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Biomedical subjects

S H Han

Publications and source records attributed to S H Han.

At least 73 records · Page 4Linked to original sources

The usefulness of orbital lines in detecting blow-out fracture on plain radiography.

The purpose of this study was to assess the diagnostic value of orbital line changes on plain radiographs in detecting blow-out fracture. 92 cases of surgically confirmed blow-out fracture were retrospectively analysed in regard to plain radiographs and CT. Anterior and posterior lamina papyracea lines (ALPL and PLPL, respectively) of the orbital medial wall as well as the posteromedial floor line (PMFL) were assessed on orbital posteroanterior projections. The inferomedial orbital line (IMOL) and the inferior wall line were assessed on Waters projections. Orbital lines on plain radiographs were compared with CT findings. Of 53 cases of lamina papyracea fracture, 47 cases showed orbital line changes on plain radiographs (sensitivity 88.7%). Changes of PLPL (41/47), IMOL (29/47), ALPL (4/47) and PMFL (2/47) were demonstrated as depression, loss, discontinuity and irregularity. In four cases showing normal radiographs, the fractures measured less than 9 mm in size on CT. All 25 cases with orbital floor fracture accompanying medial wall fracture demonstrated orbital line changes of PMFL (16/25), PLPL (14/25), ALPL (3/25) and IMOL (2/25) (sensitivity 100%). 12 of 14 cases with orbital floor fracture demonstrated changes of inferior wall line (7/12) and PMFL (6/12) (sensitivity 85.7%). Two cases demonstrated asymmetric focal soft tissue density without orbital line changes. Orbital line changes on plain radiographs corresponded well with CT findings, confirming the usefulness of plain radiographs in detecting blow-out fracture.

Adolescent↗

Molecular phylogeny of East Asian moles inferred from the sequence variation of the mitochondrial cytochrome b gene.

Taxonomic analysis has previously revealed that the species of moles that inhabit Japan are characterized by exceptional species richness and a high level of endemism. Here, we focused on the evolutionary history of the four Japanese mole species of the genera Euroscapter and Mogera, examining mitochondrial cytochrome b (cyt b) gene sequences and comparing them with those of continental Mogera wogura (Korean and Russian populations), M. insularis from Taiwan, and Talpa europaea and T. altaica from the western and central Eurasian continent, respectively. Our data support the idea that in a radiation center somewhere on the Eurasian continent, a parental stock evolved to modern mole-like morph and radiated several times intermittently during the course of the evolution, spreading its branches to other peripheral geographic domains at each stage of the radiation. Under this hypothesis, the four lineages of Japanese mole species, E. mizura, M. tokudae, M. imaizumii, and M. wogura, could be explained to have immigrated to Japan in this order. Mogera wogura and M. imaizumii showed substantial amounts of geographic variation and somewhat complicated distributions of the cyt b gene types. These intraspecific variations are likely to be associated with the expansion processes of moles in the Japanese Islands during the Pleistocene glacial ages.

Animals↗

Evolutionary trends of the mitochondrial lineage differentiation in species of genera Martes and Mustela.

We compared partial sequences (402 bp) of the mitochondrial cytochrome b gene in 68 individuals of martens (Martes), weasels (Mustela) and their relatives from the Northern Hemisphere to identify the modes of geographic differentiation in each species. We then compared complete sequences (1140 bp) of the gene in 17 species of the family Mustelidae to know the spatial and temporal modes of speciation, constructing linearized trees with transversional substitutions for deeper lineage divergences and with transversions and transitions for younger lineages. Our data suggested that these lineages of Martes and Mustela differentiated in a stepwise fashion with five radiation stages from the generic divergences (stage I) to the intraspecific divergences (stage V), during the last 10 or 20 million years as the fossil evidence suggests. In the lineage of Martes, the first offshoots are of Martes flavigula, M. pennanti, and Gulo gulo (stage II), the second is M. foina (stage III), and the third are M. americana, M. martes, M. melampus, and M. zibellina (stage IV). The divergence of the lineages of Mustela is likely to have taken place concurrently with the radiations of the Martes. These divergence processes are attributable in part to the geographic allocation along the two continents, North America and Eurasia, as well as among peripheral insular domains, such as Taiwan and the Japanese Islands. In addition, the Eurasian continent itself was shown to have been involved in the species diversification in the martens and weasels.

Animals↗

Demonstration of in vivo bioequivalence of a generic albuterol metered-dose inhaler to Ventolin.

