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Hong Tao

Publications and source records attributed to Hong Tao.

At least 19 recordsLinked to original sources
PubMed2006

The distribution of HLA alleles revealed a founder effect in the geographically isolated Chinese population, Drung.

The Drung ethnic minority is one of the smallest ethnic groups of China, geographically isolated by mountains and rivers. Before 1949, Drung society maintained many vestiges of the primitive commune system. The origin and migration of the Drung and their genetic background are still unknown because of limited records about this population. Here, we for the first time demonstrated the unique distribution of HLA alleles in the Drung by high-resolution sequence-based typing (SBT) method. Number of alleles detected is obviously less than expected and only a few alleles with a high homozygosity in each locus are predominant in this minority. The characteristics of HLA allele distribution in the Drung could reflect founder effects, suggesting the Drung probably descended from very few ancestors. The statistical analysis based on allele frequencies indicated that the Drung was an isolated ethnic group, but it also provided the clue that the Drung was genetically related to Chinese southwestern ethnic groups. Significant reduced allelic diversity and genetic isolate in the Drung make it an ideal homogeneous population and very useful model to study the evolution of HLA and the origin and migration of Chinese ethnic groups. The research paved a way to elucidate the genetic background of this mysterious minority and disease predisposition.

Alleles↗
PubMed2006

Demonstration and characterization of mutations induced by Helicobacter pylori organisms in gastric epithelial cells.

BACKGROUND: Helicobacter pylori gastritis increases gastric cancer risk. Microsatellite instability-type mutations are secondary to deficient DNA mismatch repair. H. pylori gastritis is more frequent in patients with microsatellite instability-positive gastric cancers, and H. pylori organisms independently of inflammation can reduce DNA mismatch repair protein levels, raising the hypothesis that H. pylori organisms might lead to mutagenesis during infection. MATERIALS AND METHODS: Mutations were detected using a green fluorescent protein reporter vector (pEGFP-CA13). Gastric cancer AGS cells transfected with pEGFP-CA13 were cocultured with H. pylori or Escherichia coli. The numbers of green fluorescent protein (GFP)-positive cells were determined, and GFP, hMSH2, and hMLH1 protein levels were measured by Western blot. The effect of H. pylori on CpG methylation status of hMLH1 was determined by methylation-specific polymerase chain reaction. RESULTS: GFP levels and GFP-positive cell numbers in AGS cells cocultured with H. pylori significantly increased, as the levels of hMLH1 and hMSH2 dropped. H. pylori cocultures induced low-level CpG methylation of the hMLH1 promoter. Sequence analysis of cells cocultured with H. pylori showed an increased number of frameshift mutations and point mutations as compared to cells not cocultured with H. pylori (p = .03 and p = .001, respectively). CONCLUSIONS: This is the first report showing that H. pylori bacteria may lead to accumulation of genomic mutations, independently of underlying inflammation. This is associated with reduced DNA mismatch repair, and is at least in part associated with CpG methylation of the hMLH1 promoter. These data support the notion that H. pylori-induced mutations and epigenetic alterations in gastric epithelial cells during chronic gastritis may contribute to an increased risk of gastric cancer associated with H. pylori infection.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Study on the genetic mutations of 17 alpha-hydroxylase/17,20-lyase deficiency in Chinese patients.

