Biomedical subjects

Y Han

Publications and source records attributed to Y Han.

At least 73 records · Page 4Linked to original sources

PubMed2001

nompA encodes a PNS-specific, ZP domain protein required to connect mechanosensory dendrites to sensory structures.

Mutations in the no-mechanoreceptor-potential A (nompA) gene, which eliminate transduction in Drosophila mechanosensory organs, disrupt contacts between neuronal sensory endings and cuticular structures. nompA encodes a transmembrane protein with a large, modular extracellular segment that includes a zona pellucida (ZP) domain and several plasminogen N-terminal (PAN) modules. It is specifically expressed in type I sense organs of the peripheral nervous system by the support cells that ensheath the neuronal sensory process. A green fluorescent protein (GFP)-NompA fusion protein is localized to the dendritic cap, an extracellular matrix that covers the ciliary outer segment of the sensory process and that shows organizational defects in nompA mutants. The structure and location of NompA suggest that it forms part of a mechanical linkage required to transmit mechanical stimuli to the transduction apparatus.

Amino Acid Sequence↗

PubMed2001

Identification of arabidopsis proteins that interact with the cauliflower mosaic virus (CaMV) movement protein.

Gene I of cauliflower mosaic virus (CaMV) encodes a protein that is required for virus movement. The CaMV movement protein (MP) was used in a yeast 2-hybrid system to screen an Arabidopsis cDNA library for cDNAs encoding MP-interacting (MPI) proteins. Three different clones were found encoding proteins (MPI1, -2 and -7) that interact with the N-terminal third of the CaMV MP. The interaction in the 2-hybrid system between MPI7 and CaMV MP mutants correlated with the infectivity of the mutants. A non-infectious MP mutant, ER2A, with two amino acid changes in the N-terminal third of the MP failed to interact with MPI7, while an infectious second-site mutant, that differed from ER2A by only a single amino acid change, interacted in the 2-hybrid system. MPI7 is encoded by a member of a large, but diverse gene family in Arabidopsis. MPI7 is related in sequence, size and hydropathy profile to mammalian proteins (such as rat PRA1) described as a rab acceptor. The gene encoding MPI7 is expressed widely is Arabidopsis plants. and in transgenic plants the MPI7:GFP fusion protein is localized in the cytoplasm, concentrated in punctate spots. In protoplasts transfected with CFP:MP and MPI7:YFP, CFP:MP colocalized to some of the sites where MPI7:YFP is expressed. At these sites, fluorescence resonance energy transfer (FRET) between fluorophores was observed indicating an interaction in planta between the CaMV MP and MPI7.

Amino Acid Sequence↗

PubMed2001

Effects of the oral spirochete Treponema denticola on interleukin-8 expression from epithelial cells.

This communication demonstrates that the interaction of the oral spirochete Treponema denticola 35405 with KB epithelial cells does not lead to the induction of interleukin-8 production as occurs with a variety of other bacteria. Utilizing the dentilisin protease mutant K1 of T. denticola, this property was demonstrated to be primarily a function of the expression of the protease by strain 35405.

Bacterial Proteins↗

PubMed2001

Genes determining pathogenicity to pea are clustered on a supernumerary chromosome in the fungal plant pathogen Nectria haematococca.

Three genes that contribute to the ability of the fungus Nectria haematococca to cause disease on pea plants have been identified. These pea pathogenicity (PEP) genes are within 25 kb of each other and are located on a supernumerary chromosome. Altogether, the PEP gene cluster contains six transcriptional units that are expressed during infection of pea tissue. The biochemical function of only one of the genes is known with certainty. This gene, PDA1, encodes a specific cytochrome P450 that confers resistance to pisatin, an antibiotic produced by pea plants. The three new PEP genes, in addition to PDA1, can independently increase the ability of the fungus to cause lesions on pea when added to an isolate lacking the supernumerary chromosome. Based on predicted amino acid sequences, functions for two of these three genes are hypothesized. The deduced amino acid sequence of another transcribed portion of the PEP cluster, as well as four other open reading frames in the cluster, have a high degree of similarity to known fungal transposases. Several of the features of the PEP cluster -- a cluster of pathogenicity genes, the presence of transposable elements, and differences in codon usage and GC content from other portions of the genome -- are shared by pathogenicity islands in pathogenic bacteria of plants and animals.

