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Yan Chen

Publications and source records attributed to Yan Chen.

At least 145 records · Page 8Linked to original sources

Deguelin regulates nuclear pore complex proteins Nup98 and Nup88 in U937 cells in vitro.

AIM: To investigate the anticancer effects and the molecular mechanisms of deguelin on human U937 leukemia cells, and to explore the underlying mechanism regulating nucleoporin 98 (Nup98) and nucleoporin 88 (Nup88) in vitro. METHODS: The effects of deguelin on the growth of U937 cells were studied by MTT assay. The effect of deguelin on the cell cycle of U937 cells was studied by using a propidium iodide method. The localization of the nuclear pore complex proteins Nup98 and Nup88 was investigated by using immunofluorescence and immunoelectron microscopy. The expression of Nup98 and Nup88 in U937 cells was investigated by using flow cytometry and Western blot. RESULTS: The proliferation of U937 cells was inhibited in the deguelin-treated group, with a 24-h IC(50) value of 21.61 nmol/L and a 36-h IC(50) value of 17.07 nmol/L. U937 cells treated with deguelin had reduced percentages of cells in the G(0)/G(1) phase, whereas cells accumulated in the S and G(2)/M phases. Nup88 and Nup98 were found on both the nuclear and cytoplasmic sides of the U937 cells by using immunofluorescence and immunoelectron microscopy. The expression of Nup98 was upregulated and that of the Nup88 protein was downregulated in U937 cells treated with deguelin. CONCLUSION: Deguelin is able to inhibit the proliferation of U937 cells by regulating the cell cycle such that cells are arrested at the S and G(2)/M phases, so that the proportion of cells in the G(0)/G(1) phase decreases. The antitumor effects of deguelin are related to upregulating the expression of Nup98 and downregulating the expression of Nup88 protein in U937 cells.

Antineoplastic Agents, Phytogenic↗

Mutations in the putative zinc-binding motif of UL52 demonstrate a complex interdependence between the UL5 and UL52 subunits of the human herpes simplex virus type 1 helicase/primase complex.

Herpes simplex virus type 1 (HSV-1) encodes a heterotrimeric helicase-primase (UL5/8/52) complex. UL5 contains seven motifs found in helicase superfamily 1, and UL52 contains conserved motifs found in primases. The contributions of each subunit to the biochemical activities of the complex, however, remain unclear. We have previously demonstrated that a mutation in the putative zinc finger at UL52 C terminus abrogates not only primase but also ATPase, helicase, and DNA-binding activities of a UL5/UL52 subcomplex, indicating a complex interdependence between the two subunits. To test this hypothesis and to further investigate the role of the zinc finger in the enzymatic activities of the helicase-primase, a series of mutations were constructed in this motif. They differed in their ability to complement a UL52 null virus: totally defective, partial complementation, and potentiating. In this study, four of these mutants were studied biochemically after expression and purification from insect cells infected with recombinant baculoviruses. All mutants show greatly reduced primase activity. Complementation-defective mutants exhibited severe defects in ATPase, helicase, and DNA-binding activities. Partially complementing mutants displayed intermediate levels of these activities, except that one showed a wild-type level of helicase activity. These data suggest that the UL52 zinc finger motif plays an important role in the activities of the helicase-primase complex. The observation that mutations in UL52 affected helicase, ATPase, and DNA-binding activities indicates that UL52 binding to DNA via the zinc finger may be necessary for loading UL5. Alternatively, UL5 and UL52 may share a DNA-binding interface.

Adenosine Triphosphatases↗

Infectious source factors affecting the severity of sexually transmitted acute hepatitis due to hepatitis B virus genotype C.

