Search PubMed⌕ Search

Biomedical subjects

J Hou

Publications and source records attributed to J Hou.

At least 127 records · Page 7Linked to original sources

Whole genome analysis of hepatitis B virus from four cases of fulminant hepatitis: genetic variability and its potential role in disease pathogenicity.

The precore stop-codon variant of hepatitis B virus (HBV) has been associated with fulminant hepatitis but is also found in patients with persistent infection and chronic hepatitis. We have examined the possibility that the severe outcome of infection in patients with fulminant disease may be a result of additional genomic variation. We sequenced the entire HBV genome from three patients of Greek and one patient of Chinese origin with fulminant hepatitis, and from two patients with hepatitis B e antigen (HBeAg) positive chronic infection from the same regions, using direct sequencing of amplified viral DNA. Three of the fulminant cases were infected with the precore stop-codon variant HBeAg negative) and the fourth with the wild-type (HBeAg) positive virus. We compared sequences from our four fulminant isolates, and an additional fulminant isolate reported by others, with HBeAg positive carriers from the same regions and 12 published HBV genomes. There was a higher number of nucleotide and amino-acid substitutions throughout the HBV genome in the precore variant fulminant sequences than in the wild type. A cluster of mutations previously identified in the X region (126-132) in sequences reported in Japanese patients and encompassing the Enhancer II-Core Promoter region (1751-1768), were not found in our patients. We conclude that although there are no changes common to all sequences of HBV isolates from fulminant cases, some of these changes are in recognized cis-acting regulatory elements, whilst others are in the immediate vicinity of such elements. The effect of these mutations on viral genome transcription must now be determined.

Amino Acid Sequence↗

Effects of angiotensin II infusion and inhibition of nitric oxide synthase on the rat aorta.

In previous studies, we showed that in vivo infusion of angiotensin II (Ang II) to adult rats induced vascular changes in gene expression, and this effect did not depend solely on blood pressure elevation. To determine whether nitric oxide can influence the effects of Ang II on the vessel wall, we administered to rats Ang II separately or in combination with the arginine analogue N omega-nitro-L-arginine methyl ester, which inhibits nitric oxide synthase chronically when given in vivo. We measured changes in aortic medial thickness, the association of macrophages with the endothelial surface of the aorta, the presence of proliferating cell nuclear antigen in the intima and adventitia as an index of aortic cell cycle changes, and the expression of immunodetectable fibronectin as an index of changes in the extra-cellular matrix. After 18 days of nitric oxide inhibition, the major changes were increased medial thickness and a 3.5-fold increase in the number of adherent macrophages. Rats treated with two different doses of Ang II for 3 days had a fivefold and threefold increase in the number of proliferating cells from the intimal and adventitial regions, respectively. Combined treatment resulted in increased medial thickness, intimal and adventitial cell proliferation, and macrophage adherence. An increased and altered pattern of fibronectin distribution was found in all treatment groups. Losartan administration prevented the effects of Ang II but not of nitric oxide inhibition, whereas administration of L-arginine, prevented both intimal macrophage adherence and increased adventitial proliferation in rats given combined treatment. The data suggest that nitric oxide selectively influences macrophage association with the arterial wall, whereas Ang II and nitric oxide may have opposing effects on arterial cell proliferation.

Angiotensin II↗

[Identification of vertical transmission of hepatitis B virus from mother to children by direct sequencing a segment of surface gene of hepatitis B virus].

SUBJECTIVE: To explore the reason for the failure to interrupt vertical transmission of hepatitis B virus (HBV) from mother to children in Chinese subjects by vaccination. METHODS: HBV nucleotide sequences isolated from three sets of mother/children pairs were analyzed. HBV DNA from the surface antigen region encoding the amino acids 101 to 160 of hepatitis B surface antigen (HBsAg) was amplified and sequenced from HBsAg positive mother and their children. RESULTS: Nucleotide and deduced amino acid sequences were absolutely identical in the mother and children in family one and two respectively. However, there were five nucleotides different in family one's isolates compared with the family two's isolates. All of them were a subtype. In one child of family three, with coexisted HBsAg and anti-HBs, sequencing result revealed a point mutation which predicted a change from glycine to arginine at residue 145 in the second loop of the determinant. The mother and another child had a glycine at this position. CONCLUSION: This study revealed the vertical transmission linkage of HBV between the mother and children in a molecular level, and also first described a codon 145 immune escape mutant in Chinese vaccinated children.

Adult↗

Interaction between fulvic acids of different origins and active oxygen radicals.