STUDY OBJECTIVE: To use histamine bronchoprovocation and bioassay statistical procedures to evaluate the in vivo bioequivalence of a generic albuterol metered-dose inhaler (MDI). DESIGN: A randomized, double-blind, balanced, crossover design was used to determine the potency of each generic albuterol MDI actuation relative to Ventolin (Glaxo Wellcome; Research Triangle Park, NC) administration. One treatment was administered on each of 4 study days. A histamine bronchoprovocation procedure was initiated 1.25 h before and 15 min after administration of the study treatment. PATIENTS: Twenty-four nonsmoking subjects with mild-to-moderate asthma were studied (18 to 65 years of age; FEV(1), > 60% of predicted; and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)], < or = 8 mg/mL at screening). INTERVENTIONS: One and four actuations (90 and 360 microg, respectively) of the generic MDI and of Ventolin MDI. Placebo inhalers were used to maintain blinding of inhaler and doses. MEASUREMENTS AND RESULTS: The primary outcome variable was histamine PC(20) measured after study treatment administration. A significant dose-effect relationship was present (p < 0.0001). Deviation from parallelism of the generic and Ventolin dose-response curves (p = 0.95) and differences in overall mean response between the two formulations (p = 0.68) were not significant. Using Finney 2 x 2 bioassay statistical procedures, we estimated that one actuation of the generic albuterol MDI was equivalent to 1.01 puffs of Ventolin (90% confidence interval, 0.69 to 1.50). CONCLUSION: The generic albuterol MDI delivers a quantity of albuterol to the beta(2)-receptor site in the lung that is the bioequivalent to Ventolin. Further, this study reinforces the validity of this statistical methodology for determining in vivo bioequivalence.

Adolescent↗

A case of congenital inverse Duane's retraction syndrome.

Inverse Duane's retraction syndrome is very uncommon. Congenital cases are even more unusual. A 6-year-old girl with convergent squint along with severe restriction on abduction is described. On attempted abduction, a narrowing of the palpebral fissure, upshoot and retraction of the eyeball were observed. Brain and orbit MRI demonstrated no intracranial or intraorbital mass, fracture, or entrapment of the medial rectus. Forced duction test was strongly positive. The primary lesion was found to be a tight medial rectus with shortening and soft tissue contracture. Surgical tenotomy of the medial rectus led to successful postoperative motility, but some limitation at full adduction and abduction persisted. This is a case reported with congenital medial rectus shortening, suggesting that this condition may be one of the etiologies of the rare inverse Duane's retraction syndrome.

Child↗

Ocular deviation after unilateral laser in situ keratomileusis.

Laser keratomileusis and excimer laser photorefractive keratectomy in situ are widely used therapies for treating myopia. The corrections of refractive error by glasses or contact lens result in a relatively equal refractive correction on both eyes. However, refractive surgery on a single eye can cause a focus disparity between both eyes and may result in the impairment of fusion leading to strabismus. This article aims to report a case where diplopia and esotropia occurred 1 month after laser keratomileusis (LASIK) in situ for the correction of myopia.

Adult↗

Modified Kestenbaum surgery for correction of abnormal head posture in infantile nystagmus: outcome in 63 patients with graded augmentaton.

PURPOSE: To analyze the surgical effect of modified Kestenbaum surgery and show how to determine the amount of appropriate augmentation for correction of abnormal head posture in infantile nystagmus. METHODS: We reviewed the records of 63 patients with infantile nystagmus who required surgery for a significant face turn and who were followed for at least five months after surgery. Group 1, consisting of 29 patients, received Parks' modification of the standard Kestenbaum procedure (the 5-6-7-8 mm procedure); Group 2, 32 patients, received a 20% augmentation of the original Parks recommendation; and Group 3, 2 patients, received a 30% augmentation of the original Parks procedure. Pre-and postoperative measurements with electro-oculography (EOG) using Nicolet Compact Four/CA 2000 were made. RESULTS: The average preoperative face turn in the 63 patients with horizontal nystagmus was 31.9 degrees with an average postoperative face turn of 5.2 degrees. The average net change in face turn was 26.7 degrees. The average duration of time from surgery to final examination was thirteen months. Fifty-six out of 63 patients (89%) achieved a straight head position or a residual face turn of 10 degrees or less. CONCLUSION: A Parks' modified Kestenbaum procedure, with appropriate graded augmentation up to 30% is effective for the correction of abnormal head posture in infantile nystagmus without the need for larger augmentations.