OBJECTIVE: The aim of this study was to identify clinical features and virological aspects of infectious sources that are related to the severity of sexually transmitted acute hepatitis B virus (HBV) infection in patients, especially in cases of genotype C. METHODS: Nineteen patients with acute HBV infection, 10 classified with severe acute hepatitis (SH) (prothrombin time; PT <40%) and 9 with typical acute hepatitis (AH) (PT >40%), and their infectious sources (all were sexual partners) were studied. Infectious source factors were analyzed in relation to the severity of hepatitis in the patients' partners. RESULTS: The nucleotide homology of HBV-DNA between each pair was >/=98.9%. Sixteen were infected with HBV genotype C. Among the 16 infectious sources, age, numbers with elevated alanine aminotransferase (ALT, 7/9 vs. 1/7), anti-HBe positivity (8/9 vs. 1/7) and core promoter mutations at nt 1762 (7/9 vs. 1/7), nt 1764 (8/9 vs. 1/7) and precore mutation at nt 1896 (8/9 vs. 1/7) were significantly higher in the sources of SH than in those of AH. CONCLUSION: Higher age, elevated ALT, anti-HBe positivity and core promoter/precore mutations were possible risk factors for an infectious source of the severe form of sexually transmitted acute hepatitis due to HBV genotype C.

Acute Disease↗

Co-infection with hepatitis B virus genotype D and other genotypes in Western Japan.

OBJECTIVE: Genotypes B and C are the prevalent hepatitis B virus (HBV) genotypes in eastern Asia. Although very rare in this region of the world, genotype D was found to be prevalent in a small area of western Japan. In this study, we confirm the frequency and clinical significance of co-infection with different genotypes among patients from that area infected with genotype D. METHODS: Twenty-three patients from the same area of western Japan infected with HBV genotype D, determined using a genotyping enzyme immunoassay, were studied. Cloning was done using DNA extracted from serum samples, and polymerase chain reaction assays with the restriction fragment length polymorphism for HBV genotyping were performed with 10 clones from each patient. RESULTS: Four (17.4%) of the 23 patients were found to be co-infected with HBV genotype C, and the HB surface antigen subtype was ayw in both mono- and co-infected patients. No clinical differences were found between mono-infected and co-infected patients carrying genotype D. CONCLUSION: A significant number of patients from the study area found to be infected with HBV genotype D were co-infected with genotype C. Additional study with a larger number of patients is needed to elucidate the possible clinical significance.

Adolescent↗

Atrial natriuretic peptide promotes cardiomyocyte survival by cGMP-dependent nuclear accumulation of zyxin and Akt.

This study delineates a mechanism for antiapoptotic signaling initiated by atrial natriuretic peptide (ANP) stimulation leading to elevation of cGMP levels and subsequent nuclear accumulation of Akt kinase associated with zyxin, a cytoskeletal LIM-domain protein. Nuclear targeting of zyxin induces resistance to cell death coincident with nuclear accumulation of activated Akt. Nuclear translocation of zyxin triggered by cGMP also promotes nuclear Akt accumulation. Additional supportive evidence for nuclear accumulation of zyxin-enhancing cardiomyocyte survival includes the following: (a) promotion of zyxin nuclear localization by cardioprotective stimuli; (b) zyxin association with phospho-Akt473 induced by cardioprotective stimuli; and (c) recruitment of zyxin to the nucleus by activated nuclear-targeted Akt as well as recruitment of Akt by nuclear-targeted zyxin. Nuclear accumulation of zyxin requires both Akt activation and nuclear localization. Potentiation of cell survival is sensitive to stimulation intensity with high-level induction by ANP or cGMP signaling leading to apoptotic cell death rather than enhancing resistance to apoptotic stimuli. Myocardial nuclear accumulation of zyxin and Akt responds similarly in vivo following treatment of mice with ANP or cGMP. Thus, zyxin and activated Akt participate in a cGMP-dependent signaling cascade leading from ANP receptors to nuclear accumulation of both molecules. Nuclear accumulation of zyxin and activated Akt may represent a fundamental mechanism that facilitates nuclear-signal transduction and potentiates cell survival.

Active Transport, Cell Nucleus↗

In-vitro cytotoxicity, in-vivo biodistribution and anti-tumour effect of PEGylated liposomal topotecan.

