Oxygen intercalation, stage ordering, and phase separation in La2NiO4+ delta with 0.05 <~ delta <~ 0.11.
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Biomedical subjects
Publications and source records attributed to Y Kong.
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Recently, we have demonstrated that the HLA class I regulatory complex (CRC) is conserved in a locus-specific manner with limited allelic variation. In this study, we have analyzed the CRC sequences of the alleles that showed variation from a total of 22 well-characterized, HLA-homozygous B-LCLs, using PCR amplification of genomic DNA and direct sequencing. We compared the sequences of these alleles with their respective locus consensus sequence at kappa B1, kappa B2, the IRS, the putative NRE, and the HLA counterpart of the H-2RII region, the R x R beta-binding site. The palindromic kappa B1 sequence, an active enhancer, was found to be conserved in all HLA-A and -B alleles and in one HLA-C allele. The sequences of the kappa B2 site showed locus-specific divergence with almost no allelic variation. The IRS is strictly locus specific and HLA-B and -C have identical sequences in this region. Variation in the putative NRE sequence and RII-kappa B2 junctional sequence was apparently generated by gene conversion between B and C loci. Each locus had two sequence patterns at the putative RII site. Overall, sequence analysis of variant alleles demonstrated that there is limited variation in a nonrandom fashion. These results may provide a structural basis for locus and allele-specific modulation of these genes.
In the pathogenesis of sparganosis, proteases have been considered to play important roles in tissue migration and parasite feeding. Several bands of proteolysis were observed when crude extracts of Spirometra mansoni plerocercoid (sparganum) were examined using gelatin substrate gel at neutral pH, of which two proteases of 198 and 104 kDa were purified by two chromatographic steps, and a 36 kDa protease was purified by gelatin-affinity and DEAE-anion exchange chromatography. All the purified proteases exhibited optimal activity at pH 7.5 and 0.1 M Tris-HCl. Proteolytic activities at 198 and 104 kDa were inhibited specifically by serine protease inhibitors and 4-(amidinophenyl)methanesulfonyl fluoride (APMSF, 0.5 mM) and N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK, 1 mM), which strongly suggested that these two proteases were trypsin-like proteases. The activity of the 36 kDa protease was inhibited by N-tosyl-L-phenylalanine chloromethyl ketone (TPCK, 1 mM) and chymostatin (0.1 mM), and was potentiated in 10 mM Ca2+ which showed that the protease had a chymotrypsin-like property. All the proteases were Schiff (PAS) positive. Proteases of 198 and 104 kDa degraded collagen completely within 24 h. The 36 kDa enzyme cleaved human recombinant interferon-gamma (rIFN gamma) and bovine myelin basic protein. In addition, all the purified proteins elicited strong antibody responses in the infected patients.
When immunoglobulin G (IgG) was incubated with Spirometra mansoni plerocercoid (sparganum), it was cleaved into Fab and Fc fragments. Fab/c fragments were also hydrolysed. The digestion was accelerated by dithiothreitol (DTT), indicating that cleavage of IgG heavy chain was due to a cysteine protease secreted into the medium. The responsible enzyme, of M(r) 27 (+/- 0.8) kDa, was purified by a series of thiopropyl affinity, Sephacryl S-300 HR and DEAE-anion exchange chromatographies, either from worm extracts or from excretory-secretory products (ESP). The purified, thiol-dependent protease showed an optimal activity at pH 5.7 with 0.1 M sodium acetate but was active over the pH range 4.5-8.0. Its activity was inhibited completely by 10(-5) M L-trans-epoxysuccinylleucylamido(4-guanidino) butane (E-64) and 1 mM iodoacetamide (IAA), but by only 53% using the specific cathepsin L inhibitor, Z-Phe-Phe-CHN2 (5 x 10(-5) M). Partial NH2-terminal amino acid sequence was Leu-Pro-Asp-Ser-Val-Asn-Trp-Arg-Glu-Gly-Ala-Val-Thr-Ala-Val which showed 80% homology to human cathepsin S. Immunoblot analysis showed that sera from infected patients exhibited IgE antibody reaction. It is proposed that cleavage of immunoglobulin by an excreted-secreted, cathepsin S-like, allergenic protease is a mechanism of immune evasion used by the sparganum.
