Early graft dysfunction developed within one week after renal allograft.
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Publications and source records attributed to T H Kim.
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PURPOSE: To evaluate the clinical usefulness of a stent retrieval hook in the removal of occluded lacrimal stents. MATERIALS AND METHODS: The hook consisted of an inner hook part and an outer pusher part. Under administration of local anesthetic, the retrieval hook was introduced into the nasal cavity and aimed laterally toward the inferior meatus to grasp the distal end of the stent. After grasping the end of the stent, the sheath was pushed to fully grasp it. After that, the hook was pulled out of the external naris. The retrieval hook was used to remove 267 occluded lacrimal plastic or metallic stents. RESULTS: Technical success rate was 97% in the removal of plastic stents and 96% in the removal of metallic stents. The causes of technical failure were entrenchment of granulation tissue into the stent in six plastic stents and one metallic stent, and inaccessibility of the hook to the distal tip of the stent in one plastic stent. These eight stents were removed by an otorhinolaryngologist or an ophthalmologist. Epistaxis occurred in six patients, which was controlled by a nasal pack. CONCLUSIONS: The lacrimal stent retrieval hook seems useful for the removal of occluded stents.
Twisted atrioventricular connections occur almost exclusively in the hearts with biventricular atrioventricular connections. Only one example of double inlet left ventricle has been illustrated in which the axes of the two atrioventricular valves crossed each other. We describe herein three patients, and one autopsied specimen, with double inlet right ventricle in which magnetic resonance imaging clearly demonstrated twisted atrioventricular connections.
Volatile flavor compounds of miniature beefsteakplant (Mosla dianthera Maxim.) from Vietnam were analyzed through gas chromatography-mass spectrometry-olfactometry (GC-MS-O). Sixty-two compounds were identified by GC-MS. Of these, (+/-)-carvone and (+/-)-limonene were the most abundant, followed by (Z)-limonene oxide, beta-caryophyllene, and alpha-humulene. Twenty aroma-active compounds were detected by aroma extract dilution analysis conducted on two GC columns of different polarities (DB-5MS and DB-Wax). The most intense aroma-active compounds were linalool (floral/sweet/lemon), (-)-carvone (spearminty), and 1-octen-3-one (mushroom/earthy). Other predominant aroma-active compounds included (Z)-3-hexenol (grassy/leafy/metallic), (Z)-limonene oxide (lemon/floral), myrcene (plastic/sweet), (+)-limonene (orange/lemon), alpha-thujene (soy sauce/grassy), and (Z)-dihydrocarvone (spearminty/pepperminty). On the basis of the aroma characteristics and intensity, it was concluded that (-)-carvone was responsible for the characteristic aroma of miniature beefsteakplant.
We investigated the relationship between induction of radio-adaptive response and cell death in mouse normal and neoplastic epidermal cells. Mouse normal primary keratinocytes (PK), cancer-prone cells [v-rasHa-transfected mouse keratinocytes (ras-PK), and line 308 cells (mouse skin papilloma cells which have activated rasHa gene with A-to-T transversion at codon 61) were primed with a low dose of gamma-rays (0.01 Gy), and were challenged with a high dose (4 Gy) after a 4 or 7 h interval. The induction of cell death in PK was 2-10 times higher and was also more rapid in PK than in ras-PK or 308 cells. Low-dose pretreatment with a 4 h interval decreased cell death, and this adaptive response was prominent in PK, whereas it was less obvious in the cases of ras-PK and 308 cells. The response of each protein kinase C (PKC) isozymes to high-dose radiation, especially PKCalpha, PKCdelta, PKCepsilon, and PKCeta, were different between the normal and ras oncogene-activated neoplastic keratinocytes; translocation of these isozymes to membrane occurred more rapidly in normal than in neoplastic cells. Furthermore, low-dose pretreatment did not induce the translocation of PKCdelta in PK significantly more than in ras-PK and 308. Thus, the difference in the induction of radio-adaptive responses between mouse normal and neoplastic epidermal cells reflects difference in the rapidity of cell death, and responsiveness of PKC may affect this adaptive response.