Adolescent↗

Association between apolipoprotein E polymorphism and Alzheimer's disease in Koreans.

We analyzed the aplolipoprotein E (APOE) genotypes of 110 probable AD patients and 226 cognitively normal controls in Koreans. The APOE epsilon4 allele was more prevalent in both early- and late-onset AD patients (P < 0.01) than in controls. The odds for the APOE epsilon4-heterozygous subjects were 2.7 (95% CI = 1.6-4.5), and those for the APOE epsilon4-homozygous subjects were 17.4 (95% CI = 2.0-147.3). But the odds were not uniform across age groups, and were higher in women than in men. Although the APOE epsilon2 allele frequency did not differ by diagnosis, the patients carrying an APOE epsilon2 allele showed delayed age-at-onset (P = 0.02). In conclusion, the APOE e4 allele increased the risk for AD in dose-dependent manner, and the APOE epsilon4-conferred AD risk was age- and sex-dependent in Koreans.

Age of Onset↗

Anti-dsDNA autoantibody cross-reacts with the C-terminal hydrophobic cluster region containing phenylalanines in the acidic ribosomal phosphoprotein P1 to exert a cytostatic effect on the cells.

The present study was an attempt to map the epitope in P1 protein which may cross-react with anti-dsDNA. In addition to wild-type P1, the genes of its C-terminal mutants were cloned and expressed. The binding activity of these proteins with anti-dsDNA was determined by Western blot and ELISA. The P1 mutants with complete deletion of the acidic charge and hydrophobic clusters, deletion of the hydrophobic cluster, or replacement of the phenylanlanines with alanine in the hydrophobic cluster lost the binding activity. Moreover, P1 mutants with mutation at the serine phosphorylation sites (positions 102 and 105) retained their binding activities with anti-dsDNA. However, those with mutation at the serine phosphorylation sites and without the hydrophobic cluster lost their binding activities. These findings suggest that phenylalanines in the C-terminal hydrophobic cluster region of ribosomal P proteins are essential to their cross-reactivity with anti-dsDNA.

Amino Acid Sequence↗

Suppression of the interleukin-2 gene expression by aflatoxin B1 is mediated through the down-regulation of the NF-AT and AP-1 transcription factors.

The effect of aflatoxin B1 (AFB1) on the interleukin-2 (IL-2) gene expression was investigated in thymocytes of B6C3F1 mice, Jurkat E6-1 human T-cell leukemia, and EL4.IL-2 murine thymoma. AFB1 inhibited the phorbol-12myristate-13-acetate/i6nomycin (PMA/Io)-induced IL-2 mRNA expression in the murine thymocytes and Jurkat E6-1 cells as determined by qualitative RT-PCR, while no effect was observed in the EL4.IL-2 cells. Electrophoretic mobility shift assay indicated that AFB1 treatment showed an inhibition of the NF-AT and AP-1 DNA binding in PMA/Io-stimulated thymocytes and Jurkat E6-1 cells. No effect was observed on the Oct and NF-kappaB DNA binding. Employing a reporter gene expression system with p(NF-AT)3-CAT and p(AP-1)3-CAT, treatment with AFB1 to the transfected Jurkat E6-1 cells also showed an inhibition of the PMA/Io-induced NF-AT/CAT and AP-1/CAT activities. These results suggest that suppression of the IL-2 gene expression by AFB1 is mediated through the down-regulation of the NF-AT and AP-1 activation.

Aflatoxin B1↗

The cytoplasmic domain of the lymphotoxin-beta receptor mediates cell death in HeLa cells.

Activation of lymphotoxin-beta receptor (LT-betaR) by conjugation with heterotrimeric lymphotoxin, LT-alpha1/beta2, or by cross-linking with anti-LT-betaR antibodies can trigger apoptosis. We have observed that overexpression of either LT-betaR or the cytoplasmic domain of LT-betaR (LT-betaR(CD)) also induces apoptosis, which may be attributed to the tendency of LT-betaR(CD) to self-associate. The self-association domain of LT-betaR(CD) was mapped to amino acids 324-377, a region of the protein that is also essential for LT-betaR-induced apoptosis. Furthermore, we have shown that LT-betaR(CD)-induced apoptosis could be inhibited by a TRAF3 dominant negative mutant and by the caspase inhibitors Z-VAD-FMK, DEVD-FMK, and CrmA. The ligand-independent apoptosis induced by LT-betaR(CD) will help us to further dissect LT-betaR signaling pathway.