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We tested whether, with exposure to an extraneous iron-catalyzed free radical-generating system, prevention of lipid peroxidation with U74006F, a 21-aminosteroid, could also prevent myocardial contractile dysfunction. Rabbits received either U74006F (10 mg/kg iv) or vehicle (V). Thirty minutes later the hearts were excised and perfused by a non-recirculating Langendorff technique. Six U74006F- and six V-treated hearts were exposed for 7.5 min to a .OH-generating system (H2O2 and Fe(2+)-ADP chelate). Myocardial lipid peroxides were measured by glutathione peroxidase-catalyzed oxidation of exogenous glutathione. With exposure to .OH, cytosolic lipid peroxide levels were increased threefold in V-treated hearts, but there was no increase in U74006F-treated hearts. After 30 min of recovery, developed pressure and maximum first derivative of left ventricular pressure were greater in U74006F-treated hearts than in V-treated hearts but were still 50 and 44% of levels in saline hearts, respectively. Coronary flow was markedly reduced after exposure to free radicals and was only slightly less depressed when U74006F was administered. When coronary flow following oxidant exposure was increased by nitroglycerin, U74006F again only modestly improved systolic function. Thus, although U74006F blocked lipid peroxidation, it only slightly improved the ventricular dysfunction caused by .OH. Therefore, factors other than lipid peroxidation play a major role in oxidant-induced myocardial stunning.
BACKGROUND: There has been controversy about whether early reperfusion of myocardial infarcts causes further necrosis mediated by reactive oxygen species or other mechanisms. Unequivocal evidence that therapeutic agents given only during reperfusion can prevent, rather than delay or modify, injury has been sparse. Failure to account for variables, such as collateral blood flow, that influence infarct size independently and attempts to measure infarct size too early in reperfusion may have limited the sensitivity and specificity of some previous studies. METHODS AND RESULTS: After 90 minutes of coronary occlusion and 48 hours of reperfusion in a canine model, we examined the effect on infarct size of intravenous infusion of N-(2-mercaptopropionyl)-glycine (MPG), a diffusible antioxidant. Infarct size and region at risk were measured by post-mortem dual perfusion with triphenyl tetrazolium chloride and Evans blue dyes, and regional myocardial blood flow was measured with radioactive microspheres. Infusion of MPG 100 mg.kg-1.h-1, beginning either 15 minutes before the onset of reperfusion or 30 minutes after the onset of reperfusion and continued until 4 hours of reperfusion and followed by an intramuscular dose, reduced infarct size, normalized for both region at risk and the level of collateral blood flow, by 60% and 45%, respectively. When infusion of MPG was limited to the last 15 minutes of ischemia and the first hour of reperfusion only, the normalized infarct size was reduced by 26%. Heart rate, blood pressure, and their product did not differ among the four groups studied. The plasma half-time of MPG was < 10 minutes. In in vitro experiments MPG was a scavenger of hydrogen peroxide but not of superoxide radical. CONCLUSIONS: After 90 minutes of coronary ligation, infusion of the diffusible hydrogen peroxide scavenger, MPG, for several hours, beginning as late as 30 minutes after the onset of reperfusion, substantially reduced infarct size measured 48 hours later. In this model, necrosis caused by processes during reperfusion may be more extensive than necrosis caused by ischemia alone. Since infusion of this agent for only the first hour of reperfusion was considerably less effective, it appears that most of the oxidant injury leading to necrosis occurred after the first 60 minutes but within the first 4 hours of reperfusion.
BACKGROUND: Although it has been demonstrated in short-term preparations that ischemia with early reperfusion results in coronary vascular injury manifested by abnormal endothelium-dependent relaxation and increased permeability to plasma proteins, it has not been clear whether these abnormalities are permanent or reversible. METHODS AND RESULTS: In a canine model, regional coronary ischemia was accomplished by 1 hour of left anterior descending coronary artery ligation, and follow-up studies were performed after reperfusion for 1 hour, 48 hours, 2 weeks, or 9 weeks. Vasorelaxation was measured in vitro with preconstricted epicardial coronary artery rings subjected to increasing concentrations of the endothelium-dependent vasodilator ADP and the endothelium-independent vasodilator nitroprusside. At 1 and 48 hours of reperfusion, relaxation of rings from the ischemic reperfused artery to ADP was blunted, but relaxation to nitroprusside was normal. At 2 weeks there was a nonsignificant trend toward a blunted response to ADP in the ischemic/reperfused rings, and at 9 weeks a completely normal response to ADP was observed. Coronary microvascular permeability was assessed by measurement of protein leak index (PLI), by using a double-isotope technique with autologous radiolabeled transferrin and erythrocytes. At 1 and 48 hours of reperfusion there were substantial increases in PLI in the previously ischemic regions, indicative of increased extravascular transferrin. There was a small increase in PLI at 2 weeks but a completely normal measurement at 9 weeks. Electron microscopy of ischemic/reperfused vessels demonstrated endothelial cell swelling and other abnormalities in epicardial arteries and the microcirculation at 48 hours of reperfusion but normal endothelium at 2 weeks of reperfusion. CONCLUSIONS: After 1 hour of regional coronary ischemia, coronary endothelial injury occurs early in reperfusion with abnormalities in epicardial coronary artery endothelium-dependent relaxation, coronary microvascular permeability, and both epicardial coronary artery and microvascular histology. This pattern of injury persists for at least 48 hours, but there is partial functional and complete histological recovery within 2 weeks and complete functional recovery within 9 weeks.