Amino Acid Sequence↗

PubMed2001

Effect of multiple mutations in the core promoter and pre-core/core region of hepatitis B virus genome on the response to interferon in e antigen-positive chronic hepatitis B.

BACKGROUND AND AIMS: Hepatitis B virus (HBV) genomic mutations may be one of the factors that influence the efficacy of interferon (IFN) therapy. The aim of this study was to investigate the effects of mutations in different parts of the HBV genome on IFN therapy. METHODS: We studied the baseline clinical, biochemical, serologic and virologic parameters in 17 patients with e antigen-positive chronic hepatitis B. The DNA sequence of the X gene and pre-core/core gene in serum samples of these patients was analyzed before the initiation of IFN therapy. RESULTS: All five patients with the T1762-A1764 mutation were IFN responsive, while among the 12 remaining patients, only two responded to therapy. Among five patients with both a pre-core A1896 mutation and a mutation in the epitope aa 107-118 of the core region, four were non-responders whereas the fifth responded to therapy. In three other patients with A1896 mutations, one with simultaneous mutations in five lymphocytic epitopes did not respond to therapy; the two remaining patients with concomitant mutations in one or two epitopes were responsive. Serum HBV-DNA levels were lower and titers of antibody to hepatitis B virus core antigen-immunoglobin M (anti-HBc-IgM) were higher in the responders than in the non-responders. Hepatitis B virus genotypes B and C were found to be in all these Chinese patients. CONCLUSIONS: These results suggest that HBV genomic mutations, serum viral loads and titers of anti-HBc-IgM might be predictive of the efficacy of IFN therapy. These clinical findings should be further investigated by in vivo and in vitro experiments.

Adult↗

PubMed2001

Ultrasound assessment of scald scars in Asian children receiving pressure garment therapy.

BACKGROUND/PURPOSE: Scar formation after scald injury in children is managed commonly by application of pressure garment. The duration of the treatment depends on clinical assessment. The objective of the study was to evaluate the efficacy of the pressure garment therapy and to correlate the clinical assessment scar thickness with ultrasound measurement. METHODS: Prospective study of children with hypertrophic scars receiving pressure garment therapy was carried out between 1993 and 1998. The scars were mapped with paper cutting. Representative scar sites were scored clinically according to Vancouver General Hospital Burn Assessment Scale (pigmentation, vascularity, pliability, height, pain, itchiness). Blind to the clinical results, 2 radiologists measured the scar thickness of the same sites with ultrasonography (5 to 10 MHz transducer, General Electric LOGIQ 500). The correlation between the clinical scores and ultrasound measurement of scar thickness were analysed using analysis of variance (ANOVA). RESULTS: The median age of 58 children with scald injury (M:F = 36:22) was 2.8 years (0.5 to 15.8 years). The mean percentage of scald was 8.8% (24% had scald area >10%). In addition, there were 5 children with burn from naked flame and 9 children with keloid secondary to surgical incisions. With pressure garment therapy, the scar thickness reached a plateau 1 (1/2) years after the injury and began to decline gradually thereafter. The clinical estimation of scar thickness correlated well with the ultrasound measurement (ANOVA, P =.003, Adjusted R square = 0.99). The accuracy rate of clinical thickness estimation was 67%. Overestimation and underestimation accounted for 15% and 18%, respectively. There also was good correlation between total clinical score and the ultrasound measurement (ANOVA, P <.001). CONCLUSIONS: In children with scald injury, the pressure garment needs to be continued for a minimum of 1 year. Ultrasound measurement correlates well with overall score of the Vancouver General Hospital Burn Assessment Scale but not individual components of the scoring system except wound height.

Adolescent↗

PubMed2001

Myocardial protection during ventricular fibrillation by reduction of proton-driven sarcolemmal sodium influx.