Using the spin trapping technique, the interaction between fulvic acids (FAs) of different origins and the active oxygen radicals was studied. The active oxygen radicals under study included superoxide anion (O2.-) produced by xanthine oxidase (XOD) and stimulated polymorphonuclear leukocytes (PMN) of human being and hydroxyl radical (.OH) produced from Fenton's reaction. It has been found that the FAs from both Kaschin-Beck disease (KBD) region and non-KBD region can accelerate the production of .OH and scavenge O2.-. FA from peat can scavenge both O2.- and .OH. The results show that the behavior of KBD and non-KBD FAs differs clearly from peat FA. It has been concluded that the superoxidation damage of KBD induced by FA is mainly due to hydroxyl radical reaction initiated in biological system.

Benzopyrans↗

[Using ligustrazini and angelica sinensis treat the bleomycin-induced pulmonary fibrosis in rats].

OBJECTIVE: To seek a kind of Chinese traditional medicine to treat the bleomycin-induced pulmonary fibrosis. METHODS: SD rats with bleomycin A(s) induced pulmonary fibrosis, were divided into 4 groups. Normal control group (10 rats), untreated model group (35 rats), ligustrazini group (10 rats), Angelica sinensis group (10 rats). Both ligustrazini and angelica sinensis were given intraperitoneally by injection daily for 28 days. Then all rats were put to death and took out the lungs for examination. Using histopathological examination and image processing computer assisted to evaluate the result of treatments. RESULTS: Ligustrazini could obviously reduced alveolitis and fibrosis and Angelica sinensis had the similar but lesser result. CONCLUSION: Ligustrazini and angelica sinensis have successful result of treatment for pulmonary fibrosis.

Animals↗

[A clinical study in the treatment of acute bacterial infections with fleroxacin].

The purpose of this clinical trial is to evaluate the efficacy and safety of fleroxacin and to compare with those of lomefloxacin. A randomized controlled study was carried out to treat sixty patients with urinary tract and respiratory tract bacterial infections, thirty in each group with one of the two drugs, and fifty cases were treated with fleroxacin in an open trial. Altogether there were one hundred and ten cases. Both fleroxacin and lomefloxacin were given orally, the dosage was 200 mg every 12 hours or 400 mg every 24 hours for 7-14 days. The clinical efficacy rate was 93.3%; the culturing rate in the fleroxacin group was 83.3%; the bacterial clearance rate was 92.3%, the incidence of adverse reactions was 9.4%, while in the lomefloxacin group they were 90.0%, 80.0%, 87.5% and 6.7% respectively, with no statistically significant difference between the two groups (P > 0.05). In the open and randomized trials, fleroxacin cured eighty cases of bacterial infections, the overall clinical efficacy rate was 90.0%, the culturing rate in the flero-xacin group was 83.8%, the bacterial clearance rate was 88.2% and the incidence of adverse reactions was 9.6%. It is shown that fleroxacin is an antibiotic of broad-spectrum, high efficacy and safety.

Adult↗

A 4-megabase YAC contig that spans the Langer-Giedion syndrome region on human chromosome 8q24.1: use in refining the location of the trichorhinophalangeal syndrome and multiple exostoses genes (TRPS1 and EXT1).

We have constructed a physical map covering over 4 Mb of human chromosome 8q24.1 and used this map to refine the locations of the genes responsible for Langer-Giedion syndrome. The map is composed of overlapping YAC clones that were identified and ordered in relation to sequence tagged sites mapped to the Langer-Giedion chromosomal region on somatic cell hybrids. The minimal region of overlap of Langer-Giedion syndrome deletions, previously identified by analysis of 15 patients, was placed on the map by analysis of 2 patients whose deletions define the endpoints. The chromosome 8 breakpoint of a balanced t(8;9)(q24.11;q33.3) translocation from a patient with trichorhinophalangeal syndrome (TRPS I) was found to be located just within the proximal end of the minimal deletion region. A deletion of 8q24.11-q24.3 in a patient with multiple exostoses was found to overlap the distal end of the LGS deletion region, indicating that the EXT1 gene is distal to the TRPS1 gene and supporting the hypothesis that Langer-Giedion syndrome is due to loss of functional copies of both the TRPS1 and the EXT1 genes.

Animals↗

A unique insertion in the S gene of surface antigen--negative hepatitis B virus Chinese carriers.