In attempt to increase the accumulation of topotecan in tumours and improve its anti-cancer activity, PEGylated liposome (H-PEG) containing topotecan was prepared. The in-vitro cytotoxicity, in-vivo biodistribution pattern and anti-tumour effect of H-PEG were studied systemically. Compared with free topotecan or conventional liposome (H-Lip), H-PEG improved the cytotoxic effect of topotecan against human ovarian carcinoma A2780 and human colon carcinoma HCT-8 cells. The IC50 value (concentration leading to 50% cell-killing) of H-PEG decreased 5 fold (P<0.01) and 9 fold (P<0.01) against A2780 and HCT-8 cells compared with H-Lip, respectively. The results of biodistribution studies in sarcoma S(180) tumour-bearing mice showed that liposomal encapsulation increased the concentration of total topotecan and the ratio of lactone form in plasma. H-PEG resulted in a 70-fold and 3.7-fold increase in AUC(0-->24 h) compared with free topotecan and H-Lip, respectively. Moreover, H-PEG increased the accumulation of topotecan in tumours and the relative tumour uptake ratio compared with free topotecan was 5.2, and higher than that of H-Lip. The anti-cancer effect studies in murine heptocarcinoma H(22) tumour-bearing mice showed that H-PEG improved the therapeutic efficiency of topotecan and decreased the toxicity of topotecan to a certain extent compared with H-Lip. These results indicated that PEG-modified liposome might be an efficient carrier of topotecan.

Animals↗

Methods for measuring TGF-b using antibodies, cells, and mice.

The transforming growth factor (TGF)-betas are essential in pre- and postnatal development, differentiation and morphogenesis of higher organisms. Quantitation of the levels of TGF-beta synthesis, secretion, and activation are crucial for grasping the mechanisms that control these events and ultimately control TGF-beta action. Rather than presenting a single method, we describe several methods for measuring active TGF-beta in different experimental situations. This is possible as a result of advances in transgenic mice technology that allow in vivo TGF-beta measurements in addition to the more established in vitro approaches.

Animals↗

[Genetic polymorphisms of NQO1, GSTT1, GSTM1 and susceptibility to chronic benzene poisoning].

OBJECTIVE: To explore the relationship between genetic polymorphism of quinone oxidoreductase 1 (NQO1), glutathione S-transferase theta 1 (GSTT1), glutathiones S-transferase mu 1 (GSTM1) and susceptibility to chronic benzene poisoning (BP). METHODS: The genotypes of NQO1, GSTT1, GSTM1 for 100 patients with benzene poisoning and 90 workers exposed to benzene who were engaged in the same working time and job title as patients with benzene poisoning were detected by PCR-RFLP and multi-PCR. RESULTS: There was a 2.82-fold (95% CI: 1.42 approximately 5.58, P < 0.05) increased risk of BP in the subjects with NQO1 C609T mutation genotype (T/T) compared with those carrying heterozygous (C/T) and wild type (C/C), and there was a 2.94-fold (95% CI: 1.25 approximately 6.90, P < 0.05) increased risk of BP in the subjects with NQO1 C609T T/T genotype compared with those carrying C/C genotype. The subjects with GSTT1 null genotype had a 1.91-fold (95% CI: 1.05 approximately 3.45, P < 0.05) increased risk of BP compared with those with GSTT1 non-null genotype. The interaction of two genes showed that there was a increased risk of BP in subjects with any two genotypes of NQO1 C609T T/T genotype and GSTT1 null genotype and GSTM1 null genotype, compared to the individual with any two genotypes of NQO1 C609T C/C genotype and GSTT1 non-null genotype and GSTM1 non-null genotype. The interaction of three genes showed that there was a 20.41-fold (95% CI: 3.79 approximately 111.11, P < 0.01) increased risk of BP in subjects with NQO1 C609T T/T genotype and GSTT1 null genotype and GSTM1 null genotype compared with those carrying NQO1 C609T C/T genotype and C/C genotype and GSTT1 non-null genotype and GSTM1 non-null genotype. CONCLUSIONS: The interaction of multi-genes may be an important role to BP. The genetic polymorphisms of 3 genes (NQO1, GSTT1 and GSTM1) led to declining of detoxifying ability in benzene metabolism, so the individual with NQO1 C609T T/T genotype, GSTT1 null genotype and GSTM1 null genotype is most susceptive to benzene. The results were consistent with that of the theoretic presumption. It could be suggested as a biomarker to assess the risk of benzene poisoning for individuals.