Although the inhibition of proton-driven sarcolemmal sodium influx ameliorates ischemic injury in the quiescent myocardium, the effects when ventricular fibrillation is present are largely unknown. We used an isolated rat heart model to investigate whether inhibition of the sodium-hydrogen exchanger isoform-1 (with the benzoylguanidine derivatives HOE-694 and cariporide) with or without concomitant inhibition of the sodium-bicarbonate co-transporter (with perfusate buffered with N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid [HEPES]) during ischemia and ventricular fibrillation could ameliorate functional myocardial abnormalities presumed to limit cardiac resuscitability. Ischemic contracture, which typically develops during ventricular fibrillation, was ameliorated by HOE-694 when either a bicarbonate-buffered (20 +/- 7 mm Hg vs 15 +/- 5 mm Hg, P <.05) or a HEPES-buffered (14 +/- 5 mm Hg vs 10 +/- 3 mm Hg, P <.04) perfusate was used. Maximal amelioration occurred when cariporide and HEPES-buffered perfusate were used simultaneously (25 +/- 14 mm Hg vs 11 +/- 3 mm Hg, P <.01), and this was accompanied by lesser leftward shifts of the end-diastolic pressure-volume curves after defibrillation. Intramyocardial sodium increases of 76% during ischemia and ventricular fibrillation (P <.05) were ameliorated by the sodium-influx-limiting interventions. Thus interventions limiting sarcolemmal sodium influx during ischemia and ventricular fibrillation may facilitate successful resuscitation from ventricular fibrillation.

Animals↗

PubMed2001

Effects of movement protein mutations on the formation of tubules in plant protoplasts expressing a fusion between the green fluorescent protein and Cauliflower mosaic virus movement protein.

Fusions between the green fluorescent protein (GFP) and the Cauliflower mosaic virus (CaMV) movement protein (MP) induce the formation of fluorescent foci and surface tubules in Arabidopsis thaliana leaf mesophyll protoplasts. Tubules elongate coordinately and progressively in an assembly process approximately 6 to 12 h following transfection of protoplasts with GFP-MP constructs. Tubules are not formed in protoplasts transfected by GFP-MP(ER2A), a MP mutation that renders CaMV noninfectious. A small number of short tubules are formed on protoplasts transfected by GFP-MP(N6) and GFP-MP(N13), two second-site revertants of ER2A that partially restore infectivity. Protoplasts cotransfected with cyan fluorescent protein (CFP)-MP(WT) and GFP-MP(ER2A) form tubules containing both MP fusions, indicating that although the GFP-MP(ER2A) cannot induce tubule formation, GFP-MP(ER2A) can coassemble or colocalize with CFP-MP(WT) in tubules. Thus, CaMV MP-induced tubule formation in protoplasts correlates closely with the infectivity of mutation ER2A and its revertants, suggesting that tubule-forming capacity in plant protoplasts reflects a process required for virus infection or movement.

Arabidopsis↗

PubMed2001

Regulation of monocyte chemoattractant protein (MCP)-1 transcription by interferon-gamma (IFN-gamma) in human astrocytoma cells: postinduction refractory state of the gene, governed by its upstream elements.

Monocyte chemoattractant protein (MCP)-1 is expressed by astrocytes in diverse inflammatory states and is a key regulator of monocyte recruitment to the central nervous system (CNS). In the current study, we addressed mechanisms by which transcription of the human MCP-1 gene (hMCP-1) was terminated, after induction by interferon (IFN)-gamma. Our results demonstrated that IFN-gamma-induced transcription of hMCP-1 was followed by a refractory state, during which hMCP-1 was resistant to restimulation by either IFN-gamma or heterologous activators such as TNF-alpha. This refractory state affected the hMCP-1 gene selectively, as other IFN-gamma-inducible genes remained responsive to restimulation. The IFN-gamma-induced hMCP-1 refractory state was governed at the transcriptional level and was sensitive to protein synthesis inhibitors, suggesting a requirement for newly expressed components. A minimal 213 base pair hMCP-1 regulatory element directed both IFN-gamma-mediated transcription and the subsequent refractory state. We previously demonstrated that IFN-gamma treatment resulted in coordinate protein occupancy in vivo of two hMCP-1 promoter elements, a gamma-activated site (GAS) and a GC-rich element. During the refractory state, IFN-gamma treatment failed to induce protection of either the hMCP-1 GAS element or the GC box. These results furnish insight into the expression of hMCP-1 during CNS inflammation and provide the first delineation of an IFN-gamma-induced transcriptional refractory state.

