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Biomedical subjects

J Han

Publications and source records attributed to J Han.

At least 343 records · Page 19Linked to original sources
PubMed1995

Independent human MAP-kinase signal transduction pathways defined by MEK and MKK isoforms.

Mammalian mitogen-activated protein (MAP) kinases include extracellular signal-regulated protein kinase (ERK), c-Jun amino-terminal kinase (JNK), and p38 subgroups. These MAP kinase isoforms are activated by dual phosphorylation on threonine and tyrosine. Two human MAP kinase kinases (MKK3 and MKK4) were cloned that phosphorylate and activate p38 MAP kinase. These MKK isoforms did not activate the ERK subgroup of MAP kinases, but MKK4 did activate JNK. These data demonstrate that the activators of p38 (MKK3 and MKK4), JNK (MKK4), and ERK (MEK1 and MEK2) define independent MAP kinase signal transduction pathways.

Amino Acid Sequence↗
PubMed1995

Expression of type VI collagen during glioblastoma cell invasion in brain tissue cultures.

Human glioblastoma cells, U-87 MG, were utilized in two separate rat brain tissue culture systems. In both cases, the glioblastoma cells deeply penetrated and formed tumor masses inside the brain tissues. Immunofluorescence technique, utilizing anti-type VI collagen antibodies demonstrated strong immunoreactivity of type VI collagen in the tumor masses, invading cells, and cell groups. We suggest that type VI collagen may be involved in tumor cells infiltration and invasion of healthy rat brain tissues. Furthermore, the brain tissue culture method may provide a rapid in vitro model with which cellular and extracellular determinants of invasiveness may be studied.

Animals↗
PubMed1995

The genotypic distribution of shared-epitope DRB1 alleles suggests a recessive mode of inheritance of the rheumatoid arthritis disease-susceptibility gene.

OBJECTIVE: To test whether the genotypic distribution of rheumatoid arthritis (RA)-associated DRB1 alleles suggests that the DRB1-associated disease-susceptibility gene has a recessive or additive (dominant) mode of inheritance. METHODS: Caucasian patients with RA and control subjects were recruited from a faculty outpatient practice. DRB1 typing was done by several DNA-based techniques: polymerase chain reaction (PCR), followed by dot-blot hybridization with sequence-specific oligonucleotides, conventional and PCR-based restriction fragment length polymorphisms (RFLPs), and a multiplex amplification-refractory mutation RFLP system. The genotypic distribution of shared-epitope DRB1 alleles was analyzed by antigen genotype frequency among patients. The analytical method postulates a linkage-disequilibrium model with a disease locus close to a marker locus and a marker allele in linkage disequilibrium with the disease-susceptibility allele. In this instance, the marker allele was defined alternatively by any DR4-group allele, by any DR4-group or DR1-group allele, by any DR4-group shared-epitope allele, by any DR4-group shared-epitope allele plus DRB1*0101, or by any shared-epitope DRB1 allele. Observed numbers were compared with those predicted for recessive mode or additive (dominant) mode of inheritance of the DRB1-associated RA disease-susceptibility gene. RESULTS: The genotypic distribution of shared-epitope DRB1 alleles (DRB1*0401, *0404, *0405, *0408, *0101, *0102, or *1001) fit that predicted for a recessive mode of inheritance and was significantly different from that predicted for an additive (dominant) mode. When the analysis was restricted to shared-epitope DR4 alleles alone (DRB1*0401, *0404, *0405, or *0408), the observed genotype numbers fit the recessive mode best. When DR1-group alleles were added to DR4-group alleles, or alternatively, when the major shared-epitope DR1 allele (*0101) was added to DR4-group shared-epitope alleles, there was a less significant deviation from the additive mode of inheritance. The reason for this was derived by comparison of observed genotype frequencies to those expected under Hardy-Weinberg equilibrium; there was a deficit of persons with DRB1*0401, *0101 and an excess of *0101,X. CONCLUSION: The genotypic distribution of shared-epitope DRB1 marker alleles suggests that the mode of inheritance of the DRB1-associated disease susceptibility gene must be recessive and not additive (dominant).