Sun protection factor (SPF) that measures sunscreen protection against erythema and edema may not be enough to measure a sunscreen's activity against many other biologic reactions induced by ultraviolet radiation (UV). It may be better to evaluate sunscreen efficacy using various tools including immune protection factor (IPF), mutation protection factor (MPF) and protection against photocarcinogenesis. In terms of immune protection, sunscreens protected against UV-induced immune suppression significantly. But protection in some cases was partial and often the IPF of sunscreens were less than the SPF. IPF may differ with various immunological endpoints, and it may be better to use a couple of different assays to measure sunscreen protection more objectively. Sunscreen use protects against most UV-induced non-melanoma skin cancers and actinic keratoses but its activity against melanoma is not clear. More studies with broad-spectrum stable sunscreens and better models for the investigation of malignant melanoma are required.
The photodegradation products of hydrochlorothiazide produced by ultraviolet (UV) radiation were investigated for their phototoxicity utilizing the photohemolysis and Candida albicans tests. Hydrochlorothiazide was irradiated for 30, 60, 90 and 120 min with a 250 W xenon arc lamp using a WG295 cut-off filter. Irradiation of hydrochlorothiazide resulted in the gradual decrease of all three absorption bands (225, 270 and 320 nm), the blue shift of the 225 nm band, and the appearance of a new band around 290 nm. Since previous results demonstrated that photosubstitution of chloride could occur, the main product of this photolysis most likely is ethoxyhydrochlorothiazide. The photohemolysis test revealed a significant increase in photohemolysis observed in the photodegradation products produced after 60, 90 and 120 min of UV irradiation. This increase in hemolysis value directly correlated with the UV-irradiation time. However, there was no significant phototoxic killing of yeast in the Candida albicans test. This suggests photodegradation products of hydrochlorothiazide may play an important role in phototoxicity by acting on the cell membrane, but not on DNA. Considering the high in vitro phototoxicity observed in bendroflumethiazide and the data presented here, substitution of chloride seems to be responsible for the increased phototoxicity of hydrochlorothiazide.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been reported to induce apoptosis in various tumor cells but not in nontransformed, normal cells. Preclinical studies in mice and nonhuman primates have shown that administration of TRAIL can induce apoptosis in human tumors, but that no cytotoxicity to normal organs or tissues is found. The susceptibility of tumor cells to TRAIL and an apparent lack of activity in normal cells has lead to a proposal to use TRAIL in cancer therapy. Here, we assessed the sensitivity of hepatocytes from rat, mouse, rhesus monkey and human livers to TRAIL-induced apoptosis. TRAIL induced apoptosis in normal human hepatocytes in culture but not in hepatocytes isolated from the other species. Human hepatocytes showed characteristic features of apoptosis, including cytoplasmic shrinkage, the activation of caspases and DNA fragmentation. Apoptosis and cell death in human hepatocytes was massive and rapid, occurring in more than 60% of the cells exposed to TRAIL within 10 hours. These results indicate that there are species differences in sensitivity to TRAIL, and that substantial liver toxicity might result if TRAIL were used in human cancer therapy.
PURPOSE: The purpose of this article was to identify the risk factors related to development of hemodynamically significant cardiac arrhythmias in patients with mechanical ventilation. MATERIALS AND METHODS: Holter recording and echocardiogram were performed within 24 hours of ventilator initiation in patients on mechanical ventilation (MV) owing to respiratory failure (RF) from various reasons. RESULTS: From 68 patients, hemodynamically significant cardiac arrhythmias were detected in 18 patients (26.5%). Initial mean arterial pressure, maximal heart rate, and initial pH were identified as risk factors for hemodynamically significant cardiac arrhythmias. Additionally, the patients with pressure-controlled ventilation as an initial ventilatory mode developed hemodynamically significant cardiac arrhythmias less frequently than the patients with other modes (15.8% vs. 40%, P = .03). In multivariate analysis, initial mean arterial pressure (< 70 mm Hg, odds ratio [OR]: 5.5; 95% confidence interval [CI]: 1.2 to 24.2, P = .026), maximal heart rate (> 120/min, OR: 19.7; 95% CI: 2.0 to 190.9, P = .01), and pressure-controlled ventilation (OR: 0.13; 95% CI: 0.03 to 0.55, P = .006) were associated with the development of hemodynamically significant cardiac arrhythmias. CONCLUSIONS: These findings suggest that during the early stages of mechanical ventilation with acute respiratory failure, hemodynamically significant cardiac arrhythmias are directly associated with tachycardia (> or = 120/min), initial MAP (<70 mm Hg), and, inversely, the initial use of pressure-controlled ventilation.