The presence of unique hepatitis B virus (HBV) variants has been investigated in two Chinese patients with chronic liver disease, whose sera were positive for HBV-DNA by dot blot hybridization or polymerase chain reaction (PCR) but hepatitis B surface antigen (HBsAg)-negative by conventional polyclonal antibody based immunoassays. PCR amplification of HBV-DNA followed by direct sequencing showed an insertion of six nucleotides, which introduced two additional amino acids between codons 122 and 123 in one patient (Isolate 1), whereas a nine nucleotide insertion in the other patient (Isolate 2) gave rise to three amino-acids between codons 123 and 124 immediately upstream from the 'a' determinant in the S gene. These insertions have not been described previously in any published sequences of the known subtypes and were absent from sequences of 30 HBsAg-positive Chinese patients from the same region. In the cases under study, the insertion is associated with four consecutive adenine molecules from nucleotides 516 to 519. It seems likely that this area is a hot spot for insertions in HBV. We found none of the previously described amino-acid deletions or substitutions in the pre-S1, pre-S2 and S genes, which are involved in unusual antigenic profiles. This finding suggests that genetic mutations in the S gene outside the 'a' determinant may be responsible for failure to detect HBsAg in some Chinese patients with chronic hepatitis caused by HBV infection.

Adult↗

Identification and purification of human Stat proteins activated in response to interleukin-2.

A key cytokine induced during the immune response is IL-2. Following T cell activation, the genes encoding IL-2 and the various chains of its receptor are transcriptionally induced. In turn, secreted IL-2 serves to stimulate the proliferation and differentiation of T lymphocytes. Several recent studies have implicated Jak kinases in the signaling pathway induced by IL-2. Following this lead, we set out to identify transcription factors induced in response to IL-2. Human peripheral blood lymphocytes were observed to contain several IL-2-inducible DNA binding activities. Similar activities were also observed in a transformed human lymphocyte line, termed YT. We have purified these activities and found that the principal IL-2-inducible component bears significant relatedness to a prolactin-induced transcription factor first identified in sheep mammary gland tissue. We hypothesize that activation of this protein, designated hStat5, helps govern the biological effects of IL-2 during the immune response.

Amino Acid Sequence↗

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

These studies were performed to determine if the effects of angiotensin II infusion on the development of cardiac fibrosis could be modified by the chronic inhibition of nitric oxide synthase activity. NG-nitro-L-arginine-methyl ester (L-NAME) was administered to adult Wistar rats in drinking water (40 mg/kg per d). Although blood pressure was maintained at hypertensive levels after 2 wk, cardiac hypertrophy or fibrosis did not occur. Angiotensin II, given for 3 d at a dose which induced little or no blood pressure elevation and minimal if any fibrosis, caused significant fibrosis when given to a rat pretreated for 2 wk with L-NAME. This marked fibrosis did not occur if angiotensin II was given shortly after L-NAME treatment was begun or briefly after discontinuation of L-NAME. The fibrosis that occurred with combined treatment was characterized by increased immunodetectable fibronectin, the presence of inflammatory cells within interstitial and perivascular regions, and increased steady state mRNA levels for matrix genes and atrial natriuretic protein. The data indicated a regulatory role for nitric oxide in modulating the angiotensin II-induced cardiac fibrosis and suggest a potentially important autocrine or paracrine role for nitric oxide in fibroblast proliferation.

Angiotensin II↗

[Applied study on MRI diagnosis of the oral and maxillofacial masses.].

38 cases of Oral and Maxillofacial masses were selected to be studied by MRI,combined with fine neddle aspiration cytologic examination,compared with CT scan.The authors thought that MRI was clear,high resolving power of soft tissue,able to find out the bone infiltration of the Oral Maxillofacial masses and hemangioma or lymphoangioma etc,those which were suspected to invade the crania base,tip of orbit,pterygopalatine fossa,parapharyngeal,the vital blood vessel of the neck,primary study on MRI supervising local recur after the maxillofacial tumors being resected was also done.

English Abstract↗

[Genetic variation in the cleavage site of the precore region of hepatitis B virus in Chinese patients with fulminant hepatitis].

In this study, a previously not documented variant of hepatitis B virus was described in Chinese patients with fulminant hepatitis. The entire precore/core region amplified from samples was cloned into a bacterial vector and sequenced by dideoxy chain termination reaction. Double amino acid substitutions were seen in the precore region in the isolates: one from glycine to aspartic acid at codon 29 previously reported; the other substitution of phenylalanine for valine at codon 17 in the cleavage site of hepatitis B virus. Loss of hepatitis B virus e antigen in these patients with fulminant hepatitis might therefore be due to the mutation in the cleavage site, rather than the emergence of a stop codon in the precore region of hepatitis B virus. Accumulation of hepatitis B e antigen precursor within the hepatocytes might account for the fulminant hepatitis exacerbation.