OBJECTIVE: To investigate the CYP17A1 gene mutations in Chinese patients with 17 alpha-hydroxylase/17, 20-lyase deficiency. METHODS: Clinical data were retrospectively analyzed. The CYP17A1 gene mutations were detected in 5 cases with 17 alpha-hydroxylase/17, 20-lyase deficiency and their relatives. The genomic DNA of the patients was isolated from whole blood. Seven pairs of primers were used to amplify eight exons and exon-intron boundaries of the CYP17A1 gene. The amplified PCR products were purified by agarose gel and then directly sequenced. In order to confirm the DNA sequences of different alleles, some fragments were inserted into pMD 18-T vector and then sequenced. Sequencing results were compared to the established human CYP17A1 sequence. RESULTS: Briefly, we found 2 kinds of compound mutations, of which were: (1) 6436-6438(TAC-->AA), causing amino acid Y329K, 418X; (2) 6531-6532(GC-->A), causing amino acid L361F, 418X. Among the five cases, four were homozygous for 6436-6438(TAC-->AA), whereas one was compound heterozygous for 6436-6438(TAC-->AA)/6531-6532(GC-->A). The clinical characteristics of 5 cases were all completely combined defects of 17 alpha-hydroxylase/17, 20-lyase, and they all carried two alleles of CYP17A1 gene mutations that all shifted the reading frame and resulted in truncated protein which lack of the activity center site of P450C17, of which corresponding with their clinical feature. CONCLUSION: Nine alleles have the mutation of 6436-6438(TAC-->AA), accounting for 90% of total alleles (9/10). That suggests this kind of mutation may have racial specificity. More study should be done to have better understanding of the function of the truncated P450C17 enzymes.

Adolescent↗
PubMed2005

Downregulation of EphA7 by hypermethylation in colorectal cancer.

A significant reduction of EphA7 expression in human colorectal cancers was shown using semiquantitative reverse transcription-polymerase chain reaction analysis in 59 colorectal cancer tissues, compared to corresponding normal mucosas (P=0.008), and five colon cancer cell lines. To investigate the mechanism of EphA7 downregulation in colorectal cancer, we examined the methylation status of the 5'CpG island around the translation start site in five colon cancer cell lines using restriction enzymes, methylation-specific PCR, and bisulfite sequencing and found evidence of aberrant methylation. The expression of EphA7 in colon cancer cell lines was restored after treatment with 5-aza-2'-deoxycytidine. Analysis of methylation status in totally 75 tumors compared to clinicopathological parameters revealed that hypermethylation of colorectal cancers was more frequent in male than in female (P=0.0078), and in moderately differentiated than in well-differentiated adenocarcinomas (P=0.0361). There was a tendency that hypermethylation in rectal cancers was more frequent than in colon cancers (P=0.0816). Hypermethylation was also observed in colorectal adenomas. This is the first report describing the downregulation of an Eph family gene in a solid tumor via aberrant 5'CpG island methylation. It provides the evidence that EphA7 gene is involved in human colorectal carcinogenesis.

Aged↗
PubMed2005

Bacillus clausii effect on gene expression pattern in small bowel mucosa using DNA microarray analysis.

BACKGROUND: Probiotics are widely used for the cure or prevention of several clinical conditions. However, clinical decisions need to be substantiated by an analysis of the complex bacteria-host interplay in the intestinal lumen. AIMS: To identify the gene expression pattern induced by Bacillus clausii in the intestinal mucosa of healthy individuals. METHODS: Six male patients (mean age 38+/-5 years) affected by endoscopically confirmed mild oesophagitis were treated for one month with esomeprazole, and were randomly selected to receive or not B. clausii (groups I and II, respectively). Duodenal biopsies were taken pre and post-treatment to identify the modification of gene expression, using the GeneChip Human U133A array. To validate the microarray analysis, real-time reverse transcriptase-polymerase chain reaction (PCR) of five target genes was performed. RESULTS: After B. clausii administration, a total of 158 and 265 genes were up and downregulated, respectively. Quantitative PCR confirmed the microarray data. B. clausii mainly affected the expression of genes involved in immune response and inflammation, apoptosis and cell growth, cell differentiation, cell-cell signalling, cell adhesion, signal transcription and transduction. CONCLUSIONS: Our data represent the first global analysis of B. clausii effects on the gene expression profile in normal intestine, and provide the basis to identify the mechanisms by which these agents interact with the host and exert their beneficial effects. Future studies are needed to clarify the B. clausii-induced gene pattern in the clinical disorders in which probiotics have proved to be effective.

Adult↗
PubMed2005

[Screening 21-hydroxylase deficiency carriers in androgen excess women of Chinese Han nationality].

