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K Kim

Publications and source records attributed to K Kim.

At least 379 records · Page 21Linked to original sources
PubMed1995

Illusory contours activate specific regions in human visual cortex: evidence from functional magnetic resonance imaging.

The neural basis for perceptual grouping operations in the human visual system, including the processes which generate illusory contours, is fundamental to understanding human vision. We have employed functional magnetic resonance imaging to investigate these processes noninvasively. Images were acquired on a GE Signa 1.5T scanner equipped for echo planar imaging with an in-plane resolution of 1.5 x 1.5 mm and slice thicknesses of 3.0 or 5.0 mm. Visual stimuli included nonaligned inducers (pacmen) that created no perceptual contours, similar inducers at the corners of a Kanizsa square that created illusory contours, and a real square formed by continuous contours. Multiple contiguous axial slices were acquired during baseline, visual stimulation, and poststimulation periods. Activated regions were identified by a multistage statistical analysis of the activation for each volume element sampled and were compared across conditions. Specific brain regions were activated in extrastriate cortex when the illusory contours were perceived but not during conditions when the illusory contours were absent. These unique regions were found primarily in the right hemisphere for all four subjects and demonstrate that specific brain regions are activated during the kind of perceptual grouping operations involved in illusory contour perception.

Brain Mapping↗
PubMed1995

A bivariate cumulative probit regression model for ordered categorical data.

This paper proposes a latent variable regression model for bivariate ordered categorical data and develops the necessary numerical procedure for parameter estimation. The proposed model is an extension of the standard bivariate probit model for dichotomous data to ordered categorical data with more than two categories for each margin. In addition, the proposed model allows for different covariates for the margins, which is characteristic of data from typical ophthalmological studies. It utilizes the stochastic ordering implicit in the data and the correlation coefficient of the bivariate normal distribution in expressing intra-subject dependency. Illustration of the proposed model uses data from the Wisconsin Epidemiologic Study of Diabetic Retinopathy for identifying risk factors for diabetic retinopathy among younger-onset diabetics. The proposed regression model also applies to other clinical or epidemiological studies that involve paired organs.

Adult↗
PubMed1995

Spectral characterization and chemical modification of catalase-peroxidase from Streptomyces sp.

Catalase-peroxidase was purified to near homogeneity from Streptomyces sp. The enzyme was composed of two subunits with a molecular mass of 78 kDa and contained 1.05 mol of protoporphyrin IX/mol of dimeric protein. The absorption and resonance Raman spectra of the native and its cyano-enzyme were closely similar to those of other heme proteins with a histidine as the fifth ligand. However, the peak from tyrosine ring at approximately 1612 cm-1, which is unique in catalases, was not found in resonance Raman spectra of catalase-peroxidase. The electron paramagnetic resonance spectrum of the native enzyme revealed uniquely two sets of rhombic signals, which were converted to a single high spin, hexacoordinate species after the addition of sodium formate. Cyanide bound to the sixth coordination position of the heme iron, thereby converting the enzyme to a low spin, hexacoordinate species. The time-dependent inactivation of the enzyme with diethyl pyrocarbonate and its kinetic analysis strongly suggested the occurrence of histidine residue. From the above-mentioned spectroscopic results and chemical modification, it was deduced that the native enzyme is predominantly in the high spin, ferric form and has a histidine as the fifth ligand.

Catalase↗
PubMed1995

A domain sharing model for active site assembly within the Mu A tetramer during transposition: the enhancer may specify domain contributions.

The functional configuration of Mu transposase (A protein) is its tetrameric form. We present here a model for the organization of a functional Mu A tetramer. Within the tetramer, assembly of each of the two active sites for Mu end cleavage requires amino acid contributions from the central and C-terminal domains (domains II and III respectively) of at least two Mu A monomers in a trans configuration. The Mu enhancer is likely to function in this assembly process by specifying the two monomers that provide their C-terminal domains for strand cleavage. The Mu B protein is not required in this step. Each of the two active sites for the strand transfer reaction is also organized by domain sharing (but in the reverse mode) between Mu A monomers; i.e. a donor of domain II (also the recipient of domain III) during cleavage is a recipient of domain II (and the donor of domain III) during strand transfer. The function of the Mu B protein (which is required at the strand transfer step) and that of the enhancer element may be analogous in that their interactions with Mu A (domain III and domain I alpha respectively) promote conformations of Mu A conducive to strand cleavage or strand transfer.