Mitochondrial cytochrome c release plays a critical role in apoptotic signal cascade after the activation of cell surface death receptors. We investigated the role played by nitric oxide (NO) in mitochondrial apoptotic signaling in tumor necrosis factor alpha (TNF-alpha) plus actinomycin D (TNF-alpha/ActD)-induced apoptosis. NO produced either by S-nitroso-N-acetyl-DL-penicillamine (SNAP) or inducible NO synthase (iNOS) prevented TNF-alpha/ActD-induced apoptosis in hepatocytes and also inhibited both caspase-8-like (IETDase) and caspase-3-like protease (DEVDase) activity as well as mitochondrial cytochrome c release. Recombinant human (rh) caspase-8 induced the cleavage of the cytochrome c-effluxing factor Bid and cytochrome c release from purified mitochondria in the reconstitution system with Bid(+/+) cytosol, but not with Bid(-/-) cytosol. The addition of SNAP and the caspase-8 inhibitor Ac-IETD-fmk inhibited caspase-8-dependent Bid cleavage and cytochrome c release. The inhibitory effect of NO on caspase-8 was reversed by dithiothreitol (DTT). Furthermore, rh-caspase-8 was found to be modified by S-nitrosylation with 1.7 moles of NO bound per mole of enzyme. Treatment of hepatocytes with interleukin 1beta (IL-1beta) plus interferon gamma (IFN-gamma), which induced iNOS expression and NO production, suppressed TNF-alpha/ActD-induced Bid cleavage and mitochondrial cytochrome c release. The NOS inhibitor N(G)-monomethyl-L-arginine (NMA) inhibited the protective effects of IL-1beta and IFN-gamma. The liver-specific NO donor V-PYRRO/NO also inhibited in vivo elevation of IETDase activity, Bid cleavage, and mitochondrial cytochrome c release in the livers of rats injected with TNF-alpha plus D-galactosamine. Our results indicate that one mechanism by which NO protects hepatocytes from TNF-alpha/ActD-induced apoptosis is via the interruption of mitochondrial apoptotic signaling through S-nitrosylation of caspase-8.
The Arabidopsis COP1 protein functions as a developmental regulator, in part by repressing photomorphogenesis in darkness. Using complementation of a cop1 loss-of-function allele with transgenes expressing fusions of cop1 mutant proteins and beta-glucuronidase, it was confirmed that COP1 consists of two modules, an amino terminal module conferring a basal function during development and a carboxyl terminal module conferring repression of photomorphogenesis. The amino-terminal zinc-binding domain of COP1 was indispensable for COP1 function. In contrast, the debilitating effects of site-directed mutations in the single nuclear localization signal of COP1 were partially compensated by high-level transgene expression. The carboxyl-terminal module of COP1, though unable to substantially ameliorate a cop1 loss-of-function allele on its own, was sufficient for conferring a light-quality-dependent hyperetiolation phenotype in the presence of wild-type COP1. Moreover, partial COP1 activity could be reconstituted in vivo from two non-covalently linked, complementary polypeptides that represent the two functional modules of COP1. Evidence is presented for efficient association of the two sub-fragments of the split COP1 protein in Arabidopsis and in a yeast two-hybrid assay.