OBJECTIVE: To gain a primary understanding of the prevalence of 21-hydroxylase deficiency(21-OHD) heterozygote (carrier) among androgen excess women of Chinese Han nationality, compare the molecular genetic changes therein revealed with the results of adrenocorticotropic hormone (ACTH) stimulating test, and assess the carriers' phenotype-genotype correlation. METHODS: Eighty-two androgen excess cases and 14 healthy women underwent ACTH stimulating test during the follicular phase. Molecular genetic analysis of CYP21 for 9 common mutations was performed with the method of amplification-created restriction sites. RESULTS: In androgen excess group, the basal level of F0 (P<0.01), as well as basal 17-OHP0 and the ACTH stimulated concentrations of 17-OHP60 were much higher than controls (P<0.01), and there was no obvious discrepancy in F60 (P>0.05). The net increase of 17-OHP and the ratio of net increase of 17-OHP to net increase of F were also higher than controls (P<0.01). No CYP21 gene mutations were found in control group. Four patients of the androgen excess group were identified as heterozygous carriers of CYP21 mutations. The ACTH stimulating test results from gene normal patients and from carriers overlapped to a certain extent. CONCLUSION: Among 82 patients of Chinese Han nationality androgen excess women, 4.9% were 21-OHD heterozygous. The response of serum 17-OHP is not useful for predicting CYP21 gene mutation carrier status. Genotyping is the most reliable method to detect carrier.

Adolescent↗
PubMed2005

[Effects of fluvastatin on blood levels of inflammatory cytokines in patients with unstable angina undergoing percutaneous coronary intervention].

OBJECTIVE: To investigate the effect of fluvastatin on blood levels of c-reactive protein (CRP), tumor necrosis factor alpha (TNFalpha) and cardiac troponin I (cTnI) in patients with unstable angina undergoing percutaneous coronary intervention (PCI). METHODS: Sixty patients who underwent PCI from July 2002 to April 2004 in our hospital were randomized into two groups: control group; fluvastatin group (40 mg/d). Serum levels of CRP, TNFalpha and cTnI were measured before and after two weeks treatment (in the early morning of the procedure) and at 24 hours after the procedure. RESULTS: The serum levels of CRP, TNFalpha and cTnI in fluvastatin group were distinctly lower than those in control group before (P < 0.01) and after the procedure (P < 0.01), respectively. CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI.

Angina, Unstable↗
PubMed2005

[Clinical characteristics of 17alpha-hydroxylase/17,20-lyase deficiency and long term follow up results].

OBJECTIVE: To improve the diagnosis and the treatment level of 17alpha-hydroxylase/17,20-lyase deficiency. METHODS: 24 patients suffering from this disease were diagnosed and treated in Peking Union Medical College Hospital from 1978 to 2002. All the patients had comprehensive hormone assay and some had bone mineral density detection. RESULTS: 20 patients with complete combined defect in this study had typical clinical presentation of hypertension and hypokalemia and presented both karyotype 46, XX or 46, XY. All had female external genitalia and lacked spontaneous puberty. The circulating concentrations of cortisol and gonadal steroids were reduced and that of gonadotropin was elevated, whereas in the remaining 4 cases with partial combined deficiencies, adrenal corticotropic hormone stimulating test as well as the results of the sex hormone determination suggested that there was partial 17alpha-hydroxylase/17,20-lyase enzyme activities in their adrenal glands or sexual glands. Long term follow up data showed that in most of the patients, small doses of dexamethasone (0.1 - 0.375 mg per day) could achieve good control of hypertension and correct hypokalemia, but in five patients other drugs were needed for normalization of blood pressure. With sex hormone replacement, the patients could keep adult female appearance, but did not have reproductive function. CONCLUSIONS: In clinical work it is necessary to enhance the recognition of partial combined 17alpha-hydroxylase/17,20-lyase deficiency. Long term regulation treatment can achieve good control of blood pressure and rectify the low blood potassium.

Adolescent↗
PubMed2005

[Study on the relation between concentration of circulating non-host fetal DNA in pregnant women and pre-eclampsia].

