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Biomedical subjects

K Lee

Publications and source records attributed to K Lee.

At least 451 records · Page 25Linked to original sources

Nitrogen dioxide in indoor ice skating facilities: an international survey.

An international survey of nitrogen dioxide (NO2) levels inside indoor ice skating facilities was conducted. One-week average NO2 concentrations were measured inside and outside of 332 ice rinks located in nine countries. Each rink manager also completed a questionnaire describing the building, the resurfacing machines, and their use patterns. The (arithmetic) mean NO2 level for all rinks in the study was 228 ppb, with a range of 1-2,680 ppb, based on a sample collected at breathing height and adjacent to the ice surface. The mean of the second indoor sample (collected at a spectator's area) was 221 ppb, with a range of 1-3,175 ppb. The ratio of the indoor to outdoor NO2 concentrations was above 1 for 95% of the rinks sampled, indicating the presence of an indoor NO2 source (mean indoor:outdoor ratio = 20). Estimates of short-term NO2 concentrations indicated that as many as 40% of the sampled rinks would have exceeded the World Health Organization 1-hour guideline value of 213 ppb NO2 for indoor air. Statistically significant associations were observed between NO2 levels and the type of fuel used to power the resurfacer, the absence of a catalytic converter on a resurfacer, and the use of an ice edger. There were also indications that decreased use of mechanical ventilation, increased number of resurfacing operations per day, and smaller rink volumes were associated with increased NO2 levels. In rinks where the main resurfacer was powered by propane, the NO2 concentrations were higher than in those with gasoline-powered resurfacers, while the latter had NO2 concentrations higher than in those using diesel. Rinks where the main resurfacer was electric had the lowest indoor NO2 concentrations, similar to the levels measured outdoors.

Air Pollution, Indoor↗

Dental implant infections.

Dental implants provide a restorative tool to support crowns, bridge abutments, and removable dentures. Osseointegrated implants are titanium posts that are surgically implanted in alveolar bone. A tight immobile bond (osseointegration) forms between bone and titanium, and prosthetic and restorative fixtures are attached to the implants. Titanium implants differ from natural teeth, which may make them more susceptible to mechanical stress. A small proportion of implants are not successful and may fail due to infection. The microbiota of implants is similar to that of teeth in similar clinical states. Implants that fail because of mechanical stress are colonized by species associated with healthy teeth. Infected implants are colonized by subgingival species, including Porphyromonas gingivalis, Bacteroides forsythus, Fusobacterium nucleatum, Campylobacter gracilis, Streptococcus intermedius, and Peptostreptococcus micros. Different patients may be colonized by different microbial complexes, indicating that optimal treatment should be directed to the specific infection.

Bacterial Infections↗

Spread of the serotype 23F multidrug-resistant Streptococcus pneumoniae clone to South Korea.

Thirty-eight antibiotic-resistant isolates of Streptococcus pneumoniae recovered in a hospital in Seoul, Korea, between February 1990 and March 1992 were analyzed for serotype, antibiotic susceptibility patterns, and chromosomal relatedness using pulsed-field gel electrophoretic (PFGE) analysis of SmaI chromosomal digests. Most of the isolates were from sputum samples, and a few strains were from otitis media and meningitis. The great majority of isolates (34 of 38, or 89%) were multiresistant, sharing virtually identical, elevated minimal inhibitory concentration (MIC) values (microgram/ml) for penicillin (1-2), chloramphenicol (12-25), tetracycline (25-30), and sulfamethoxazole/trimethoprim (> 100). Twenty of the isolates were also resistant to erythromycin, and all isolates were also considered to be resistant to ceftriaxone and cefotaxime (1-2) according to the new breakpoint definitions. The most frequent serotypes were 23F (17 of 38) and 19F(14 of 38); 2 belonged to serotype 15B and 1 of 24F. Of the remaining 4 isolates (2 serotype 3, 1 type 6B, and 1 type 9V) all were resistant to tetracycline and sulfamethoxazole/trimethoprim and with the exception of 1 of the type 3 strains, were also resistant to chloramphenicol. Eleven of the 14 serotype 19F isolates shared a relatively homogeneous PFGE pattern, which was indistinguishable from the PFGE pattern shown by most (12 of 17) of the 23F isolates. The PFGE pattern of these 19F and 23F isolates was also indistinguishable from the PFGE pattern shown by representative multiresistant capsular type 23F isolates from Croatia, Portugal, and New York City and the findings document the extensive geographic spread of this multidrug-resistant S. pneumoniae clone. The data also suggests in vivo capsular transformation of the multiresistant clone from serotype 23F to serotype 19F.