Among fluoroquinolone antibiotics, ofloxacin (OFL) and norfloxacin (NOR) have piperazinyl groups but flumequine (FLU) does not have this substitutent. The emission spectra of OFL and NOR are strong, broad structureless bands with large Stokes' shifts in water but the emission intensities are very weak in organic solvents. Thus we find that these compounds exist as different chemical species in various solvents. A continuous red shift in the emission bands for OFL and NOR is observed as the water concentration within the aerosol-OT (AOT; sodium 1,4-bis[2-ethylhexyl]sulfosuccinate) micelle increases or temperature of this solution rises. From the fluorescence anisotropy measurements of OFL and NOR, we assume the intramolecular charge transfer after excitation from the nitrogen of the piperazinyl group to the keto oxygen. Theoretical calculations further support this observation. Multifrequency phase and modulation experiments and time-resolved emission spectra clearly show the occurrence of intramolecular charge transfer and the subsequent nanosecond water reorganization around OFL or NOR in the AOT micelle. Upon increasing the water concentration within the AOT micelle, the relaxation rate increases because of the large amount of free water. The emission spectra of FLU do not exhibit any significant response to the physical properties of their environment.
We purified and characterized a serine proteinase secreted by Acanthamoeba healyi to evaluate it as a possible virulence factor in the pathogenesis of granulomatous amoebic encephalitis (GAE). Ammonium sulfate precipitated culture supernatant of A. healyi OC-3A strain was purified by chromatography on CM-Sepharose, Sephacryl-S200, and Q-2 anion-exchange columns. The purified 33-kDa enzyme had a pH optimum of 8.0 and a temperature optimum of 40 C. Phenylmethylsulfonylfluoride and diisopropyl fluorophosphate, serine proteinase inhibitors, diminished activity of the enzyme to near zero. In addition to types I and IV collagen and fibronectin, the main components of the extracellular matrix, other proteins such as fibrinogen, IgG, IgA, albumin, and hemoglobin were also degraded by the enzyme. The broad substrate specificity of this secreted serine proteinase suggests that it may play an important role in pathogenesis of GAE by A. healyi.
Park, S-H., Lee, S-J., Chung, H-Y., Kim, T-H., Cho, C-K., Yoo, S-Y. and Lee, Y-S. Inducible Heat-Shock Protein 70 Is Involved in the Radioadaptive Response. The thermoresistant (TR) clone of radiation-induced fibrosarcoma (RIF) cells showed an adaptive response, i.e. a reduced effect, after exposure to a higher challenging dose (4 Gy) when the priming dose (1 cGy) was given 4 or 7 h earlier, but RIF cells did not. Since inducible Hsp70 expression was different in cells of these two cell lines, the role of inducible Hsp70 in the adaptive response was examined. When inducible Hsp70 was transfected into RIF cells, the adaptive response was acquired. Transfection of inducible Hsp70 to NIH 3T3 mouse embryo cells also conferred radioresistance to the cells as assayed by clonogenic survival, [(3)H]thymidine incorporation, and an ELISA cell death detection kit. An increased tendency for the induction of an adaptive response was also observed. Interestingly, basal levels of Ca(2+)-dependent and independent Pkc activities were increased by transfection with inducible Hsp70 compared to those of control vector cells. Irradiation with gamma rays induced activation of Pkc within minutes in control vector cells, while transfection with inducible Hsp70 did not. Cellular redistribution to particulate fractions of Pkca, d and z after exposure gamma rays also was not detected. Furthermore, radioresistance by transfection with inducible Hsp70, as tested by clonogenic survival, disappeared after pretreatment with Pkc inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7), prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), and GF109203X. Taken together, these data suggest that radioresistance inducible by Hsp70 is associated with an elevated level of Pkc activity.