OBJECTIVE: To explore the diagnostic value of plasma fetal DNA level in preeclampsia. METHODS: Thirty cases of pregnant women with preeclampsia (at 33 weeks and 3 days) and 30 cases of normal pregnant women (at 34 weeks and 3 days) were selected. All the pregnant women carried a male fetus by B-ultrasound, and were sampled at gestational 20 weeks, third trimester and at 1 hour, 3 hours, 6 hours after delivery. SRY levels in maternal blood were quantitated by polymerase chain reaction (QF-PCR). The endotheliotoxin (ET) level was measured with RIA. RESULTS: (1) Mean fetal DNA level of patients with preeclampsia at 20 weeks of gestation was (316 +/- 61) copy/ml. They were (266 +/- 79) copy/ml, (396 +/- 91) copy/ml, (165 +/- 43) copy/ml for light and severe preeclampsia women and normal pregnant women, respectively. Maternal blood fetal DNA levels in pregnant women with preeclampsia at 20-weeks of gestation were significantly higher than those normal pregnant women (P < 0.01). (2) Mean fetal DNA level of patients with preeclampsia in third trimester was (970 +/- 413) copy/ml. They were (758 +/- 357) copy/ml, (1285 +/- 573) copy/ml, (319 +/- 99) copy/ml for light and severe preeclampsia and normal pregnant women, respectively. Maternal blood fetal DNA levels in pregnant women with preeclampsia in third trimester were significantly higher than those normal pregnant women (P < 0.01). (3) Maternal blood mean fetal DNA level of patients with preeclampsia were (139 +/- 45) copy/ml, (76 +/- 31) copy/ml, (44 +/- 13) copy/ml at 1 hour, 3 hours, and 6 hours after delivery, respectively. Mean fetal DNA level was (102 +/- 42) copy/ml, (57 +/- 25) copy/ml, (36 +/- 12) copy/ml for patients with light preeclampsia, (209 +/- 51) copy/ml, (97 +/- 40) copy/ml, (52 +/- 17) copy/ml for patients with severe preeclampsia, and (33 +/- 13) copy/ml, (9 +/- 5) copy/ml, 0 copy/ml for normal pregnant women. Significant difference was found between preeclampsia and control groups (P < 0.01). (4) The mean endotheliotoxin level for preeclampsia women was (80 +/- 18) ng/L. For light preeclampsia, severe preeclampsia and normal pregnant women ET levels were (74 +/- 14) ng/L, (89 +/- 32) ng/L, (50 +/- 11) ng/L, respectively. ET levels in pregnant women with preeclampsia were significantly higher than those normal pregnant women (P < 0.01). (5) A positive correlation was found between fetal DNA levels and ET levels in preeclampsia group (r = 0.748, P < 0.01). CONCLUSION: The fetal DNA determination may help diagnose preeclampsia.

Adult↗
PubMed2004

Inactivating mutations of the human base excision repair gene NEIL1 in gastric cancer.

Oxidized DNA base lesions, such as thymine glycol (Tg) and 8-hydroxyguanine, are often toxic and mutagenic and have been implicated in carcinogenesis. To clarify whether NEIL1 protein, which exhibits excision repair activity towards such base lesions, is involved in gastric carcinogenesis, we examined 71 primary gastric cancers from Japanese patients and four gastric cancer cell lines for mutations and genetic polymorphisms of the NEIL1 gene. We also examined 20 blood samples from Chinese patients for NEIL1 genetic polymorphisms. Three mutations (c.82_84delGAG:p.Glu28del, c.936G > A and c.1000A > G:p.Arg334Gly) and two genetic polymorphisms were identified. When the excision repair activity towards double-stranded oligonucleotide containing a Tg:A base pair was compared among six types of recombinant NEIL1 proteins, p.Glu28del-type NEIL1, found in a primary case, was found to exhibit an extremely low activity level. Moreover, c.936G > A, located in the last nucleotide of exon 10 and detected in the KATO-III cell line, was shown to be associated with a splicing abnormality using an in vivo splicing assay. An immunofluorescence analysis showed that the wild-type NEIL1 protein, but not the truncated protein encoded by the abnormal transcript arising from the c.936G > A mutation, was localized in the nucleus, suggesting that the truncated protein is unlikely to be capable of repairing nuclear DNA. An expression analysis revealed that NEIL1 mRNA expression was reduced in six of 13 (46%) primary gastric cancer specimens that were examined. These results suggest that low NEIL1 activities arising from mutations and reduced expression may be involved in the pathogenesis in a subset of gastric cancers.

