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Biomedical subjects

N Kim

Publications and source records attributed to N Kim.

At least 73 records · Page 4Linked to original sources
PubMed1999

Isolation of rice allergenic cDNA clones from a rice cDNA library by immunoscreening with a polyclonal antibody specific to 16 kD rice allergenic protein.

Clinical cases of type-1 hypersensitive reaction to rice (Oryza sativa) have been reported in western countries as well as in Japan. Among rice proteins, 14-16 kD globulin proteins encoded by multiple gene family have been identified as major rice allergens. In this study, a rice cDNA library was constructed using lambda UniZap vector and screened with a rat anti-16 kD globulin protein polyclonal antibody in order to isolate Korean rice allergenic cDNA clones. Five independent cDNA clones, termed RAK1-5, were obtained after second rounds of plaque assay and immunoblot analysis. These clones encoded 13-19 kD recombinant proteins upon IPTG induction, which were identified by the polyclonal antibody in immunoblot analysis. DNA sequencing analysis showed that RAK1-4 have 99% sequence homology with RA5b, and RAK5 is closely related with RA14c. This result indicated that RA5b gene is widely distributed in our cDNA library among other possible rice allergenic genes, and more study is needed to isolate heterogeneous or novel rice allergen genes.

Allergens↗
PubMed1999

Percutaneous penetration enhancement activity of aromatic S, S-dimethyliminosulfuranes.

The activity of three series of iminosulfuranes (classes I-III) as potential transdermal penetration enhancers was investigated. These dimethyl sulfoxide (DMSO) related compounds were synthesized from activated DMSO by trifluoroacetic anhydride. Structure confirmation was accomplished by 1H NMR, and 13C NMR spectroscopy and elemental analysis prior to in vitro testing. Hydrocortisone (HC) was used as a model drug, and the effect of the iminosulfuranes on the penetration of HC through hairless mouse skin was evaluated. All enhancers tested were applied to the skin as saturated suspensions in propylene glycol to ensure their maximum thermodynamic activity. Three compounds, S,S-dimethyl-N-(4-bromobenzoyl)iminosulfurane (9), S,S-dimethyl-N-(5-nitro-2-pyridyl)iminosulfurane (13), and S, S-dimethyl-N-(4-phenylazaphenyl)iminosulfurane (16) showed statistically significant activity quantitated by amounts of model drug permeated through the skin in 24 h (Q(24)), and flux values, compared to control (propylene glycol without enhancer). Highest Q(24) and flux values were obtained for 9: 996.2+/-192.5 microg/cm(2) and 42.9+/-7.5 microg/cm(2) per h, respectively. All arylsulfonyl substituted compounds showed lower or similar enhancement activity when compared to control. S, S-dimethyl-N-(benzenesulfonyl)iminosulfurane (1), S, S-dimethyl-N-(2-methoxycarbonylbenzenesulfonyl)iminosulfurane++ + ( 7) and S,S-dimethyl-N-(4-chlorobenzenesulfonyl)iminosulfurane (8) decreased the permeation of HC significantly (P<0.05). It is possible that these agents work as retardants under these experimental conditions. None of the enhancers tested showed significant skin model drug retention, suggesting that these compounds could be useful for increasing systemic rather than local drug delivery.

Animals↗
PubMed1999

Different mismatch repair deficiencies all have the same effects on somatic hypermutation: intact primary mechanism accompanied by secondary modifications.