OBJECTIVE: Diagnosis of cerebral paragonimiasis in its early active stage is important because curative chemotherapy is possible. Accordingly, this study was undertaken to evaluate the CT and MR features of early active cerebral paragonimiasis. MATERIALS AND METHODS: We retrospectively reviewed the CT scans (n = 29) and MR images (n = 7) of the brain in 20 patients between 7 and 59 years old who had cerebral paragonimiasis in the early active stage. The diagnosis was based on a positive antibody test by enzyme-linked immunosorbent assay (ELISA) for paragonimiasis in serum and CSF. The diagnosis was confirmed surgically in seven patients. RESULTS: The most common and characteristic imaging finding was a conglomerate of ringlike enhancing lesions (grape-cluster appearance) with surrounding edema in one cerebral hemisphere in 11 patients (55%). Other nonspecific findings included a solitary ringlike lesion (n = 4) or irregular enhancing lesions (n = 2), localized hemorrhage with (n = 3) or without (n = 2) enhancing lesions, and a poorly defined non-hemorrhagic, nonenhancing lesion (n = 1). CONCLUSION: CT and MR findings of clustered ring-enhancing lesions, seen in approximately half of the cases of early cerebral paragonimiasis, are suggestive of cerebral paragonimiasis.
We have shown previously that a 500-bp region of the human insulin receptor promoter (-0.3 to -1.8 kb) was able to stimulate transcription from a heterologous thymidine kinase promoter in HepG2 hepatoma cells but not in HeLa fibroblasts. Footprint analysis localized the transcription factor binding sites to a 36-bp region at -1420. In this paper, we analyze the factors that recognize this element and show that it contains binding sites for the CAAT/enhancer binding protein C/EBP and nuclear factor 1 (NF-1). In addition we show that both C/EBP alpha and the C/EBP beta can transactivate the human insulin receptor promoter in a dose-dependent manner.
A seroepidemiologic observation of anti-Spirometra erinacei plerocercoid (sparganum) antibody (IgG) in serum was made in normal adult and epileptic patients in Korea from February, 1987 to September, 1990. Sera were tested by enzyme-linked immunosorbent assay (ELISA) for anti-sparganum antibody together with anti-Taenia solium metacestode, and anti-Paragonimus westermani antibodies. Sera reacted positively to sparganum antigen only were considered. Positive rate for anti-sparganum antibody in 850 normal adults was 1.9% (standardized rate by provincial population was 1.7%). In 2,667 randomly selected patients of epilepsy at 28 local centers of the Changmi Club, positive rate was 2.5% (standardized rate: 2.3%). In both normal adult and patient groups, the higher antibody rates were observed in Kangwon and Chonnam Provinces. Positive rates were 10 times higher in male than in female in normal adults and 4.5 times in male epileptic patients. The rates were elevated especially with age over 30-year. Odd ratio of the antibody was 1.32 which indicated an ambiguous etiologic factor for epilepsy.
In the definitive hosts, metacercariae of Paragonimus westermani excyst in host duodenum, penetrate intestinal wall, migrate peritoneal and thoracic cavities, and develop to sexual maturity in 8 weeks. This study was undertaken to examine the age of the maturing P. westermani when their infectivity to the other definitive hosts was retained. On 3, 7, 10, 14, 21 and 28 days after feeding the metacercariae to cats through a gastric tube, the developing worms were harvested. The juveniles of different age were fed again to other experimental cats. One to 12 weeks after the oral-transfer infections, the experimental cats were examined for establishment of infections. In the cats to which 3-day and 7-day old juveniles (grown up to 1.4 mm long) were fed, 31.4% and 22.6% of the transferred worms were found infected. The worms of 10-28 days old were not infective. Early maturing stages grown up to 7 days maintained their infectivity to the other definitive hosts.