Alternative Splicing↗
PubMed2004

A novel splice-site variant of the base excision repair gene MYH is associated with production of an aberrant mRNA transcript encoding a truncated MYH protein not localized in the nucleus.

The MYH gene encodes a DNA glycosylase involved in the excision repair of adenines paired with 8-hydroxyguanines, a major component of oxidative DNA damage, and bi-allelic germline MYH mutations have been reported to predispose individuals to multiple colorectal adenomas and carcinoma. To determine whether the MYH gene is involved in gastric carcinogenesis, we examined blood specimens from 20 Japanese familial gastric cancer (GC) patients for MYH mutations by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis followed by direct sequencing. Bi-allelic germline MYH mutations were not found in any of the specimens, but in addition to four known variants, a novel splice-site variant, IVS10-2A > G (c.892-2A > G), was found in two patients as its heterozygote. Reverse transcription-PCR analysis revealed that the IVS10-2A > G variant caused the production of an aberrant mRNA transcript encoding a truncated MYH protein. Immunofluorescence analysis showed that the wild-type MYH protein, but not the variant-type, is localized in the nucleus. We then searched for the IVS10-2A > G variant in 128 digestive tract cancer patients by PCR with confronting two-pair primers, and eight cancers from six patients with the IVS10-2A/G genotype were identified. However, no other germline MYH mutations or inactivation of the remaining wild-type allele was detected. We next tested the presumed correlation of the IVS10-2G allele with GC risk in a case-control study of 148 GC cases and 292 controls, but no significant difference in the distribution of the IVS10-2A > G variant was found between the cases and controls. Interestingly, the homozygote for the IVS10-2G allele was found in one GC case, but not in any controls. These results suggested that the ability to repair 8-hydroxyguanine in nuclear DNA may differ among Japanese individuals due to the splicing abnormality based on the MYH IVS10-2A > G variant, and that the bi-allelic IVS10-2A > G variation may be responsible for the occurrence of GC.

Adult↗
PubMed2004

IgE enhances parasite clearance and regulates mast cell responses in mice infected with Trichinella spiralis.

Trichinella spiralis infection elicits a vigorous IgE response and pronounced intestinal and splenic mastocytosis in mice. Since IgE both activates mast cells (MC) and promotes their survival in culture, we examined its role in MC responses and parasite elimination in T. spiralis-infected mice. During primary infection, wild-type but not IgE-deficient (IgE(-/-)) BALB/c mice mounted a strong IgE response peaking 14 days into infection. The splenic mastocytosis observed in BALB/c mice following infection with T. spiralis was significantly diminished in IgE(-/-) mice while eosinophil responses were not diminished in either the blood or jejunum. Similar levels of peripheral blood eosinophilia and jejunal mastocytosis occurred in wild-type and IgE-deficient animals. Despite the normal MC response in the small intestine, serum levels of mouse MC protease-1 also were lower in parasite-infected IgE(-/-) animals and these animals were slower to eliminate the adult worms from the small intestine. The number of T. spiralis larvae present in the skeletal muscle of IgE(-/-) mice 28 days after primary infection was about twice that in BALB/c controls, and the fraction of larvae that was necrotic was reduced in the IgE-deficient animals. An intense deposition of IgE in and around the muscle larvae was observed in wild-type but not in IgE null mice. We conclude that IgE promotes parasite expulsion from the gut following T. spiralis infection and participates in the response to larval stages of the parasite. Furthermore, our observations support a role for IgE in the regulation of MC homeostasis in vivo.