We previously demonstrated the protective effect of the small heat-shock protein against oxidative damage induced by tumor necrosis factor alpha. Here we have extended our studies of the possible role of Hsp25 in ionizing radiation-induced damage. For these studies, we transfected murine fibroblast L929 cells with the Hsp25 gene and selected three stably transfected clones. Hsp25 overexpression conferred radioresistance as detected by clonogenic survival and induction of apoptosis. Interestingly, the Hsp25-transfected cells showed an increase in the level of the anti-apoptosis molecule Bcl2. We also observed alterations of cell growth in the Hsp25-transfected cells. The cell cycle time of Hsp25-transfected cells was 3-4 h slower than that of vector-transfected control cells. Flow cytometry analysis of synchronized cells at late G(1) phase by mimosine treatment also showed the growth delay in Hsp25-overexpressing cells. In addition, reduced cyclin D1, cyclin A and Cdc2 levels and increased levels of Cdkn1a (also known as p21(Waf)) were observed in Hsp25-transfected cells, which probably caused the reduction in cell growth. In addition, synchronization by mimosine treatment only partially altered radioresistance in the Hsp25-transfected cells. Taken together, these data suggest that Hsp25-induced radioresistance is associated with growth delay as well as induction of Bcl2.
OBJECTIVE: The objective of this study was to investigate the usefulness of helical CT angiography in the evaluation of total anomalous pulmonary venous connections. MATERIALS AND METHODS: Fourteen patients with total anomalous pulmonary venous connections underwent helical CT angiography and subsequent three-dimensional (3D) reconstruction. They ranged in age from 3 days to 8 months (median age, 2.3 months) and in weight from 2.3 to 7.1 kg (median weight, 4.3 kg). The types of total anomalous pulmonary venous connections and the number of pulmonary veins were evaluated on axial and 3D images. Qualitative evaluations were performed for extent of pulmonary vascular enhancement and contrast- or motion-induced artifacts. RESULTS: In all patients, helical CT angiography correctly depicted total anomalous pulmonary venous connections. Seven cases were the supracardiac type, four cases were the cardiac type, one case was the infracardiac type, and two cases were the mixed type. The detection rate of the pulmonary vein in 3D reconstruction images (95-98%) was slightly lower than that of the pulmonary vein in the axial images (100%), but the difference between axial and 3D reconstruction images was not statistically significant (p > 0.1). No statistically significant differences were noted among 3D reconstruction images in the detection rates of the pulmonary vein (p > 0.1). The extent of contrast enhancement of the pulmonary vein was good or excellent in all patients. In five patients, there were contrast-induced artifacts that made some surrounding vascular distortion but did not interfere with the pulmonary vein analysis, except in one patient. Motion-induced artifacts were observed in nine patients. One of them had an obstacle in pulmonary vein analysis. CONCLUSION: The combination of axial and 3D images in helical CT angiography is helpful in the assessment of a total anomalous pulmonary venous connection containing the individual pulmonary vein, and this combination can be a good diagnostic tool in preoperative evaluation of neonates and infants with a total anomalous pulmonary venous connection.
It has been generally accepted that high density lipoprotein cholesterol (HDL-C) level decreases with menopause in women. However, recent reports show different results. There is very little data concerning perimenopausal women. To verify these findings, lipids and lipoprotein(a) [Lp(a)] levels were compared among pre-, peri- and postmenopausal women of similar mean ages. Postmenopausal women had higher HDL-C levels than premenopausal women (p<0.001) and there was no difference between peri- and postmenopausal women. LDL-C level in perimenopausal women was lower than in postmenopausal women (p<0.001) and higher than in premenopausal women with borderline significance (p=.051). Total cholesterol levels showed stepwise elevation from premenopause to postmenopause. Perimenopausal women had lower Lp(a) levels than postmenopausal women (p<0.0005) and similar levels to premenopausal women. Lp(a) levels between 0.1 to 10.0 mg/dL were the most prevalent in pre- and perimenopausal women, and those between 10.1 to 20.0 mg/dL in postmenopausal women. In conclusion, menopause itself is associated with the elevation of HDL-C level, and the postmenopausal increase of coronary artery disease is not related to postmenopausal change of HDL-C level. Perimenopausal status, although transient, may favor Lp(a) and lipid profiles for delaying atherosclerosis.