DNA Fingerprinting↗

Sarcomatous transformation of neurofibromas. Comparative imaging with Ga-67, Tl-201, Tc-99m pentavalent DMSA and Tc-99m MIBI.

A 29-year-old man, with a history of von Recklinghausen's disease, presented with progressive dyspnea associated with a rapidly growing mass on the right chest wall. Plain radiograph and CT of the chest revealed a huge soft-tissue mass with central low-density area involving the right upper lung and chest wall. SPECT imaging with Ga-67 citrate, Tl-201 chloride, Tc-99m pentavalent DMSA (V-DMSA), and Tc-99m MIBI were performed to characterize the mass. The tumor concentrated Ga-67, Tl-201, and Tc-99m (V) DMSA, but not Tc-99m MIBI. Punch biopsy of the lesion revealed malignant transformation of a thoracic neuroma (neurofibrosarcoma). Subsequently, findings compatible with the presence of a multidrug resistance-1 (MDR1) gene in the tumor was documented, which may explain the poor uptake of Tc-99m MIBI. The patient did not respond to intensive chemotherapeutic regimens, and died 3 months later. This case demonstrates the potential use of combined radionuclide imaging for the detection of malignant transformation of neurofibroma, as well as for predicting tumor response to chemotherapy.

Adult↗

Loosening and osteolysis of cemented joint arthroplasties. A biologic spectrum.

The purpose of this study was to characterize the cell types (using immunohistochemistry) and cytokine expression (using in situ hybridization) of tissues surrounding well fixed and loose cemented prostheses undergoing revision. Clinical and radiographic data were gathered prospectively for a series of cemented total joint replacements undergoing revision. Three groups were identified: (1) loose implants with osteolysis (10 specimens), (2) loose implants without osteolysis (11 specimens), and (3) well fixed implants (7 specimens). At surgery, a specimen was harvested from the bone cement interface. Immunohistochemical staining was performed using monoclonal antibodies to identify macrophages and lymphocyte subgroups. Human antisense probes were selected to identify the mRNA for specific cytokines using in situ hybridization. The percentage of positively staining cells was determined for each antibody or probe using a grid counting technique. Tissues from loose cemented prostheses with osteolysis contained significantly greater numbers of macrophages and T lymphocytes compared with tissues from loose and well fixed cemented prostheses without osteolysis. The number of interleukin-1 and interleukin-6 positive cells was highest in specimens with osteolysis and lowest in specimens from well fixed prostheses. These cytokines modulate the growth and differentiation of cells in the immune system and the monocyte and macrophage system and mediate the remodeling of bone and mesenchymal tissues. Specific cell populations and cytokine profiles appear to be involved in periprosthetic osteolysis; this information may be useful in planning strategies for prevention and treatment.

Aged↗

More does not mean better: prenatal visits and pregnancy outcome in the Hispanic population.

Early and consistent prenatal care (PNC) is thought to play an important role in the reduction of low birthweight (LBW) in the United States. It has been reported that LBW and delayed PNC are common to the Hispanic woman. In California, this cultural group comprises approximately 26% of the population, and much debate concerning health care reform has been targeted at this problem. A comparative study was conducted in California to examine the number of prenatal visits and the outcomes of Mexico-born Hispanics and U.S.-born Hispanics. Obstetric and medical record review for 783 women was done. The results show that more prenatal visits did not improve the outcome during pregnancy, labor, or the postpartum period. Because a large portion of PNC is now delivered by the advanced practice nurse, implications for practice include exploring alternatives for the delivery of culturally relevant care, addressing the barriers to caring for this population, and finding alternative models of care that have the potential to produce positive outcomes.

Adolescent↗

Stereospecific oxidation of (R)- and (S)-1-indanol by naphthalene dioxygenase from Pseudomonas sp. strain NCIB 9816-4.