Adjuvants, Immunologic↗
PubMed2004

Splice-site genetic polymorphism of the human kallikrein 12 (KLK12) gene correlates with no substantial expression of KLK12 protein having serine protease activity.

The human kallikrein 12 (KLK12) gene is a new member of the KLK gene family, some members of which are implicated in the initiation and progression of cancer. In this study, we examined 50 non-cancerous tissues from Japanese patients with primary gastric cancer to determine the presence of genetic polymorphisms in the KLK12 gene using polymerase chain reaction (PCR)-single-strand conformation polymorphism and sequencing. Four different types of genetic polymorphisms were identified: one at a splice-donor site of intron 4 (c.457+2T>C), two in exon 6 (c.618_619delTG:p.Cys206fsX72 and c.735G>A:p.Met245Ile), and one in intron 3. The c.457+2T>C polymorphism was observed at a high frequency (allele frequency:0.63), compared to the frequencies of the two polymorphisms in exon 6 (allele frequency:0.01). Reverse transcriptase (RT)-PCR and Western blot analyses revealed that the c.457+2T>C polymorphism was associated with a splicing abnormality and that the expression of the human KLK12 protein (hK12), corresponding to the putative serine protease, was absent in individuals with a c.457+2C/C genotype but not in individuals with the T/T or T/C genotypes. We also found that recombinant His6-tagged hK12 has activity that cleaves chromogenic substrate (H-D-Pro-L-Phe-L-Arg-p-nitroaniline dihydrochloride), that is, serine protease activity. These results indicate that individuals with the c.457+2C/C genotype have no substantial expression of hK12 serine protease.

Carcinoma↗
PubMed2004

Alterations of DNA mismatch repair proteins and microsatellite instability levels in gastric cancer cell lines.

Alterations in DNA mismatch repair (MMR) proteins result in microsatellite instability (MSI), increased mutation accumulation at target genes and cancer development. About one-third of gastric cancers display high-level microsatellite instability (MSI-High) and low-level microsatellite instability (MSI-Low) is frequently detected. To determine whether variations in the levels of MMR proteins or mutations in the main DNA MMR genes are associated with MSI-Low and MSI-High in gastric cancer cell lines, the MSI status (MSI-High, MSI-Low or MS-Stable (MSS)) of 14 gastric cancer lines was determined using multiple clone analysis with a panel of five microsatellite markers. Protein levels of hMLH1, hMSH2, hMSH6, hPMS2 and hPMS1 were determined by Western blot. Sequence analysis of hMLH1 and hMSH2 was performed and the methylation status of the hMLH1 promoter was examined. The cell lines SNU1 and SNU638 showed MSI-High, decreased to essentially absent hMLH1 and hPMS2 and reduced hPMS1 and hMSH6 protein levels. The hMLH1 promoter region was hypermethylated in SNU638 cells. The MKN28, MKN87, KATOIII and SNU601 cell lines showed MSI-Low. The MMR protein levels of cells with MSI-Low status was similar to the levels detected in MSS cells. A marked decrease in the expression levels of MutL MMR proteins (hMLH1, hPMS2 and hPMS1) is associated with high levels of MSI mutations in gastric cancer cells. Gastric cancer cell lines with MSI-Low status do not show significant changes in the levels of the main DNA MMR proteins or mutations in the DNA mismatch repair genes hMSH2 and hMLH1. These well-characterized gastric cancer cell lines are a valuable resource to further our understanding of DNA MMR deficiency in cancer development, progression and prognosis.

Adaptor Proteins, Signal Transducing↗
PubMed2004

[Molecular characterization of mutations and phenotype/genotype correlation in Chinese patients with 21-hydroxylase deficiency].