Bacteriophage mu↗
PubMed1995

Both nuclear and mitochondrial cytochrome c oxidase mRNA levels increase dramatically during mouse postnatal development.

The steady-state levels of 13 of 16 cytochrome c oxidase (COX) mRNAs and mitochondrial DNA were measured during the postnatal development of mouse skeletal muscle, ventricle, kidney and brain as well as during the differentiation of mouse myoblasts into myofibres in cell culture. These experiments indicate that large co-ordinated increases in COX mRNA levels and isoform switching are important for the elaboration of this enzyme during postnatal development and demonstrate the importance of gene-regulatory mechanisms in controlling COX activity. On a per nucleus basis, the levels of the mitochondrial- and most nuclear-encoded COX mRNAs co-ordinately increase 3-10-fold during postnatal development, with the highest levels obtained in ventricle and skeletal muscle. However, concentrations of mitochondrial and nuclear COX mRNAs remain constant during the differentiation of myoblasts into fibres in cell culture. A gradual change from the liver to the heart isoform of COX subunit VIa mRNA occurs during postnatal development of skeletal muscle and ventricle and is nearly complete 3 days after the formation of myofibres in cell culture. Mitochondrial DNA increases proportionally with COX mRNAs during mouse postnatal development but not during myoblast differentiation in cell culture, in which mitochondrial DNA levels increase 5-fold and mitochondrial mRNA levels remain constant. This suggests that mitochondrial DNA replication may control mitochondrial RNA concentrations during postnatal development but not during myoblast differentiation in cell culture.

Animals↗
PubMed1995

Step-arrest mutants of phage Mu transposase. Implications in DNA-protein assembly, Mu end cleavage, and strand transfer.

We describe the isolation and characterization of Mu A variants arrested at specific steps of transposition. Mutations at 13 residues within the Mu A protein were analyzed for precise excision of Mu DNA in vivo. A subset of the defective variants (altered at Asp269, Asp294, Gly348, and Glu392) were tested in specific steps of transposition in vitro. It is possible that at least some residues of the Asp269-Asp294-Glu392 triad may have functional similarities to those of the conserved Asp-Asp-Glu motif found in several transposases and retroviral integrases. Mu A(D269V) is defective in high-order DNA-protein assembly, Mu end cleavage, and strand transfer. The assembly defect, but not the catalytic defect, can be overcome by precleavage of Mu ends. Mu A(E392A) can assemble the synaptic complex, but cannot cleave Mu ends. A mutation of Gly348 to aspartic acid within Mu A permits the uncoupling of cleavage and strand transfer activities. This mutant is completely defective in synaptic assembly and Mu end cleavage in presence of Mg2+. The assembly defect is alleviated by replacing Mg2+ with Ca2+. Some Mu end cleavage is observed with this mutant in the presence of Mn2+. When presented with precleaved Mu ends, Mu A(G348D) exhibits efficient strand transfer activity.

Amino Acid Sequence↗
PubMed1995

Mouse silver mutation is caused by a single base insertion in the putative cytoplasmic domain of Pmel 17.

This laboratory has established in previous studies that Pmel 17, a gene expressed specifically in melanocytes, maps near the silver coat color locus (si/si) on mouse chromosome 10. In the current study, we have focused on determining whether or not the si allele carries a mutation in Pmel 17. Pmel 17 cDNA clones, isolated from wild-type and si/si murine melanocyte cDNA libraries, were sequenced and compared. A single nucleotide (A) insertion was found in the putative cytoplasmic tail of the si/si Pmel 17 cDNA clone. This insertion is predicted to alter the last 24 amino acids at the C-terminus. Also predicted is the extension of the Pmel 17 protein by 12 residues because a new termination signal created downstream from the wild-type reading frame. The mutation was confirmed by the sequence of the PCR-amplified genomic region flanking and including the mutation site. The fact that si/si Pmel 17 was not recognized by antibodies directed toward the C-terminal 15 amino acids of wild-type Pmel 17, indicated a defect in this region. We conclude from these results that silver pmel 17 protein has a major defect at the carboxyl terminus. The chromosomal location and the identification of a potentially pathologic mutation in si-Pmel 17 support our conclusion that Pmel 17 is encoded at the silver locus.

Amino Acid Sequence↗
PubMed1995

Observations on the developmental patterns and the consequences of pancreatic exocrine adenocarcinoma. Findings of 154 autopsies.