Somatic hypermutation of Ig genes is probably dependent on transcription of the target gene via a mutator factor associated with the RNA polymerase (Storb, U., E.L. Klotz, J. Hackett, Jr., K. Kage, G. Bozek, and T.E. Martin. 1998. J. Exp. Med. 188:689-698). It is also probable that some form of DNA repair is involved in the mutation process. It was shown that the nucleotide excision repair proteins were not required, nor were mismatch repair (MMR) proteins. However, certain changes in mutation patterns and frequency of point mutations were observed in Msh2 (MutS homologue) and Pms2 (MutL homologue) MMR-deficient mice (for review see Kim, N., and U. Storb. 1998. J. Exp. Med. 187:1729-1733). These data were obtained from endogenous immunoglobulin (Ig) genes and were presumably influenced by selection of B cells whose Ig genes had undergone certain mutations. In this study, we have analyzed somatic hypermutation in two MutL types of MMR deficiencies, Pms2 and Mlh1. The mutation target was a nonselectable Ig-kappa gene with an artificial insert in the V region. We found that both Pms2- and Mlh1-deficient mice can somatically hypermutate the Ig test gene at approximately twofold reduced frequencies. Furthermore, highly mutated sequences are almost absent. Together with the finding of genome instability in the germinal center B cells, these observations support the conclusion, previously reached for Msh2 mice, that MMR-deficient B cells undergoing somatic hypermutation have a short life span. Pms2- and Mlh-1-deficient mice also resemble Msh2-deficient mice with respect to preferential targeting of G and C nucleotides. Thus, it appears that the different MMR proteins do not have unique functions with respect to somatic hypermutation. Several intrinsic characteristics of somatic hypermutation remain unaltered in the MMR-deficient mice: a preference for targeting A over T, a strand bias, mutational hot spots, and hypermutability of the artificial insert are all seen in the unselectable Ig gene. This implies that the MMR proteins are not required for and most likely are not involved in the primary step of introducing the mutations. Instead, they are recruited to repair certain somatic point mutations, presumably soon after these are created.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Telomerase activity in ductal carcinoma in situ and invasive breast cancer.

The increasing number of breast carcinoma in situ detected by screening procedures makes it imperative to develop improved markers to stratify the risk of invasive cancer. Telomerase is detectable in invasive cancer, but not in normal tissues. We have microdissected frozen tissue blocks containing both DCIS and invasive cancer to assay the telomerase activity of these two lesions. The 46 available cases of concurrent DCIS and invasive breast cancer resulted in 43 DCIS samples and 38 invasive cancer samples adequate for analysis. Seventy per cent of the DCIS and all invasive cancer samples tested had detectable telomerase activity. In addition, we analysed telomerase activity in ten cases of DCIS that were not associated with invasive cancer, and detected telomerase activity in seven (70%). Mixing experiments showed no evidence of telomerase inhibitors in telomerase negative samples. Furthermore, periductal inflammatory infiltrates were shown to be a potential confounding source of telomerase activity. Since DCIS lesions appear to be heterogeneous with respect to telomerase activity, and telomerase activation appears to precede the development of invasive cancer, telomerase activity may be a useful adjunct in stratifying the risk of developing invasive breast cancer in patients with DCIS.

Adult↗
PubMed1999

Cripto-1 indirectly stimulates the tyrosine phosphorylation of erb B-4 through a novel receptor.

Cripto-1 (CR-1) is a recently discovered protein of the epidermal growth factor family that fails to directly bind to any of the four known erb B type 1 receptor tyrosine kinases. The present study demonstrates that CR-1 indirectly induces tyrosine phosphorylation of erb B-4 but not of the epidermal growth factor-related receptors erb B-2 and erb B-3 in different mouse and human mammary epithelial cell lines. In addition, down-regulation of erb B-4 in NMuMG mouse mammary epithelial cells and in T47D human breast cancer cells, using an anti-erb B-4 blocking antibody or a hammerhead ribozyme vector targeted to erb B-4 mRNA, impairs the ability of CR-1 to fully activate mitogen-activated protein kinase. Finally, chemical cross-linking of 125I-CR-1 to mouse and human mammary epithelial cell membranes results in the labeling of two specific bands with a molecular weight of 130 and 60 kDa, suggesting that the CR-1 receptor represents a novel receptor structurally unrelated to any of the known type I receptor tyrosine kinases. In conclusion, these data demonstrate that CR-1, upon binding to an unknown receptor, can enhance the tyrosine kinase activity of erb B-4 and that a functional erb B-4 receptor is required for CR-1-induced MAPK activation.