Apoptosis↗

Acetylaminofluorene inhibits nitric oxide production in LPS-stimulated RAW 264.7 cells by blocking NF-kappa B/Rel activation.

The mechanism by which 2-acetylaminofluorene (AAF) inhibited nitric oxide (NO) formation, in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells was investigated. The decrease in NO, as demonstrated by measurement of nitrite was found to correlate well with a decrease in inducible nitric oxide synthase (iNOS) mRNA. Since the promoter in iNOS gene contains binding motifs for NF-kappa B/Rel, AP-1, and NF-IL6 which appear to be important for LPS-mediated iNOS induction, the effect of AAF on the activation of these transcription factors was determined. Treatment of AAF to RAW 264.7 cells induced a dose-related inhibition of NF-kappa B/Rel in chloramphenicol acetyltransferase activity, while either AP-1 or NF-IL6 activation was not affected by AAF. Treatment of RAW 264.7 cells with AAF inhibited protein/DNA binding of NF-kappa B/Rel to its cognate site as measured by electrophoretic mobility shift assay. In addition, AAF treatment caused a significant reduction of nuclear c-rel, p65, and p50 protein levels, and this decrease was paralleled by the accumulation of cytoplasmic c-rel, p65, and p50. These data suggest that AAF inhibits iNOS gene expression by a mechanism involving a blockade of LPS-induced nuclear translocation of NF-kappa B/Rel.

2-Acetylaminofluorene↗

NF-kappa B-dependent Fas ligand expression.

Apoptosis of lymphocytes is triggered by different stimuli through the induced expression of Fas and Fas ligand (FasL). Using T cell activation-induced Fas/FasL expression as a model system, we observed a differential regulation of the induction of Fas and FasL. cAMP inhibited activation-induced apoptosis by an effective suppression of TCR-coupled FasL expres sion. In contrast, cAMP weakly interfered with activation-induced Fas expression, and the remaining Fas molecules on cAMP-treated T cells still mediated apoptosis. Among the major transcription elements on the FasL promoter, the activation of NF-kappaB, but not of NF-AT and AP-1, was suppressed by cAMP. The prominent role of NF-kappaB was further demonstrated by a better activation of the FasL promoter and an elevated expression of FasL induced by p65 (RelA) overexpression than those induced by AP-1 or NF-AT. Our results demonstrate the essential role of NF-kappaB for the expression of the death receptor ligand FasL, and suggest a direct link between NF-kappaB activation and the expression of FasL. NF-kappaB may be the common mediator in the induction of FasL through TCR activation and by various stress stimuli.

Antibodies, Monoclonal↗

Effect of ursodeoxycholic acid on ischemia/reperfusion injury in isolated rat heart.

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, 37 degrees C) on a Langendorff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 microM or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint of reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC (EC25=97.3 microM), reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and 160 microM significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

Animals↗

The birthdates of GABA-immunoreactive amacrine cells in the rat retina.

The birthdates of GABAergic amacrine cells in the rat retina were investigated by immunocytochemistry using anti-GABA and anti-bromodeoxyuridine (BrdU) antisera. The ratio of co-localization of GABA to BrdU increased gradually from embryonic-day 13 (E13) and showed a peak value on E18 in the central retina and on E20 in the periphery. After birth, until postnatal-day 3 (P3), a few co-localized cells were observed in the inner nuclear layer (INL). However, in the peripheral retina, co-localized cells were observed in the INL and ganglion cell layer until P5. Our results suggest that the birthdates of GABA-immunoreactive cells vary, depending on cell-type and that there is a temporal lag in the GABA-immunoreactive cell production in the peripheral retina relative to the central retina.

Animals↗

Cloning and cytotoxicity of fusion proteins of EGF and angiogenin.