OBJECTIVE: To improve our future care of the patient with exocrine pancreatic cancer by seeking, within the limitations of our present approaches, additional information on the growth and spread of the cancer and its influences on the patient. DESIGN: Consecutive autopsies of all patients with exocrine pancreatic cancer were reviewed retrospectively by two surgeons and three pathologists. SETTINGS: Three teaching hospitals of the Medical College of Ohio, Toledo. MATERIALS: One hundred fifty-four consecutive autopsies of patients with exocrine pancreatic cancer during the period between 1952 and 1992. RESULTS: Intrapancreatic metastases or multicentric cancers were found in 12 patients. In 32 patients, pancreatic cancer skipped the lymph nodes, primarily draining the respective areas of the pancreas to metastasize to the secondary chain of nodes. In 13 patients, pulmonary metastases occurred without hepatic metastasis. Intrapancreatic contiguous extension was identified in 34 patients. Carcinoma of the body and/or tail of the pancreas was characterized by transperitoneal as well as hematogenous dissemination to a greater extent than was carcinoma of the head of the pancreas. Seven of 11 small tumors (< 2 cm in diameter) were associated with remote metastases. Relatively severe chronic obstructive pancreatitis was found to have resulted from pancreatic carcinoma in 18 cases, whereas in seven patients, pancreatic carcinoma probably developed in preexisting chronic pancreatitis. Thromboembolic disease was found in 30 patients, more frequently in the patients with the mucin-producing tumors of the pancreatic body and tail. In 21 patients, the amount of ascites was not proportional to the severity of peritoneal dissemination, vessel invasion, or recognizable hepatic dysfunction. Thromboembolic disease, severe infection, stress ulcer, and acute hemorrhagic erosive gastroenteritis were frequent systemic complications contributing to death. Malnutrition in the form of cachexia was undoubtedly a major, even dominant, feature in many patients that could not be quantitated from this data. CONCLUSIONS: Metastasizing cells frequently bypass the initial filters in lymph nodes, liver, or lung to become established in secondary or tertiary sites. Intrapancreatic metastases or multicentric tumors also may develop more frequently than generally has been recognized. Small cancers (< 2 cm in diameter) are often associated at autopsy with remote metastases. These facts would appear to limit the usefulness of the current staging of resected cancers of the pancreas. Cancers of the body or tail are characterized by transperitoneal and hematogenous spread to a greater extent than are those of the head. Anatomical studies often do not explain the cause or the extent of ascites associated with pancreatic adenocarcinoma. As previously indicated, chronic pancreatitis appears to be further confirmed as a precursor of pancreatic cancer.

Adenocarcinoma↗
PubMed1995

Steroid-responsive pulmonary disorders associated with myelodysplastic syndromes with der(1q;7p) chromosomal abnormality.

We report three patients with pulmonary disorders associated with myelodysplastic syndromes (MDS). All three patients had symptoms of pyrexia and respiratory discomfort. One patient had pulmonary eosinophilia with bilateral pleural effusion, one had interstitial pneumonia, and one had bilateral pleural effusion caused by systemic vasculitis. Elevated C-reactive protein (CRP) levels, polyclonal hypergammaglobulinemia, and morphological abnormalities in peripheral blood were observed in all three patients. The bone marrow of these patients revealed trilineage dysplasia and eosinophilia. Cytogenetic analysis showed [46,XY,-7,+der(1q;7p)]. Antibiotic treatment was not effective. However, improvement was dramatic after corticosteroid treatment; CRP levels were reduced and the hypergammaglobulinemia was improved. These cases suggest that MDS with [-7,+der(1q;7p)] may be correlated with bone marrow eosinophilia and that an immunologic abnormality may be involved in the pulmonary disorders.

Adrenal Cortex Hormones↗
PubMed1995

Toxoplasma gondii: stable complementation of sag1 (p30) mutants using SAG1 transfection and fluorescence-activated cell sorting.