Animals↗
PubMed1999

Smoking cessation following treatment in a smoke-free Navy Alcohol Rehabilitation program.

The purpose of this study was to examine changes in smoking behavior and attitudes following treatment in the smoke-free Navy Alcohol Rehabilitation program (NARC) and to evaluate changes in staff attitudes toward the smoke-free policy. Consecutive patients (N = 404; 93.8% male) admitted to the NARC between February 1, 1993 and September 30, 1993 were studied, of whom 54.7% were current smokers. Measures included patient surveys administered repeatedly at admission and discharge and at 12 months following the 4-week treatment program. The staff were also administered a survey 2 months before (N = 86) and 6 months after (N = 104) policy implementation. Results indicate that alcohol treatment in a smoke-free environment did not markedly affect the smoking status of patients; the proportion of current smokers at discharge was 54.7%. Significant reductions in cigarettes smoked per day (p < .001) were observed among patients from admission to discharge. However, no statistically significant change in readiness to consider smoking cessation scores was detected. Results indicated no significant change in patient smoking status at 12-month follow-up, although the survey response rate was low (35.1%; N = 142). Six months following implementation of the smoke-free policy, 84.6% of staff indicated that the NARC should remain smoke-free and 84.6% recommended that other alcohol and drug treatment facilities be smoke-free.

Adult↗
PubMed1999

TRANCE, a TNF family member, activates Akt/PKB through a signaling complex involving TRAF6 and c-Src.

TRANCE, a TNF family member, and its receptor, TRANCE-R, are critical regulators of dendritic cell and osteoclast function. Here, we demonstrate that TRANCE activates the antiapoptotic serine/threonine kinase Akt/PKB through a signaling complex involving c-Src and TRAF6. A deficiency in c-Src or addition of Src family kinase inhibitors blocks TRANCE-mediated PKB activation in osteoclasts. c-Src and TRAF6 interact with each other and with TRANCE-R upon receptor engagement. TRAF6, in turn, enhances the kinase activity of c-Src leading to tyrosine phosphorylation of downstream signaling molecules such as c-Cbl. These results define a mechanism by which TRANCE activates Src family kinases and PKB and provide evidence of cross-talk between TRAF proteins and Src family kinases.

Animals↗
PubMed1999

Sequential priming in hierarchically organized figures: effects of target level and target resolution.

Three experiments are reported in which participants identified target letters that appeared at either the global or local level of hierarchically organized stimuli. It has been previously reported that response time is facilitated when targets on successive trials appear at the same level (L. M. Ward, 1982; L. C. Robertson, 1996). Experiments 1 and 2 showed that this sequential priming effect can be mediated by target-level information alone, independent of the resolution, or actual physical size, of targets. Target level and resolution were unconfounded by manipulating total stimulus size, such that global elements of the smaller stimuli subtended the same amount of visual angle as local elements of the larger stimuli. Experiment 3, however, showed that when level information is less useful than resolution in parsing targets from distractors, resolution does become critical in intertrial priming. These data are discussed as they relate to the role of attention in local vs. global (part vs. whole) processing.

Attention↗
PubMed1999

Continuity and change in the social competence of children with autism, Down syndrome, and developmental delays.