Adult↗

[Analysis of the methylation in the promoter of LRP15 gene and its expression].

To study the methylation in the promoter of LRP15 gene and its relationship with gene expression and to explore the possible mechanism of regulating LRP15 gene methylation, the methylation in the promoter of LRP15 gene in K562 cell line was detected by MS-PCR. Then K562 was exposed to 5-aza-2'-deoxycytidine (CdR) and trichostatin (TSA), to determine whether the silencing of LRP15 gene by de novo methylation could be reversed. As a result, it was confirmed by MS-PCR that the promoter of LRP15 was hypermathylated in K562 cell line, and lost its transcription activity. After CdR, with or without TSA, the silencing of LRP15 gene by de novo methylation can be reversed. Observation demonstrated that the expression of LRP15 was controlled by methylation in its promoter in K562. It is suggested that methyltransferase inhibitor and deacetylase inhibitor may be effective agents in leukemia therapy.

Azacitidine↗

[Effect of coagulation on preventing membrane from fouling].

In this experiment, the effects on improve of flux and prevention of membrane from fouling is studied. The results demonstrate that after backwashing, the flux was completely recovered by addition of 4mg/L and l0mg/L(as Al), while the flux was only 40% of initial flux without coagulation pretreatment. It is also observed that whether or not prevention of fouling by coagulation are depended on the characteristics of cake layer formed on membrane surface during membrane filtration. In the presence of filtration of coagulation floc suspension, coagulation can form cake layer on membrane surface, thus prevent membrane from fouling effectively, while in the presence of filtration of supernatant, fouling are occurred due to cake layer comprising small, neutral, hydrophilic compounds, which can not remove by backwash.

Equipment Failure↗

[The predictive value of the ambulatory blood pressure monitoring parameters on left ventricular hypertrophy and carotid artery intima-media thickness in hypertensives].

OBJECTIVE: To investigate the predictive value of the ambulatory blood pressure monitoring parameters on left ventricular hypertrophy (LVH) and carotid artery intima-media thickness (IMT) in the hypertensives. METHODS: We evaluated 147 hypertensive patients who were never treated regularly before. All patients underwent ultrasound examinations of the heart and the IMT of carotid arteries. We classified them as LVH group (n = 45) or no LVH group (n = 102), and as IMT increased group (n = 52) or no IMT increased group (n = 95). The record of medical history, physical examination and 24 h ambulatory blood pressure monitoring (ABPM) were performed in all the patients. The biochemical parameters such as blood lipids, glucose and so on were tested. Then the data comparison was made. RESULTS: (1) There were no significant differences in clinical manifestations and biochemical parameters between the LVH and no LVH groups (P > 0.05). Age (68.3 +/- 6.2) year vs (65.6 +/- 5.8) year, male 75.6% vs 66.7%, body mass index (24.1 +/- 4.1) vs (23.8 +/- 4.7) (kg/m(2)), diabetes mellitus and(or) impaired glucose tolerance 40.0% vs 38.2%, angina pectoris 42.3% vs 38.9%, cerebral vascular diseases 19.2% vs 15.7%, total cholesterol (5.40 +/- 1.42) vs (5.28 +/- 1.46) mmol/L, triglycerides (1.80 +/- 1.02) vs (1.74 +/- 1.08) mmol/L, low-density lipoprotein cholesterol (4.03 +/- 1.43) vs (4.06 +/- 1.48) mmol/L, high-density lipoprotein cholesterol (1.00 +/- 0.30) vs (0.99 +/- 0.26) mmol/L. (2) The parameters of ABPM in LVH group were higher than those in no LVH group. There were significant differences (P < 0.05) in 24 h mean systolic blood pressure (140.7 +/- 14.1) vs (128.3 +/- 12.3) mm Hg, 24 h mean diastolic blood pressure (86.4 +/- 8.9) vs (81.6 +/- 9.3) mm Hg, daytime mean systolic blood pressure (142.8 +/- 13.9) vs (130.9 +/- 11.1) mm Hg, daytime mean diastolic blood pressure (86.9 +/- 8.8) vs (83.4 +/- 9.0) mm Hg, nighttime mean systolic blood pressure (129.0 +/- 13.2) vs (114.6 +/- 11.4) mm Hg, nighttime mean diastolic blood pressure (77.2 +/- 9.4) vs (67.5 +/- 8.1) mm Hg, 24 h pulse pressure (54.2 +/- 10.2) vs (46.9 +/- 9.6) mm Hg, daytime pulse pressure (55.9 +/- 10.5) vs (47.5 +/- 9.1) mm Hg, nighttime pulse pressure (51.8 +/- 10.7) vs (47.1 +/- 8.7) mm Hg, 24 h systolic blood pressure variance (8.4 +/- 2.0) vs (7.2 +/- 1.9), 24 h diastolic blood pressure variance (9.5 +/- 2.2) vs (8.0 +/- 2.1), the non-dipper rhythm of ambulatory blood pressure 55.6% vs 25.5%. (3) There were also no significant differences in clinical manifestations between the IMT increased and no IMT increased group (P > 0.05). While there were significant differences between the IMT increased and no IMT increased group in those parameters of ABPM (P < 0.05). CONCLUSION: There were more LVH or IMT increased persons in the hypertensives whose ABPM parameters were abnormal.