To investigate characteristics of CYP21 mutations in Chinese patients with 21-hydroxylase deficiency (21-OHD) and the relationship between genotype and phenotype, a time saving, reliable molecular diagnosis method was developed. Eight patients with NC 21-OHD, 35 patients with classical ones and 34 normal controls were studied as followed: CYP21 gene was amplified into fragment 1 (exon1 --> exon3) and fragment 2 (exon3 --> exon10) through PCR with specific primers. The second round PCR was carried out using fragment 1 and 2 as template, and PCR products were digested by restrictive enzymes to analyze nine mutations, including Del, Exon3 Del8 bp, Q318X, R356W, Exon6Cluster, i2g, l172N, P30L and V281L. The most frequent mutation in 43 cases of Chinese 21-OHD was l172N (36.0%), followed by i2g (20.9%), Del (8.6%), P30L (7.0%), Q318X (7.0%), V281L (4.7%), R356W (2.3%), E6Cluster (2.3%) and Exon3 Del8 bp (1.2%). The most common CYP21 gene defect in salt wasting, simple virilizing and nonclassical form was Del (44.4%), l172N (44.2%) and P30L (37.5%) respectively. In addition, genotype was classified into three (severe, moderate and mild) groups according to the degree of 21-hydroxylase enzymatic compromise caused by the mutation. Age of first visit, basal 17-OHP, composition of disease subtype were significantly different among the three groups, P < 0.05. In conclusion, the most common mutations in Chinese 21-OHD were l172N, i2g and Del. The genotype of Chinese 21-OHD has strong correlation with the phenotype.

Adolescent↗
PubMed2003

[Study on the strategy of Japanese encephalitis immunization using live attenuated vaccine combined with inactivated vaccine].

OBJECTIVE: Using the advantages of Japanese encephalitis live attenuated and inactivated vaccine, to reduce the rate of immunization reaction and to increase the effect, we conducted a study on the strategy of immunization in Japanese encephalitis using live attenuated vaccine combined with inactivated vaccine. METHODS: Observing the safety and immune effects of different groups. RESULTS: Data on side effect showed that the rate of moderate and severe systematic reactions of the group who were inoculated with combined vaccine was 0.73%, with local reaction 1.46% while the combined rate of moderate and severe systematic reaction of the group who were inoculated with inactivated vaccine was 2.8%. Under the detection of serum neutralizing antibody, the GMT rose from 1:1.05 - 1:3.35 before vaccination to 1:47.34 - 1:101.30 after vaccination in the different groups. Neutralizing antibody was detected in 97.67% of the combined group. There was a significant difference by comparing neutralizing antibody seroconversion rate of the combined group with the inactivated group (chi(2) = 3.89, P < 0.05), but no significant difference with attenuated group (chi(2) = 0.74, P > 0.05). CONCLUSION: Results showed that in children who previously had been immunized with two doses of inactivated vaccine, the booster administration of live attenuated vaccine was both effective and safe.

Antibodies, Viral↗
PubMed2003

[A clinical analysis of 103 cases of adrenal incidentaloma].

OBJECTIVE: To improve the diagnosis and treatment of adrenal incidentaloma (AI). METHODS: Retrospective analysis of 103 AI patients in PUMC Hospital from 1994 to 2002. RESULTS: Of the 103 cases (43 men and 60 women), most patients were 40-60 years old. Eighty-five cases (82.5%) were benign masses, of which 36 (35.0%) were non-functional adrenal cortical adenoma, and 12 (11.7%) were pheochromocytoma, 1 (1%) was Cushing's syndrome and 1 for aldosteronomas. Three cases did not show clinical feature and the diagnosis of pheochromocytoma were based on 131I-MIBG. Among 18 (17.5%) malignant tumors, adrenal carcinomas account for the majority (8 cases, 7.8%). Patients with malignant masses were significantly younger than patients with adenomas (P < 0.05), and the adenomas were significantly smaller than malignancy (P < 0.001). A cut-off at 4.0 cm of tumor mass size was set for differentiating benign and malignant tumors. CONCLUSIONS: During the diagnosis of AI, it's essential to evaluate hormonal activity and assess for the risk of malignancy. If the mass size is 4 cm or larger, the risk of malignancy increases. More attention should be paid to subclinical hyperfunctional state.

Adenoma↗