Amino Acid Sequence↗

Intact and functional fibroblast growth factor (FGF) receptor-1 trafficks near the nucleus in response to FGF-1.

Exogenous fibroblast growth factor-1 (FGF-1) associates with the nucleus in a receptor-dependent manner during the entire G1 period of the BALB/c 3T3 cell cycle (Zhan, X., Hu, X., Friesel, R., and Maciag, T. (1993) J. Biol. Chem. 268, 9611-9620). To further study the role of the FGF receptor (FGFR) during this translocation, the intracellular fate of FGFR-1 protein and enzymatic activity was examined. Immunoprecipitation using multiple FGFR-1 antibodies followed by an in vitro tyrosine kinase activity assay enabled us to identify FGFR-1 as a 130-kDa phosphotyrosine-containing protein associated with the nuclear fraction of NIH 3T3 cells exposed to FGF-1. While FGFR-1 tyrosine kinase activity could be detected as a nuclear-associated protein after a 2-h exposure of the NIH 3T3 cells to FGF-1, this activity appeared to be maximal in the nuclear fraction between 4 and 12 h after FGF-1 treatment. In addition, analysis by confocal immunofluorescence microscopy of quiescent and FGF-1-stimulated NIH 3T3 cells reveal a prominent perinuclear FGFR-1 staining pattern in the cells exposed to FGF-1 but not in the quiescent population. We also observed FGFR-1 associated with the nuclear fraction in FGFR-1-transfected L6 rat myoblasts, which are known to be refractive to exogenous FGF-1 and express relatively low levels of endogenous FGFR-1. In addition, these cells also exhibited the presence of a 145-kDa phosphoprotein in the nuclear fraction that was recognized by FGFR-1 antibodies. These results suggest that the FGFR-1 may be translocated near the nucleus upon interaction with its ligand during the entire G1 period of the NIH 3T3 cell cycle as a structurally intact and functional tyrosine kinase that may be accessible to perinuclear polypeptides as a regulatory enzyme.

3T3 Cells↗

Regulatory elements and transcription factors controlling basal and cytokine-induced expression of the gene encoding intercellular adhesion molecule 1.

The gene encoding intercellular adhesion molecule 1 (ICAM-1) is transcriptionally induced in response to inflammatory and immunomodulatory cytokines. To investigate the mechanisms controlling ICAM-1 gene expression, we have identified regulatory DNA sequences responsible for maintaining basal and mediating induced transcription in response to tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). Regulatory elements centered 115, 60, and 40 bp upstream from the ICAM-1 transcription start site were implicated in cytokine-independent gene expression. Regulatory elements dedicated to TNF-alpha and IFN-gamma were identified 190 and 90 bp, respectively, upstream from the ICAM-1 transcription start site. A combination of mutagenesis and DNA-binding assays revealed that the TNF-alpha response element is composite, consisting of binding sites for both C/EBP and NF-kappa B. The IFN-gamma response element behaved as a simple regulatory element that selectively binds to an IFN-gamma-inducible activity composed, at least in part, of p91. These observations provide a framework for understanding how extracellular signals dynamically regulate the adhesive properties of mammalian cells.

Base Sequence↗

An interleukin-4-induced transcription factor: IL-4 Stat.

Interleukin-4 (IL-4) is an immunomodulatory cytokine secreted by activated T lymphocytes, basophils, and mast cells. It plays an important role in modulating the balance of T helper (Th) cell subsets, favoring expansion of the Th2 lineage relative to Th1. Imbalance of these T lymphocyte subsets has been implicated in immunological diseases including allergy, inflammation, and autoimmune disease. IL-4 may mediate its biological effects, at least in part, by activating a tyrosine-phosphorylated DNA binding protein. This protein has now been purified and its encoding gene cloned. Examination of the primary amino acid sequence of this protein indicates that it is a member of the signal transducers and activators of transcription (Stat) family of DNA binding proteins, hereby designated IL-4 Stat. Study of the inhibitory activities of phosphotyrosine-containing peptides derived from the intracellular domain of the IL-4 receptor provided evidence for direct coupling of receptor and transcription factor during the IL-4 Stat activation cycle. Such observations indicate that IL-4 Stat has the same functional domain for both receptor coupling and dimerization.

Amino Acid Sequence↗