Aged↗

[Expressions of cyclooxygenase-2 and matrix metalloproteinase-2 and airflow obstruction in patients with chronic obstructive pulmonary disease].

OBJECTIVE: To investigate the expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) in induced sputum and airway obstruction in patients with stable chronic obstructive pulmonary disease (COPD). METHODS: Fifty-five patients with stable COPD and 10 age-matched controls were enrolled in the study. Sputum induction was collected by inhalation of 3% sodium chloride. Cell numbers and differentials in sputum suspension were counted with Wright's stain. The concentrations of prostaglandin E(2) (PGE(2)) and MMP-2 in sputum supernatant were measured by ELISA. COX-2 protein expression in the cells was detected by Western blot. RESULTS: The total sputum cells, the numbers of alveolar macrophages (AM) and neutrophils (Neu) in COPD patients were significantly higher than those in the control group (P < 0.05 or P < 0.01). The number of AM and Neu was inversely correlated with FEV(1)%pred and FEV(1)/FVC (r = -0.280, P < 0.05, r = -0.345, P < 0.01; r = -0.677, r = -0.773, all P < 0.01). The level of COX-2 protein expression was higher in induced sputum in COPD patients than that in the control group. Concentrations of PGE(2) in the control group and in COPD patients with grade 0, I, IIA, IIB and III were (81 +/- 18), (111 +/- 17), (117 +/- 23), (118 +/- 29), (153 +/- 24), (194 +/- 28) ng/L, respectively. Concentrations of MMP-2 in the control group and in COPD patients with grade 0, I, IIA, IIB and III were (0.7 +/- 0.4), (4.0 +/- 0.9), (4.5 +/- 1.5), (7.7 +/- 3.1), (11.9 +/- 3.5), (18.5 +/- 5.0)microg/L, respectively. Concentrations of PGE(2) and MMP-2 in sputum in COPD patients were significantly higher than those in the control group (all P < 0.01). PGE(2) and MMP-2 were inversely correlated with FEV(1)%pred, FEV(1)/FVC in stable COPD patients (r = -0.748, r = -0.750, P < 0.01; r = -0.801, r = -0.816, all P < 0.01). Concentrations of PGE(2) were positively correlated with MMP-2 in COPD patients (r = 0.775, P < 0.01). CONCLUSIONS: (1) There is chronic inflammatory process in airway of stable COPD. AM and Neu contribute to the process. (2) COX-2 and MMP-2 may be involved in the airway inflammatory process and contribute to airway remodeling in COPD.