Adult↗
PubMed1995

Hemagglutination by Staphylococcus aureus strains responsible for human bacteremia or bovine mastitis.

Although hemagglutination by Staphylococcus aureus has been associated with the pathogenesis of bovine mastitis, this trait has not been characterized with regard to human disease. In this study, the prevalence of hemagglutination in 100 strains of S. aureus responsible for bovine mastitis or human bacteremia, was characterized. Under optimum conditions hemagglutination was noted in 23% of the bovine strains, but only 13% of human strains, leading us to conclude that this trait is not a significant virulence determinant in human systemic infection. Additional studies indicate the hemagglutinin of S. aureus strains responsible for human bacteremia is proteinaceous in character.

Animals↗
PubMed1995

Assessment of stenoses in the aortoiliac tract by calculation of a vascular resistance change ratio before and after exercise.

OBJECTIVES: Intraarterial pressure measurement is the most reliable method to assess haemodynamically significant stenoses in the aortoiliac tract. We have tried to develop a simple and quick, non-invasive method to assess stenoses of this type. DESIGN: Prospective semi-blinded clinical study. METHODS: It was postulated that a haemodynamically significant aortoiliac tract stenosis would result in a lesser degree of vascular resistance decrease after vasodilatation, compared to patients only suffering from femorodistal stenoses. We approximated vascular resistance by: (brachial pressure-ankle pressure)/femoral artery mean Doppler velocity. By dividing vascular resistance at rest by vascular resistance after exercise, we calculated the Resistance Change Ratio (RCR). PATIENTS AND RESULTS: In 34 patients (50 legs) with arterial stenoses, the pressure gradient over the aortoiliac segment was compared to the RCR. Legs were divided in three groups: group 1 consisted of 22 legs that showed a pressure gradient > 10 mmHg at rest; group 2 showed a pressure gradient > 10 mmHg after papaverine; group 3 showed a pressure gradient of 10 mmHg or less. The median RCR was: 0.74 (range: 0.23-4.04) for group 1, 0.71 (range: 0.36-1.80) for group 2 and 0.93 (range 0.36-2.06) for group 3. There was no significant difference between the groups (p = 0.19). CONCLUSION: The RCR could not be used to accurately detect stenoses in the aortoiliac.

Aorta, Abdominal↗
PubMed1995

Recurrent mis-splicing of fibrillin exon 32 in two patients with neonatal Marfan syndrome.

The Marfan syndrome (MFS) is an autosomal dominant heritable disorder of connective tissue. Variable and pleiotropic clinical features are observed in the skeletal, ocular, and cardiovascular systems. The most severe end of the phenotypic spectrum of this disorder comprises a group of patients usually diagnosed at birth, who have a life expectancy of little more than a year. To distinguish this group of patients from those with classical MFS, we refer to them as neonatal Marfan syndrome (nMFS). These infants usually die of congestive heart failure rather than aortic aneurysmal disease, the most frequent cause of morbidity and mortality in classical MFS. Defects in fibrillin, an elastin-associated microfibrillar glycoprotein, are now known to cause both the classical and neonatal forms of MFS. Here we report the recurrent mis-splicing of fibrillin (FBN1) exon 32, a precursor EGF-like calcium binding domain, in two unrelated infants with nMFS. The mis-splicing, in one patient, was due to an A-->T transversion at the -2 position of the consensus acceptor splice site; while that in the second patient was caused by a G-->A transition at the +1 position of the donor splice site. Characterization of FBN1 mutations in individuals at the most severe end of the Marfan syndrome spectrum should provide greater understanding of the multiple domains and regions of fibrillin.

Alleles↗
PubMed1995

Characterization of the hemagglutinin of Staphylococcus epidermidis.