Astrocytoma↗

PubMed2001

Comparative study of platelet activation markers in diabetes mellitus patients complicated by cerebrovascular disease.

Cerebrovascular disease and other vascular diseases are common complications of non-insulin-dependent diabetes mellitus (NIDDM) and are associated with its increased morbidity and mortality. Platelet activation plays an important role in the pathomechanisms of these vascular diseases. Although several indices have been used to assess platelet activation, few data are available indicating which are more sensitive or more valuable in this situation. We have measured platelet arachidonic acid metabolites [thromboxane B2 (TXB2) and 11-dehydro-thromboxane B2 (TXB2)] and plasma P-selectin, platelet fibrinogen binding and membrane glycoproteins in 47 well-characterized NIDDM patients with cerebrovascular disease, 38 NIDDM patients without vascular diseases, and 36 age-matched healthy individuals. Our study shows that platelets were remarkably activated in NIDDM patients with cerebrovascular diseases. The measurement of plasma 11-dehydro-TXB2 and the determination of fibrinogen binding to, and P-selectin expression on platelets would reveal a higher diagnostic sensitivity for detecting in vivo platelet activation than other markers.

Adult↗

PubMed2001

Effects of a modified sandblasting surface treatment on topographic and chemical properties of titanium surface.

A modified sandblasting surface treatment (a noncoating, roughening surface modification of dental implants) has been developed that will overcome the defects of conventional coating techniques. To verify the feasibility and reliability of this method at the chemical and topographic levels, scanning electron microscopy, x-ray diffraction, and a titanium ion releasing test were used; the topography of titanium surface, the embedding of sandblasting particles, nonpollution of heteroelements, and anticorrosiveness of titanium were criteria. Results showed that the rough surface created by sandblast was rather irregular, full of sharp tips and many embedded sandblast particles, and its corrosive rate was increased. These characteristics were modified by oxalic acid attack; the contour of the rough surface became more regular and round, the embedded particles and the heteroelement pollution were thoroughly removed, and the Ti corrosive rate decreased dramatically. Oxalic acid attack modification also created numerous secondary micropores (2.0-micron diameter) on the basis of sandblasted surface macrotexture. This modified sandblasting surface treatment is feasible and reliable to apply to dental implants and does not decrease the biocompatibility of titanium.

Aluminum Oxide↗

PubMed2001

Human parainfluenza virus type 3 inhibits gamma interferon-induced major histocompatibility complex class II expression directly and by inducing alpha/beta interferon.

Human parainfluenza virus type 3 (HPIV3) is one of the major causes of bronchiolitis, pneumonia, and croup in newborns and infants. Cellular immunity involving major histocompatibility complex (MHC) class I and class II molecules plays an important role in controlling virus infection. Several viruses have been shown to down-regulate gamma interferon (IFN-gamma)-mediated MHC class II expression. In this communication, we show that HPIV3 strongly inhibits the IFN-gamma-induced MHC class II expression in HT1080 human fibrosarcoma cells. The culture supernatant of HPIV3-infected cells also inhibited IFN-gamma-induced MHC class II expression, a phenomenon that was found to be due, in large part, to alpha/beta interferon (IFN-alpha/beta). Expression of MHC class I and intercellular adhesion molecule 1 occurred efficiently in cells simultaneously infected with HPIV3 and treated with IFN-gamma, indicating that the inhibitory effect of HPIV3 was specific to MHC class II. STAT1 activation was not affected by HPIV3 at early postinfection times but was partially inhibited at later times. These data suggested that the potent inhibition of MHC class II expression was, in major part, due to a defect downstream of STAT1 activation in the IFN-gamma-induced MHC class II expression pathway. Class II transactivator (CIITA) is the unique mediator of IFN-gamma-induced transcription from the MHC class II promoter. By RNase protection analysis, CIITA expression was found to be strongly inhibited in HPIV3-infected cells. The culture supernatant containing IFN-alpha/beta, on the other hand, inhibited MHC class II expression without affecting STAT1 and CIITA expression. These data indicate that HPIV3 inhibits IFN-gamma-induced MHC class II expression primarily by the viral gene products targeting CIITA and additionally by inducing IFN-alpha/beta to target one or more steps further downstream.