Adult↗

Detection of chromosome aberrations in Chinese children with autism using G-banding and BAC FISH.

OBJECTIVE: To detect the characteristic chromosomal changes in Chinese children with infantile autism. METHODS: Chromosome aberrations in 68 cases of infantile autism were analyzed by high-resolution G-banding and fluorescence in situ hybridization (FISH) with bacterial artificial chromosome (BAC) clones. RESULTS: Chromosomal changes were detected in 4 cases by high-resolution G-banding: one case with t(4;6)(q23-24;p21), one case with longer p arm of chromosome 21 (21p+), and two cases with pericentric inversion of chromosome 9 (inv(9)) which was confirmed by C-banding. BAC FISH analysis was performed to confirm these observations and changes in chromosomes 2, 7 and 15, which are often found in autistic children. There could exist the translocation of t(4;6) (q25-26;p21.1). Chromosome changes often reported previously in chromosomes 2, 7 and 15 were not detected in this study. Inv(9) and 21p+ were not confirmed with present BAC clones. CONCLUSION: Chromosomal changes were detected in four cases of infantile autism, with a detectability of 5.9% , far lower than that (10% to 48%) reported in literature. The breakpoint of translocation could be detected more accurately using BAC FISH method.

Autistic Disorder↗

[Effect of curcumin on caspase 8- and caspase 9- induced apoptosis of lymphoma Raji cell].

Curcumin is a crucial component of curcuma. Recently more attention has been paid to the effect of curcumin on specific proliferative inhibition and inducing apoptosis of tumor cells. This study was aimed to investigate the anticancer activities of curcumin and its molecular mechanism. Raji cells (lymphoma cell line) were selected as studying targets, peripheral blood mononuclear cells (PBMNC) obtained from healthy donors were separated by Ficoll solution and suspended in RMPI 1640. The inhibition rates of Raji cells and PBMNC after treatment with curcumin at various concentrations and different times were determined by MTT method and were compared. The expressions of caspase 8 and caspase 9 in Raji cells after treatment with curcumin at 25 micromol/L (IC(50)) and for 24 hours were detected by Western blot. The results showed that curcumin could inhibit proliferation of Raji cells in dose-and time-dependent manner. Curcumin could remarkablely enhance the Raji cell apoptosis at 25 micromol/L and 24 hours (P < 0.01), and its effect was dose-dependent and time-selective. Curcumin had no remarkable effect on PBMNC at certain concentrations, which demonstrated that curcumin could selectively inhibit tumor cell proliferation. It is concluded that the expression of caspase 8 and caspase 9 plays an important role in the proliferation and apoptosis of Raji cells, so that curcumin showed inhibitive effect on Raji cells at various concentrations.

Antineoplastic Agents, Phytogenic↗

[Preparation of cardiomyocyte-targeting liposomes and their targeting ability in vitro].

AIM: To prepare the cardiomyocyte-targeting liposomes and investigate their cardiomyocyte targetability in vitro. METHODS: Liposomes modified with compound PAC were prepared (PAC-L); The uptake of PAC-L by cardiomyocytes was studied by incubating fluorescence labeled liposomes with cardiomyocytes in vitro and measuring the association of liposomes by a fluorescence spectrophotometer. RESULTS: A high affinity of PAC-L to the cardiomyocytes was observed, the amount of cell uptake of PAC-L by cardiomyocytes was higher than that by nonmyocyte (P < 0.001); The amount of cardiomyocyte uptake of PAC-L on the normoxia condition 2 h was 2.9-fold higher than that of plain-L, and the increase was 5.2-fold when hypoxia occured; The form of liposome uptake changed, the amount of cardiomyocyte uptake of Plain-L by internalization was only 11%, while that of PAC-L was 56%. CONCLUSION: It is indicated that PAC-L was a potential drug carrier for targeting to ischemic myocardium.

Adrenergic beta-Antagonists↗

[Serological antibodies comparison of a hepatitis E outbreak].