The aims of this longitudinal study were: (1) to assess the continuity and change in diagnosis, intelligence, and language skills in children with autism, Down syndrome, and other developmental delays, (2) to specify the deficits in social competence and language skills in these children, and (3) to identify precursors in the preschool period of gains in language skills and of peer engagement in the mid-school years. The initial sample consisted of 70 children with autism, 93 children with Down syndrome, 59 children with developmental delays, and 108 typically developing children, with the first three groups of children studied when they were between 2 and 6 years of age. At follow-up, 51 children with autism, 71 children with Down syndrome, and 33 children with developmental delays were assessed at mean ages around 10-13 years. The long-term follow-up showed little change in the diagnosis of autism but sizeable improvements in intellectual and language abilities within the autistic group, a pattern that was not seen in the children with Down syndrome. Unique deficits in joint attention, some forms of representational play, responsiveness to the emotions of others, and initiation of peer engagement were identified in the autistic children, whereas the children with Down syndrome seemed to have a specific deficit only in language. Joint attention skills were concurrently associated with language abilities in all groups and predicted long-term gains in expressive language for the children with autism. Children with autism, regardless of their level of functioning, were less socially engaged with classmates than the other developmentally disabled children because they infrequently initiated and accepted play bids, not because they were rebuffed by peers. Early nonverbal communication and play skills were predictors of the frequency of initiations of peer play for the children with Down syndrome as well as the extent of peer engagement of the children with autism. These results suggest that improvements in early communication and play skills may have long-term consequences for later language and social competence in these groups of children.

Adolescent↗
PubMed1999

Chronic estrogen treatment increases levels of endothelial nitric oxide synthase protein in rat cerebral microvessels.

BACKGROUND AND PURPOSE: A number of studies indicate that the female gonadal hormone, estrogen, confers protection against cerebrovascular disorders such as stroke. One postulated mechanism for these effects of estrogen is an action on the enzyme endothelial nitric oxide synthase (eNOS), which produces the vasodilatory molecule NO. We have investigated the hypothesis that estrogen increases expression of eNOS in cerebral microvessels of male and female rats. METHODS: We measured levels of eNOS protein by Western blot in cerebral microvessels isolated from 7 groups of animals: females, ovariectomized females, ovariectomized females treated with estrogen, males, castrated males, castrated males treated with estrogen, and castrated males treated with testosterone. RESULTS: Ovariectomized female rats treated with estrogen had 17. 4-fold greater levels of eNOS protein in cerebral microvessels than ovariectomized females, and intact females had 16.6-fold greater levels than ovariectomized females (P<0.01). In intact females, cerebral microvessel eNOS protein levels were 9.2-fold higher than those of intact males (P<0.05). Levels of eNOS protein in castrated males, castrated males treated with testosterone, and males were not different from each other. Estrogen treatment of castrated animals resulted in an 18.8-fold increase in cerebral microvessel eNOS protein (P<0.05). CONCLUSIONS: Chronic estrogen treatment increases levels of eNOS protein in cerebral microvessels of male and female rats. This increase in eNOS protein correlates with our previous functional findings indicating that estrogen exposure increases NO modulation of cerebrovascular reactivity in both male and female animals. Upregulation of eNOS expression may contribute to the neuroprotective effect of estrogen.

Animals↗
PubMed1999

Effect of eradication of Helicobacter pylori on the benign gastric ulcer recurrence--a 24 month follow-up study.

OBJECTIVES: To evaluate the effect of eradication of Helicobacter pylori (H. pylori) on the recurrence of benign gastric ulcer (BGU) in the patients with BGU. METHODS: This study was performed for 40 H. pylori-positive BGU patients cured of BGU and H. pylori eradicated, and for 25 H. pylori-positive patients (non-eradicated group) who were not treated with H. pylori eradication regimen or H. pylori was not eradicated. Four different methods--CLOtest, microscopy of Gram stained mucosal smear, culture and histology of modified Giemsa staining--were taken for identifying colonization of H. pylori before treatment, and 4 weeks after completion of triple therapy. For the control group in which triple therapy was not tried, follow-up gastroscopy was done to confirm the healing of the ulcer. To detect BGU recurrence, the gastroscopy was performed at 6, 12, 18, and 24 months after therapy. RESULTS: In the non-eradicated group, the BGU recurrence rate was 16% within 6 months, 40% within 1 year, 56% within 18 months and 60% within 2 years. The respective recurrence rates in the 40 patients in whom the bacteria had been eradicated were 0%, 7.5%, 10% and 10% (4 patients), respectively. Among the four BGU-recurred patients in whom H. pylori had been eradicated, one patient was found to have BGU recurring with H. pylori positive again in one year, and another two patients had NSAIDs ingestion history. CONCLUSION: The eradication of H. pylori in patients with BGU reduces the recurrence of BGU. In addition, the major causes of BGU recurrence look like NSAIDs ingestion and reinfection of H. pylori.