Animals↗

PubMed2001

Ocular responses to head rotations during mirror viewing.

The gain of the human vestibuloocular reflex (VOR) is influenced by the proximity of the object of regard. In six human subjects, we measured the eye rotations induced by passive, sinusoidal, horizontal head rotations at 2.0 Hz during binocular fixation of a stationary far target at 7 m; a stationary target close to the subject's near point of fixation (<15 cm); and the bridge of the subject's own nose, viewed through a mirror positioned so that, for each subject, the angle of vergence was similar to that during viewing of the near target. The median gain of compensatory eye movements for the group of subjects during far viewing was 0.99 (range 0.80-1.04), during near viewing was 1.21 (range 0.88-1.47), and during mirror viewing was 0.85 (range 0.71-1.01). The gain during near and mirror viewing was significantly different for each subject (P < 0.001) even though the vergence angles were similar. The lower gain values during mirror viewing can be attributed to the geometric relationship between the head rotation, the position of the eyes in the head, and the movement of the subject's virtual image in the mirror. To determine whether visually mediated eye movements were responsible for the observed gain values, we conducted a control experiment in which subjects were rotated using a sum-of-sines stimulus that minimized the effects of predictive visual tracking; differences of gain values between near- and mirror-viewing conditions were similar to those during rotation at 2 Hz. We conclude that, in these experiments, target proximity and vergence angle were not the key determinants of gain of the visuo-vestibular response during head rotation while viewing a near target but that contextual cues from motion vision were more important in generating the appropriate response.

Adult↗

PubMed2001

TNF-alpha mediates SDF-1 alpha-induced NF-kappa B activation and cytotoxic effects in primary astrocytes.

Stromal-derived cell factor-1 alpha (SDF-1 alpha; CXCL12) and its receptor, CXCR4, are constitutively expressed on neuroepithelial cells and are believed to be involved in both development and pathological processes, such as AIDS-associated neurologic disorders. Here, we demonstrate that SDF-1 alpha activates NF-kappa B, stimulates production of chemokines and cytokines, and induces cell death in primary astrocytes, effects that depend on ongoing secretion of TNF-alpha. SDF-1 alpha upregulated TNF-alpha mRNA and protein secretion, as well as TNF receptor 2 expression. TNF-alpha treatment mimicked SDF-1 alpha induction of NF-kappa B, IL-1 alpha/beta, and RANTES, as well as cell death; neutralizing antibodies against TNF-alpha opposed these responses. We also found that SDF-1 alpha activated Erk1 and Erk2 (Erk1/2) MAPK in a biphasic fashion. Early Erk1/2 activation was stimulated directly by SDF-1 alpha and late activation was mediated by TNF-alpha. PD98059 suppression of early Erk1/2 activation correlated with reduction of SDF-1 alpha-induced TNF-alpha expression. Late Erk1/2 activation was involved in TNF-alpha-stimulated NF-kappa B activation and cytokine induction. SDF-1 alpha was induced in reactive CXCR4-positive astrocytes near axotomized spinal cord motor neurons, consistent with autocrine SDF-1/CXCR4 signaling in these cells. We propose that these novel effects of SDF-1 alpha are relevant to the pathogenic and developmental roles of SDF-1 alpha in the CNS.

Animals↗

PubMed2001

Spontaneous platelet aggregation with congenital giant platelet containing large granules and thick membrane.

Inherited giant platelet disorders are a heterogeneous group of disorders. In the current study, a patient was reported with moderate bleeding tendency, giant platelets, and spontaneous platelet aggregation, which were not affected by the administration of aspirin or ticlopidine. The electron microscopy of platelets showed a black and thick plasma membrane with crystal-like fine hairs in the exterior coat and more large and variously shaped granules in the cytoplasm. The expression of glycoprotein (GP) Ib, GP IIb, and GP IIIa on platelet surface was normal, and no mutations in genes for GP Ib alpha, GP Ib beta, and GP IX were detected. These phenomena are so distinguishable from those of Mondreal platelet syndrome and other hereditary giant platelet disorders, that we propose that this patient probably has a novel platelet disorder, which has not yet been reported.