OBJECTIVE: To compare the serological characters of an outbreak of hepatitis E and evaluate sensitivity and specificity of anti-HEV E2-IgM. METHODS: The sera collected from the employees of an outbreak unit were detected for anti-HEV E2-IgM and IgG, and the serum samples from a neighboring department were used as control. The results detected with anti-HEV E2-IgM, IgG and Genelab anti-HEV IgM, IgG in some samples were compared. RESULTS: The positive rate of anti-HEV E2-IgM in the control group was 0.11%. The results between the positive and the negative samples can be distinguished easily. The specificity of anti-HEV E2-IgM is about 99.89%. The positive rate of anti-HEV E2-IgM in outbreak stricken population was 8.66%, significantly higher than that in the control group (P < 0.001). The results from HEV patients' serial samples in the outbreak unit showed that the anti-HEV E2-IgM titer was high 30-60 days after the infected and then declined clearly. The positivity seemed unrelated to neither sex nor age. Among the 115 positive to anti-HEV E2-IgM, 27 were negative to Genelab anti-HEV IgG, the fact indicated a rather high risk of misdiagnosis of about 23.48%. In the 179 randomized samples of the control group, the positive rate of Genelabs anti-HEV IgG was about 11.17%. In 110 samples for the positive anti-HEV E2-IgM, the positive ratio of Genelabs anti-HEV IgG was about 76.36%, and that of Genelabs anti-HEV IgM only 69.09%. There were 16 samples negative for both Genelabs anti-HEV IgG and IgM. The ratio of the difference between the Genelabs anti-HEV IgG and IgM was about 25.45%. CONCLUSION: The specificity of anti-HEV E2-IgM was about 99%, and false positive rate was low. The sensitivity of anti-HEV E2-IgM in acute hepatitis E infection was 25%-30% higher than that of Genelabs anti-HEV IgM,IgG. The infected persons in the outbreak unit can be preferably distinguished from the non-infected persons by anti-HEV E2-IgM. Anti-HEV E2-IgM can image the characters of the outbreak of HEV and played a great role in the control of outbreak and in the early diagnosis for hepatitis E.

Antibodies, Viral↗

[Altered expression of myostatin gene in the progressive muscular dystrophy patients].

Progressive muscular dystrophy is a group of inherited disorders characterized by progressive skeletal muscle wasting and weakness, which is not of neurogenic origin. Myostatin, a new member of the TGF-beta super-family, is a negative regulator of skeletal muscle growth. To investigate the possible involvement of myostatin in the development of progressive muscular dystrophy, we cloned and sequenced myostatin cDNAs from the progressive muscular dystrophy patients by RT-PCR. Levels of myostatin mRNA and protein in the patients were analyzed by semi-quantitative RT-PCR and Western blot,respectively. We did not find any mutations in the myostatin cDNA sequences from the progressive muscular dystrophy patients in this study. However, we found that the levels of myostatin transcripts were reduced in some patients and the processing and maturation of myostatin protein were inhibited in some patients. Our data demonstrated that the pathogenesis of some types or subtypes of progressive muscular dystrophy is probably associated with the altered myostatin expression and the processing inhibition of myostatin protein.

Blotting, Western↗

[Neuronal activities related to right-sided mastication detected with functional magnetic resonance imaging].

OBJECTIVE: To observe neuronal activities related to right-sided mastication in cortex and to explore the effect of mastication on brain function. METHODS: Neuronal activities related to right-sided mastication were detected with functional magnetic resonance imaging in 10 healthy volunteers. Image data was analyzed by SPM99 software with the use of t test. RESULTS: Localization of activation in brain was different among subjects. Brain activation during mastication included left basal ganglion, Broca's area, angular gyrus and right supramarginal gyrus. CONCLUSIONS: The functional areas related to right-sided mastication and speech were closely connected, which indicated close relationship between mastication and speech. The central control of mastication might share part of common neural mechanism with that of speech. The roles of activated brain regions in mastication still remained to be elucidated.

Adult↗