Adult↗
PubMed1998

Thiolated Salmonella antibody immobilization onto the gold surface of piezoelectric quartz crystal.

An improved antibody-coated sensor system based on quartz crystal microbalance analysis on Salmonella spp. was developed making use of thiolated antibody immobilization onto one gold electrode of the piezoelectric quartz crystal surface. The best results in sensitivity and stability were obtained with the thin layer of a thiol-cleavable, heterobifunctional cross-linker, sulfosuccinimidyl 6-[3-(2-pyridyldithio)propionamido]hexanoate (sulfo-LC-SPDP). The long bridge of this reagent could function as a spacer, facilitating antibody-Salmonella interaction on the gold electrode. After the addition of a S. typhimurium suspension into a reaction cell with 0.1 M sodium phosphate buffer, pH 7.2, the resonant frequency decreased conspicuously. The time required for maximum frequency shift was about 30-90 min. Sensor response was observed for the microbial suspensions ranging from 9.9 x 10(5) to 1.8 x 10(8) CFU/ml.

Antibodies, Bacterial↗
PubMed1998

Cyanide determination by an ISFET-based peroxidase biosensor.

Horseradish peroxidase immobilized on the surface of an Ion Sensitive Field Effect Transistor (ISFET) can be used for the determination of cyanide ions in aquatic media. When the enzyme is immobilized in BSA gel, the resulting sensor can determine 10(-5)-10(-3) M cyanide. Enzyme immobilization into a positively charged polymer, poly(4-vinylpyridine-co-styrene) (PVPy), seems to cause an increase in cyanide inhibition effects because of anion accumulation in the polymeric matrix, and the resulting sensor can measure cyanide concentration in the range 10(-7)-10(-5) M. Fifty percent peroxidase inactivation was observed with 80 microM KCN in the case of BSA-entrapped enzyme, and with only 0.6 microM KCN when the enzyme was covered by PVPy film. Because of the reversible nature of peroxidase inhibition with cyanide ions, restoration of the enzyme activity after inhibition can be obtained by sensor rewashing in fresh buffer.

Biosensing Techniques↗
PubMed1998

Cell cycle and adhesion defects in mice carrying a targeted deletion of the integrin beta4 cytoplasmic domain.

The cytoplasmic domain of the integrin beta4 subunit mediates both association with the hemidesmosomal cytoskeleton and recruitment of the signaling adaptor protein Shc. To examine the significance of these interactions during development, we have generated mice carrying a targeted deletion of the beta4 cytoplasmic domain. Analysis of homozygous mutant mice indicates that the tail-less alpha6beta4 binds efficiently to laminin 5, but is unable to integrate with the cytoskeleton. Accordingly, these mice display extensive epidermal detachment at birth and die immmediately thereafter from a syndrome resembling the human disease junctional epidermolysis bullosa with pyloric atresia (PA-JEB). In addition, we find a significant proliferative defect. Specifically, the number of precursor cells in the intestinal epithelium, which remains adherent to the basement membrane, and in intact areas of the skin is reduced, and post-mitotic enterocytes display increased levels of the cyclin-dependent kinase inhibitor p27(Kip). These findings indicate that the interactions mediated by the beta4 tail are crucial for stable adhesion of stratified epithelia to the basement membrane and for proper cell-cycle control in the proliferative compartments of both stratified and simple epithelia.

Animals↗