Blood Platelet Disorders↗

PubMed2001

Do underrepresented minority medical students differ from non-minority students in problem-solving ability?

BACKGROUND: In medical education, examinations must assess a logical progression toward problem-solving skills. Differences in cognitive development between underrepresented minority students (URMs) and non-URMs may affect examination performance and subsequent attrition rates. PURPOSE: The authors investigated URM and non-URM performances by retrospectively analyzing success rates on exam items of differing cognitive demand. METHOD: Mean correct responses to exam items classified as Recall, Interpretation, or Problem-Solving questions were calculated. Both URM and non-URM groups were stratified by grade point average (GPA) and scores on the Medical College Admission Test (MCAT). Differences were investigated with analysis of variance and general linear models. RESULTS: For all students, performance levels decreased as the cognitive demands of the exam items increased. When stratified by GPA and MCAT score, several important differences were found between URM and non-URM performance. CONCLUSIONS: Because cognitive measures fail to account for the majority of performance differences, noncognitive attributes must contribute to the poorer performance of URMs.

Chicago↗

PubMed2001

Effect of voluntary wheel-running on insulin sensitivity and responsiveness in high-fat-fed rats.

The effect of voluntary wheel-running on insulin resistance was studied in high-fat-fed rats. A sequential hyperinsulinemic euglycemic clamp procedure was employed (insulin infusion rates: 3 and 30 mU/kg BW/min) in 14 high-fat-fed rats and 7 chow-fed rats under the awake condition. The high-fat-fed rats were further divided into a sedentary (n=7) and a voluntary wheel-running (n=7) groups. Blood glucose was clamped at the fasting level in each rat. Plasma insulin levels during the 3- and 30-mU/kg BW/min insulin infusions were 40-50 and 450-550 microU/ml, respectively. At both 3 and 30 mU/kg BW/min insulin infusions, high-fat-feeding showed a significant decrease in glucose infusion rate (GIR), compared with the chow-fed rats. However, decreased GIRs were restored by the 4-wk wheel-running and reached similar levels as the chow-fed rats. Therefore, it could be concluded that voluntary wheel-running prevents insulin resistance induced by high-fat feeding.

Animals↗

PubMed2001

Reduction of listeria monocytogenes on green peppers (Capsicum annuum L.) by gaseous and aqueous chlorine dioxide and water washing and its growth at 7 degrees C.

Reduction of Listeria monocytogenes Scott A on uninjured and injured surfaces of green peppers after 0.3- and 3-mg/ liter gaseous and aqueous ClO2 treatment and water washing for 10 min at 20 degrees C was studied. Growth of the L. monocytogenes untreated or treated with 0.6 mg/liter ClO2 gas for 30 min at 20 degrees C on green peppers also was investigated. A membrane-surface-plating method was used for resuscitation and enumeration of L monocytogenes treated with ClO2. The bacterial viability on pepper surfaces was visualized using confocal laser scanning microscopy (CLSM). Live and dead cells of L. monocytogenes were labeled with a fluorescein isothiocyanate-labeled antibody and propidium iodide, respectively. More than 6 log CFU/5 g L. monocytogenes on uninjured surfaces and about 3.5 log CFU/5 g on injured surfaces were inactivated by both 3-mg/liter and 0.6-mg/liter ClO2 gas treatments. The 3-mg/liter aqueous ClO2 treatment achieved 3.7- and 0.4-log reductions on uninjured and injured surfaces, respectively; whereas, water washing alone showed 1.4- and 0.4-log reductions, respectively. ClO2 gas treatment was the most effective in reducing L. monocytogenes on both uninjured and injured green pepper surfaces, when compared with aqueous ClO2 treatment and water washing. The significant difference (P < 0.05) between log reductions on uninjured and injured surfaces and the results from CLSM analysis suggested that injured surfaces protected more bacteria from sanitation treatments than did uninjured surfaces. Not only could L. monocytogenes grow on green pepper surfaces at 7 degrees C, bacteria that survived the 0.6-mg/liter ClO2 gas treatment also could grow.

Capsicum↗