On June and July 1994, two cases of vivax malaria were consecutively diagnosed at the Yongsan Hospital, Chung-Ang University in Seoul. The first patient was a soldier serving in western parts of the demilitarized zone (DMZ) while the second case was a resident of a village near DMZ. Neither patients had history of being abroad. Republic of Korea (ROK) has been free of malaria since the mid-1970s except for imported cases. The two vivax malaria cases, together with an additional patient detected in 1993, occurred in relatively small areas near DMZ. This necessitated an epidemiologic surveillance. When medical records and blood smears in the areas were examined, no other cases were found. Of 7,723 mosquitoes collected by a black light trap for two nights in June, 7,066 (91.5%) were Anopheles sinensis. In order to evaluate a significance of the recent malaria occurrence, a surveillance system should be operated in the areas.
We report the case of a 28-year-old male who had been ill with headache and motor weakness for a month and developed sudden pain and blindness of the right eye. During ophthalmoscopy, a worm was recognized penetrating the iris, occupying the anterior chamber for a brief period, returning back behind the iris, and leaving corneal edema with hyphyema. Enucleation was performed to prevent the worm's escape from the eye. The enucleated eye revealed areas of a focal degeneration of sclera and intraocular hemorrhage. Microscopic findings of an abrupt tissue defect and few inflammatory reactions in the uvea suggested very recent migration of a moving worm. The flatworm detected in the anterior chamber was identified to be a juvenile Fasciola sp. This case is presumed to be the first case of intraocular fascioliasis reported in the literature.
We studied the relationship between the histopathology of biliary atresia and its clinical significance. Liver biopsies were made in 30 patients and ductal remnants of porta hepatis were studied in 20. The criteria for the pathological diagnosis of hepatic fibrosis were described. We think that judging the severity of hepatic fibrosis may be useful in selecting the mode of Kasai's operation and estimating the prognosis of patients with biliary atresia.
The adsorption of Na+ on gamma-alumina surfaces at four coverages of Na2CO3[5, 10, 15 and 20% w/w)] was characterized by solid-state 23Na and 27Al nuclear magnetic resonance (NMR) spectroscopy. The experimental results suggest that two distinct adsorbed species are present on the alumina surface: surface species and surface salts. At the lower coverages of Na2CO3 (5 and 10%), the surface species is predominant, in which the Na+ cations are associated with the oxygen atoms of gamma-alumina. Increasing the loading level to 15% results in the appearance of a second adsorbed species that is attributed to the surface salt, Na2CO3, deposited on the solid surface. Further adsorption of Na2CO3 leads to an increase in the amount of surface salt while the amount of surface species remains unchanged. 1H-27Al Cross-polarization magic angle spinning (CP-MAS) experiments give the evidence that some Na+ cations in the form of surface species are coordinated with the Brönsted acid sites of gamma-alumina. This may be the main driving force that improves appreciably the catalytic efficiency of an Na2CO3-Al2O3 catalyst.
MRF4 is a member of the muscle-specific basic helix-loop-helix transcription factor family that also includes MyoD, myogenin, and Myf-5. Each of these proteins, when overexpressed in fibroblasts, converts the cells to differentiated muscle fibers that express several skeletal muscle genes, such as those for alpha-actin, muscle creatine kinase, and troponin I. Despite the fact that MRF4 functions as a positive transcriptional regulator, the MRF4 protein is subject to negative regulation by a variety of agents, most notably by exposure of cells to purified growth factors, such as basic fibroblast growth factor (bFGF). In an effort to establish whether bFGF inhibits MRF4 activity through specific posttranslational modifications, we examined whether MRF4 exists in vivo as a phosphoprotein and whether the phosphorylation status of the protein regulates its activity. Our results indicate that MRF4 is phosphorylated predominantly on serine residues, with weak phosphorylation occurring on threonine residues. Both cyclic AMP-dependent protein kinase (PKA) and protein kinase C (PKC) phosphorylate MRF4 in vitro as well as in vivo, and the overexpression of each kinase inhibits MRF4 activity and thus blocks terminal differentiation. PKC-directed phosphorylation of a conserved threonine residue (T-99) situated within the DNA-binding domain inhibits MRF4 from binding in vitro to specific DNA targets. However, although T-99 itself is essential for myogenic activity, our studies demonstrate that the phosphorylation status of T-99 does not play a major role in regulating MRF4 activity in vivo, since PKA, PKC, and bFGF inhibit the activity of MRF4 proteins in which the identified PKA and PKC sites have been mutated. We suggest that the negative regulation of MRF4 imposed by bFGF does not involve a direct modification of the protein at the identified PKA and PKC sites but instead may involve the modification of specific coregulators that interact with this muscle regulatory factor.