Toxoplasma gondii and the related Apicomplexan protozoan pathogens, Plasmodium, Cryptosporidium, and Eimeria, are obligate intracellular parasites which cause severe disease in their hosts. The recent development of transient transfection of Toxoplasma permits the development of strategies utilizing "reverse genetics" to identify molecules critical to parasite survival within the host. We have utilized transfection of Toxoplasma tachyzoites to stably complement a sag1 (or p30) mutant that does not make detectable SAG1. Transfection of mutants with the wild-type SAG1 gene resulted in transient expression of SAG1 in approximately 15-20% of the transfected population. Stable transformants were enriched by repeated sorting of live parasites using a fluorescein-labeled monoclonal antibody specific for SAG1. Cloned recombinant parasites expressed SAG1 at wild-type levels and maintained expression for over 5 months after transfection (approximately 300 divisions). Cloned transformants (which proved to be siblings) carried both the mutated gene and one copy of the transfected gene which had inserted randomly into the Toxoplasma genome.

Animals↗
PubMed1995

Overexpression of HER2/neu oncogene in pancreatic cancer correlates with shortened survival.

For the purpose of determining the prognostic significance of HER2/neu oncogene in pancreatic and ampullary cancers, 21 pancreatic cancers of ductal origin and six cancers of the ampulla of Vater were studied immunohistochemically using the monoclonal antibody (MAb) CB11, specifically reactive with HER2/neu product. Staining of the epithelium of the normal duct and acini was negative or weakly positive. Moderately and strongly positive reactions indicated the overexpression of this gene, and were found in 10 of 21 (47.6%) pancreatic cancers of ductal origin and in 2 of 6 (33.3%) ampullary adenocarcinomas. Overexpression of HER2/neu was closely and inversely related to the survival of the patients with pancreatic cancer of ductal origin: 19.1 +/- 11.7 mo for those not overexpressing vs 7.3 +/- 3.8 mo for the overexpressors (p < 0.01). Among the pancreatic cancer group, 11 patients underwent cancer resection. The average survival for the 7 with nonoverexpressing cancer was 21.4 +/- 14.3 mo vs 10.5 +/- 3.6 mo for those with overexpressing tumor. Among those not undergoing resection, the average survival for the 4 with nonoverexpressing cancer was 15.0 +/- 3.8 mo as contrasted to 5.2 +/- 2.1 mo for the overexpressors (p < 0.01). Although the number of patients is small, these findings suggest that the overexpression of HER2/neu gene product may be frequently found in pancreatic cancer of ductal origin and may be one of the useful prognostic biomarkers for this cancer.

Adenocarcinoma↗
PubMed1995

Personal and behavioral predictors of automobile crash and injury severity.

The purpose of this paper is to develop a statistical model explaining the relationships between certain driver characteristics and behaviors, crash severity, and injury severity. Applying techniques of categorical data analysis to comprehensive data on crashes in Hawaii during 1990, we build a structural model relating driver characteristics and behaviors to type of crash and injury severity. The structural model helps to clarify the role of driver characteristics and behaviors in the causal sequence leading to more severe injuries. From the model we estimate the effects of various factors in terms of odds multipliers--that is, how much does each factor increase or decrease the odds of more severe crash types and injuries. We found that driver behaviors of alcohol or drug use and lack of seat belt use greatly increase the odds of more severe crashes and injuries. Driver errors are found to have a small effect, while personal characteristics of age and sex are generally insignificant. We conclude with a discussion of our modeling approach and of the implications of our findings for appropriate traffic safety interventions and future research.

Accidents, Traffic↗
PubMed1995

Extradural tumor causing spinal cord compression in Klippel-Trenaunay-Weber syndrome.

BACKGROUND: Myelopathy in Klippel-Trenaunay-Weber syndrome is uncommon but has been reported secondary to spinal vascular malformations. REPORT: A patient with Klippel-Trenaunay-Weber syndrome who presented with spinal cord compression from a spinal extradural mass lesion (angiomyolipoma) is described. DISCUSSION: This association has not been reported previously but is consistent with the segmental vascular abnormalities observed in Klippel-Trenaunay-Weber syndrome.

Adult↗
PubMed1995

Restriction enzyme-mediated integration elevates transformation frequency and enables co-transfection of Toxoplasma gondii.

This report describes the use of restriction enzyme-mediated integration (REMI) to increase the transformation frequency and allow co-transfection of several unselected constructs under the selection of a single selectable marker. We found that while BamHI (the enzyme used to originally demonstrate REMI (Schiestl, R.H. and Petes, T.D. (1991) Integration of DNA fragments by illegitimate recombination in Saccharomyces cerevisiae. Proc. Nati. Acad. Sci. USA 88, 7585-7589) increased the number of transformants by 2-5-fold over the control without added enzyme, NotI proved to be a further 29-46-times more effective in enhancing stable transformation. This simple technique was used in the transformation of three non-selective markers (two modified membrane proteins and beta-galactosidase) with a selectable construct expressing chloramphenicol acetyltransferase. Following chloramphenicol selection, four out of ten independent transformants stably acquired all four constructs with at least two expressing all four genes at the protein level. These results demonstrate that REMI may be used in the efficient stable transformation and co-transfection of this and perhaps other protozoan parasites.

