acids. CONCLUSIONS: The identification of the mutation in the candidate gene indicates that this novel gene is responsible for EXT2 (one of the disease-causing gene of EXT).

Amino Acid Sequence↗
PubMed1999

[An approach to the cytologic diagnostic criteria of hepatocellular carcinoma by fine needle aspiration biopsy].

OBJECTIVE: To identify useful cytologic features for diagnosis of hepatocellular carcinoma (HCC). METHODS: Fine needle aspiration(FNA) smears from 61 patients with proven HCC, 19 patients with metastatic tumors in the liver and 16 patients with non-neoplastic lesion of the liver were reviewed in order to detect the relevant cytologic changes associated with HCC. Step-wise logistic regression analysis was done to select useful cytologic features in discriminating HCC from metastatic tumors and non-neoplastic lesions of liver. RESULTS: Nine cytologic features observed were significantly associated with HCC: abundant tissue fragments(91.8%); trabecular pattern(91.8%); sinusoidal endothelial cells (47.5%); polygonal cells with centrally placed nuclei(82.0%); increased nuclear to cytoplasmic ratio(95.1%); large nucleoli(55.7%); bile granules(31.1%); cytoplasmic vacuoles(27.9%) and atypical naked hepatocyte nuclei(88.5%). In distinquishing HCC from metastatic tumors, polygonal cells with centrally placed nuclei, bile granules and trabecular pattern were useful cytologic features. Of the 61 patients with HCC, the logistic model correctly predicted 60(98.4%) as having HCC, while of the 19 patients with metastatic tumors, 18(94.7%) were correctly predicted. In distinquishing HCC from non-neoplastic liver disease, abundant tissue fragments, trebecular pattern, increased nuclear to cytoplasmic ratio and atypical naked hepatocyte nuclei were selected. When the four criteria were used, the sensitivity of diagnosing HCC was 100% and the specificity was 93.8%. CONCLUSION: Abundant tissue fragments, polygonal cells with centrally placed nuclei, increased nuclear to cytoplasmic ratio, trebecular pattern, atypical naked hepatocyte nuclei and bile granules are useful features for identifying HCC by FNA biopsy.

Biopsy, Needle↗
PubMed1999

[Effects of methylmercury on embryonic cell behavior and expression of related gene].

OBJECTIVE: To explore the mechanism of embryonic developmental toxicity of methyl mercury at cellular and gene levels. METHODS: Effects of methylmercury on embryonic cell behavior and gene expression in rats were observed with in vitro (0, 0.05, 0.10, 0.20, 0.40, 0.80 and 1.60 mg/L of methylmercury) and in vivo (0, 0.2, 0.4, 0.8, 1.6 and 3.2 mg/L of methylmercury) rat models, in situ hybridization and TdT-induced dUTP nick end labeling techniques. RESULTS: Methylmercury could pass through yolk-sac placenta quickly, and inhibit placenta development and blood vessel differentiation there at higher concentration. There was a dose-response relationship between concentration of methylmercury and its embryonic developmental toxicity. Its developmental toxicity mainly characterized as patent neural tube and anomalous flexion. Methylmercury could induce excessive apoptosis of embryonic cells, inhibit apparently the synthesis of cellular DNA and RNA and damage its cellular ultrastructure. It also could induce significantly the expression of heat shock protein 70 mRNA and inhibit the expression of fibronectin and p16 mRNA. There was relationship between heat shock protein 70 mRNA, Ca(2+), apoptosis and teratogenesis. CONCLUSION: Disturbance of embryonic cell behavior and related gene expression played important roles in developmental toxicity caused by methylmercury.

Animals↗
PubMed1999

[Significance of telomerase activity detection by fine-needle aspiration in patients with breast cancer].

OBJECTIVE: To study the telomerase activity in samples of breast fine-needle-aspiration specimens and to investigate its potential clinical implications. METHODS: Ninety nine fine-needle aspiration specimens from 83 patients with breast cancers, 12 with benign lesions and 4 with breast inflammation, were studied for the presence of telomerase activity by a PCR-based telomere repeat amplification protocol (PCR-TRAP). RESULTS: Among 83 fine-needle aspiration specimens from patients with breast cancer, telomerase activity was detected in 61 of 69 cytologic-positive specimens, 5 of 7 cytologic-suspicious specimens and 4 of 7 cytologic-negative specimens. Sensitivity of telomerase activity detection was 84.3% (70/83); the coincidence rate between telomerase detection and cytologic confirmation was 77.1% (64/83). Of 12 specimens from patients with benign breast lesions, 4 were positive for telomerase activity, but 4 specimens from patients with breast inflammation were all negative. The Combined use of cytological and telomerase detection can improve the detection rates from 83.1% (69/83) to 93.9% (78/83). CONCLUSION: Detection of telomerase in breast tissue samples by fine-needle aspiration is a sensitive and specific method, which implies that it would be helpful in preoperative cytological diagnosis of breast cancer.

Biopsy, Needle↗