Targeted toxins represent a new approach to specific cytocidal therapy. Immunotoxins based on plant and microbial toxins are very immunogenic. To develop a targeted therapy that is less immunogenic and easily invades target tissues, four fusion proteins containing human angiogenin targeted by human EGF have been constructed. EGF is a single chain polypeptide, which binds to epidermal growth factor receptor (EGFR) and is known to be internalized by endocytosis. Angiogenin has been separately fused either at the amino terminus or the carboxyl terminus of EGF via linkers, giving rise to angiogenin-gly-EGF, angiogenin-(gly)4ser-EGF and EGF-angiogenin, EGF-gly-angiogenin, respectively. The fusion proteins were over-expressed in Escherichia coli and purified from periplasmic eluents by affinity chromatography. EGF-angiogenin and EGF-gly-angiogenin maintained receptor-binding activity of EGF and RNase activity of angiogenin in a single peptide and actively inhibited growth of human EGFR-positive target cells in culture. They are expected to have a very low immunogenic potential in humans because of their endogenous origin and also to have another potential therapeutic advantage because these fusion proteins may have overcome conventional immunotoxin and possess increased ability to penetrate because of their small size.

Angiogenesis Inducing Agents↗

Inhibitory effects of electroacupuncture on stress responses evoked by tooth-pulp stimulation in rats.

The mechanism of electroacupuncture (EA) on the stress responses induced by tooth-pulp stimulation was investigated in anesthetized adult female Sprague-Dawley rats. The Hoku point in the Chinese meridian was used for acupuncture stimulation. Constant rectangular current (1 mA) pulses of 5-ms duration were delivered at 3 Hz through a pair of needles for 15 min. As for stress response indexes, we have monitored changes in arterial blood pressure and the levels of blood catecholamines, corticosterone, and ACTH. Arterial blood pressure was increased by high frequency stimulation (0.1 mA, 0.5 ms, 100 Hz for 15 s) of tooth-pulp in the control condition. After EA, we did not observe the same responses of the arterial blood pressure changes with the same stimuli. The tooth-pulp stimulation increased the concentrations of plasma norepinephrine (NE), epinephrine (E), dopamine (DA), corticosterone, and ACTH significantly from the levels of those before stress. After treatment with EA, the stress-induced increase in NE, DA, corticosterone, and ACTH but not the rise in E, were inhibited. When naloxone, an opioid antagonist, was administered intraperitoneally before EA, the effects of EA on stress responses were reduced. In this study, it can be suggested that EA has not only an analgesic effect but also suppressive effects on the stress responses primarily through the mediation of an endogenous opioid.

Adrenocorticotropic Hormone↗

Mu-opioid agonist-induced activation of G-protein-coupled inwardly rectifying potassium current in rat periaqueductal gray neurons.

The characteristics of the inwardly rectifying K+ current activated by a mu-type opioid agonist, D-Ala2,N-MePhe4,Gly5-ol-enkephalin (DAMGO), were examined in the acutely dissociated rat periaqueductal gray neurons using the nystatin-perforated and the conventional whole-cell recording modes under voltage-clamp conditions. DAMGO activated inward currents in a concentration- and voltage-dependent manner. The DAMGO-induced current was an inwardly rectifying K+ current (I(DAMGO)) which was sensitive to K+ channel blockers, quinine and Ba2+ but insensitive to Cs+ and tetraethylammonium. In the conventional whole-cell clamp mode, guanosine 5'-O-(2-thiodiphosphate) trilithium salt (GDPbetas, 0.4 mM) inhibited the amplitude of I(DAMGO) to 28% of that of the initial current. After the intracellular perfusion with guanosine 5'-O-(3-thiotriphosphate) tetralithium salt (GTPgammas, 0.4 mM) for 1 min, the first application of DAMGO irreversibly activated I(DAMGO). By the extracellular application of N-ethylmaleimide at a concentration of 50 microM for 2 min, I(DAMGO) was completely abolished. When a conventional whole-cell patch was made with a patch-pipette containing 1 microg/ml of pertussis toxin together with 1 mM of beta-nicotinamide adenine dinucleotide, I(DAMGO) gradually declined to about 41% of its initial amplitude. The extracellular application of second messenger modulators including protein kinase inhibitor (staurosporin), protein kinase A activators (forskolin, 3-isobutyl-l-methyl-xanthine and dibutyryladenosine 3'5'-cyclic monophosphate) and protein kinase C activators (phorbol-12-myristate-13-acetate and 1-oleoyl-2-acetyl-sn-glycerol) had no effect on I(DAMGO). These results suggest that (i) DAMGO-activated inwardly rectifying K+ current is mediated by pertussis toxin-sensitive guanine nucleotide binding proteins (G-proteins); (ii) the types of G protein involved in I(DAMGO) are Gi and/or Go; and (iii) the G-proteins exert their roles in I(DAMGO) without any mediation of the second messenger systems.

Animals↗