Animals↗
PubMed1995

Complementation of a Toxoplasma gondii ROP1 knock-out mutant using phleomycin selection.

The ROP1 gene of Toxoplasma gondii encodes a rhoptry protein that has been implicated in host cell invasion by this obligate intracellular protozoan. To further explore the function of this protein, we created a ROP1 deletion mutant by transfection with a plasmid encoding the bacterial chloramphenicol acetyltransferase (cat) gene flanked by ROP1 genomic sequences. Selection for chloramphenicol resistance yielded the desired ROP1-deleted or 'knock-out' mutant. Analysis of this mutant both in vitro and in vivo shows no significant alterations in growth rate, host specificity, invasiveness or virulence and thus the ROP1 gene is not obligatory for the RH strain, at least under the conditions tested. However, electron microscopy reveals that the mutant strain's rhoptries are altered in ultrastructure; they are thinner and homogeneously electron-dense compared with the thicker and normally mottled or honeycombed appearance of wild-type rhoptries. The knock-out mutant was rescued using co-transfection of a cosmid carrying the ROP1 gene together with a plasmid encoding a new selectable marker for T. gondii, the bleomycin resistance gene (ble) from Streptoalloteichus. Southern blot analysis showed that both DNAs were stably integrated into the Toxoplasma genome, although not into the ROPI locus. The resulting strain showed wild-type levels of ROP1 expression and rescue of the ultrastructural phenotype (i.e., the rhoptries returned to their normal, mottled appearance), thus establishing a cause/effect relationship between the absence of ROP1 and the electron-opacity. These results demonstrate the utility of the reverse genetic approach in the study of Toxoplasma gene function and provide a further selectable marker for such manipulations.

Animals↗
PubMed1995

SEQPWR and SEQOPR: computer programs for design of maximum information trials based on group sequential logrank tests.

The maximum information trial paradigm for clinical trials with failure time data was recognized and has been investigated. With the maximum information trial paradigm, a study is concluded when a prespecified maximum number of events of interest, thus maximum information, has been accrued if there was no early stopping due to treatment difference or lack thereof. We present two interactive FORTRAN programs for use in designing maximum information trials based on group sequential logrank tests. The program SEQPWR computes the attainable power of group sequential logrank tests given the combinations of the accrual and follow-up durations. The program SEQOPR allows the users to investigate the operating characteristics of the maximum information trial given the information fractions of interim analyses. A clinical trial from the Eastern Cooperative Oncology Group is provided to illustrate the usage and features of the programs.

Algorithms↗
PubMed1995

Malignant islet cell tumor associated with hypercalcemia.

BACKGROUND: Three cases of islet cell tumors of the pancreas with hypercalcemia were studied, and 16 similar cases have been found in a 25-year review of the English-language literature. The purpose of the study was to review the cause of the hypercalcemia and the clinical characteristics of the tumors. METHODS: Tumor tissue retrieved from paraffin-embedded blocks was studied immunohistochemically for both parathyroid hormone (PTH) and PTH-related protein (PTHrP). PTH was measured in the serum in each patient and the serum PTHrP was measured by immunoassay in one patient. RESULTS: One of our patients had a fatal serum calcium level of 26.4 mg/dl. PTHrP stains were positive in two of our tumors, and one patient had an elevated PTHrP serum level. Serum PTH levels were normal or low in each patient. All three tumors were malignant and extremely vascular. The total group of 19 patients have in common hypercalcemia associated with a normal or low serum PTH level. Although the cause of hypercalcemia has not been proved, the tumors apparently produce PTHrP, because seven of eight tumors stained positive for PTHrP and each of the four patients tested had an elevated PTHrP serum titer. The tumors are extremely vascular, are usually malignant (17 of 18), and become large, but they are compatible with a relatively long patient survival time. CONCLUSIONS: These neuroendocrine tumors associated with hypercalcemia share several characteristics, but a claim that they represent another type of "functioning islet cell tumor" should await a clearer delineation of the cause of the hypercalcemia.

Adenoma, Islet Cell↗