Adherence to biomaterials and production of biofilm is thought to be pivotal in the pathogenesis of prosthetic device infection by Staphylococcus epidermidis. In this study a strong association (P < .001) of hemagglutination with adherence and biofilm production was observed. Hemagglutination was not associated with cell surface hydrophobicity (P = .906). Hemagglutination inhibition studies revealed that hemagglutination was not affected by heat, pH, cation concentration, proteolytic enzymes, biologic detergent, serum proteins, or subinhibitory antibiotics. Hemagglutination was abolished by periodate oxidation and digestion with glycosidases. It was markedly inhibited by beta-lactose and its monosaccharide constituents in a concentration-dependent fashion. Hemagglutinin expression depended on the presence of glucose. Chemical analysis of a partially purified hemagglutinin preparation and cell-free hemagglutinating supernatants revealed little or no protein and small quantities of reducing sugars, pentose, ketose, hexosamine, uronic acid, and phosphate. Hemagglutinin of S. epidermidis appears to be a polysaccharide distinct from other known adhesins of S. epidermidis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

A technique for calibrating measurements from photographs of sliced specimens.

Determining the geometry of articular joint surfaces is critical to the study of human joint mechanics. Photographs of sliced specimens (PSS) is currently one of the most popular methods used to determine surface geometry. This study sought to improve the photographs of sliced specimens method through a new calibration technique that includes a mathematical model and a precise plastic grating (calibration grid). Simulations showed that calibration results for x and y coordinates using the new technique attained a high degree of accuracy that was independent of camera and projector lens quality, degree of parallelity between the projector and digitizing table and selection of the area to be calibrated.

Calibration↗
PubMed1995

Pulmonary oxygen toxicity in mice is characterized by alterations in ascorbate redox status.

Pulmonary oxygen toxicity results from disruption of the usual antioxidant defenses of the body. We therefore investigated whether mice that suffer from oxygen toxicity show significant alterations in the redox status of ascorbate, an important antioxidant, as reflected by changes in the relative amounts of its oxidized and reduced forms. Mice were exposed to air or hyperoxia (> 97% O2, 760 mmHg). After 5 days, plasma and saline-perfused lungs were removed and levels of ascorbate (AA), oxidized ascorbate [dehydroascorbate (DHAA)], and total ascorbate species ([AA+DHAA]) were determined by a sensitive and specific high-performance liquid chromatography assay; lungs were also assayed for total glutathione and glutathione disulfide (GSSG), an established marker of oxidative stress. We found that with hyperoxic exposure plasma AA increased by 32%, plasma DHAA increased substantially from previously undetectable levels, and the DHAA-to-[AA+DHAA] ratio increased. In contrast, in lung, [AA+DHAA] decreased by 41%. Plasma AA, DHAA, and [AA+DHAA] each correlated inversely with lung [AA+DHAA] and directly with lung GSSC. We conclude that alterations in plasma ascorbate redox status reflect pulmonary oxygen toxicity in mice. Our results suggest that further investigations are warranted to determine whether similar findings occur in humans and have clinical utility.

Animals↗
PubMed1995

Assignment of the human heart tetrodotoxin-resistant voltage-gated Na+ channel alpha-subunit gene (SCN5A) to band 3p21.

The chromosomal location of SCN5A, the gene encoding the principal voltage-gated Na+ channel expressed in human heart, has been determined by three independent methodologies: somatic cell hybrid mapping, chromosomal microdissection-polymerase chain reaction, and fluorescence in situ hybridization. The SCN5A gene was assigned to the short arm of chromosome 3 (band 3p21) by all three approaches. These data are further evidence that striated muscle Na+ channel genes are dispersed in the genome.

Animals↗
PubMed1995

Biosynthesis of type VI collagen by glioblastoma cells and possible function in cell invasion of three-dimensional matrices.

The biosynthesis of type VI collagen was studied in human glioblastoma cell line, U-87 MG. The effects of ascorbic acid on type VI collagen synthesis and secretion were investigated. After ascorbic acid treatment, type VI collagen in cell layers increased from 4.48% in control to 6.63% in the ascorbic acid treated cultures, an increase of 48%. The effect of ascorbic acid on type VI collagen synthesized by glioblastoma cells was lower than that reported for osteosarcoma cells (Engvall et al., 1986). The reason for these differences is still under investigation. The function of type VI collagen in glioblastoma cells is still unknown. We utilized the collagen gel system to elucidate the possible roles of type VI collagen in glioblastoma cells in vitro. Glioblastoma cells in collagen gels showed a stellate shape with long, branched processes in all directions. The strong positive reactivity of type VI collagen detected on cell bodies and cell processes by anti-type VI collagen antibody indicated that this specific collagen was associated with cell surfaces and processes, without releasing or diffusing into the gels. Type VI collagen was directly involved in the cell process extension. When living cells were treated with anti-type VI collagen antibody, a variation of cell morphology was observed. Instead of a stellate shape with processes, cells formed clusters without or with very short processes. These data suggest that type VI collagen, synthesized and secreted by glioblastoma cells, may play a role in tumor cell adhesion and spreading, and enhance cell process extension, penetration, and invasion into collagen gels.

Antibodies↗
PubMed1995

[Determination of psoralen and isopsoralen in tincture of fructus Psoraleae by HPLC].

A reversed-phase HPLC method was described for the determination of psoralen and isopsoralen in tincture of Fructus Psoraleae. After adding the internal standard and diluting the sample to a definite volume, the sample was injected and analysed. The RSDs were within 2% and the minimum working concentrations below 1 microgram/ml; the average recoveries of psoralen and isopsoralen 102.8% and 99.5% respectively and the linear ranges of psoralen and isopsoralen 12-200 micrograms/ml and 13-210 micrograms/ml (r = 0.999) respectively.

Chromatography, High Pressure Liquid↗
PubMed1995

Extensive wound excision in shock stage in patients with major burns.

To stop excessive plasma loss, alleviate noxious effects of devitalized tissues on the body and shorten the hospitalization time, we performed extensive escharectomy during the shock period in extensively burned patients. Group A consisted of 21 patients aged 9-45 years (26.1 +/- 7.9 years), with a mean total burn area of 63.2% +/- 18.1% TBSA, and full-thickness injury involving 35.9% +/- 19.6% TBSA. The first escharectomy was done at 24.1 +/- 13.9 hours postburn, and excision area averaged 32.3% +/- 6.7% TBSA (24%-46%). In 15 of them, Swan-Ganz catheter was introduced to monitor the hemodynamic changes. It was found that RAP, PAP, PAWP, ABP, HR, CO and CI were all stable during and after the operation. Group B consisted of 29 patients aged 11-50 years (30.4 +/- 11.7 years), in whom escharectomy was begun 4-5 days postburn. The mean healing time of the patients in group A was 33.1 days, shorter than that of group B patients (40.1 days). The duration of hemoconcentration was shorter in group A. The amount of blood transfusion was almost 700 ml less in group A during the first two weeks. Less antibiotics were used with fewer visceral complications in group A. We believe that escharectomy during the burn shock stage is feasible.

Adolescent↗
PubMed1995

Cloning, expression and purification of the ligand-binding region of human IL-6R in E. coli and its preliminary functional identification.

The ligand-binding region of human IL-6R is taken as the target gene fragment to be cloned and expressed. With pET-3b as expressing vector, two recombinants pET-6R(B) and pET-6R(B)4 have been constructed encoding the ligand-binding region (28 kD) of hIL-6R and its dimmer (53 kD), respectively. After induction with IPTG, they produced two proteins rIL6R-28 of 28 kD and rIL6R-53 of 53 kD amounting to 50% and 30% of total bacteria proteins, respectively. The expressed products were mainly recovered as inclusion bodies. After purification and renaturation, both of them were capable of augmenting the growth-stimulating effect of IL-6 on 7TD1 cells, an IL-6 dependent cell line. The result of ELISA also revealed that both rIL6R-28 and rIL6R-53 had the obvious ligand-binding activity.

Antigens, CD↗