A recombinant Escherichia coli strain which expresses naphthalene dioxygenase (NDO) from Pseudomonas sp. strain NCIB 9816-4 oxidized (S)-1-indanol to trans-(1S,3S)-indan-1,3-diol (95.5%) and (R)-3-hydroxy-1-indanone (4.5%). The same cells oxidized (R)-1-indanol to cis-1,3-indandiol (71%), (R)-3-hydroxy-1-indanone (18.2%), and cis-1,2,3-indantriol (10.8%). Purified NDO oxidized (S)-1-indenol to both syn- and anti-2,3-dihydroxy-1-indanol.

Dioxygenases↗

Hir1p and Hir2p function as transcriptional corepressors to regulate histone gene transcription in the Saccharomyces cerevisiae cell cycle.

The HIR/HPC (histone regulation/histone periodic control) negative regulators play important roles in the transcription of six of the eight core histone genes during the Saccharomyces cerevisiae cell cycle. The phenotypes of hir1 and hir2 mutants suggested that the wild-type HIR1 and HIR2 genes encode transcriptional repressors that function in the absence of direct DNA binding. When Hir1p and Hir2p were artificially tethered to yeast promoters, each protein repressed transcription, suggesting that they represent a new class of transcriptional corepressors. The two proteins might function as a complex in vivo: Hir2p required both Hir1p and another Hir protein, Hir3p, to repress transcription when it was tethered to an HTA1-lacZ reporter gene, and Hir1p and Hir2p could be coimmunoprecipitated from yeast cell extracts. Tethered Hir1p also directed the periodic transcription of the HTA1 gene and repressed HTA1 transcription in response to two cell cycle regulatory signals. Thus, it represents the first example of a transcriptional corepressor with a direct role in cell cycle-regulated transcription.

Bacterial Proteins↗

Biochemical and immunocytochemical properties of peroxisomes and mitochondria in bovine chromaffin cells.

The biochemical and immunocytochemical properties of peroxisomal and mitochondrial beta-oxidation enzymes in bovine adrenal chromaffin cells were investigated. Peroxisomes were detectable by immunofluorescence staining using antibodies against acyl-CoA oxidase, peroxisomal 3-ketoacyl-CoA thiolase and catalase. The mitochondria were abundantly stained with antibody against mitochondrial 3-ketoacyl-CoA thiolase. The biosynthesis and intracellular processing of acyl-CoA oxidase and the peroxisomal 3-ketoacyl-CoA thiolase was slower than that in fibroblasts. The peroxisomal beta-oxidation activities shown by [1-14C] lignoceric acid oxidation were slightly lower than those in fibroblasts, whereas the mitochondrial beta-oxidation activities shown by [1-14C] palmitic acid oxidation were almost identical to those in fibroblasts. Adrenal chromaffin cells are useful materials for investigating the peroxisomal and mitochondrial metabolism of autonomic neurons and may contribute to the clarification of neuronal dysfunction in peroxisomal and mitochondrial disorders.

Acetyl-CoA C-Acyltransferase↗

Release of lactate by the lung in acute lung injury.

UNLABELLED: The pathogenesis of hyperlactatemia during sepsis is poorly understood. We have previously described an increase in lactate concentration across the lung in the dog during early endotoxemia. Accordingly, we sought to determine if the lung releases lactate in humans and what relation this has with lung injury. METHODS: We measured lactate concentrations across the lung and lung injury scores (LIS) in two groups of patients. Group 1 consisted of nine patients with acute lung injury (LIS > or = 2.0) and elevated lactate concentrations (> 2.0 mmol/L). Group 2 contained 12 patients with no acute lung injury (LIS scores < or = 1.5), with or without increased lactate concentrations. Simultaneous measurements of plasma lactate and blood gases were obtained from indwelling arterial and pulmonary artery catheters. Measurements of cardiac output were also obtained. Lactate measurements were done using a lactate analyzer (YSI; Yellow Springs, Ohio). RESULTS: For each patient with acute lung injury and hyperlactatemia, an arterial-venous lactate gradient existed demonstrating release of lactate by the lung. This gradient persisted after correction for changes in hemoconcentration across the lung. The lactate gradient across the lung was 0.4 +/- 0.2 mmol/L for group 1 vs 0.05 +/- 0.1 mmol/L for group 2 (p = 0.001). This corresponded to a mean pulmonary lactate flux of 231.3 +/- 211.3 vs 5.0 +/- 37.2 mmol/h (p = 0.001). The lactate flux and the arterial-venous lactate difference correlated with LIS both for the entire sample and for the subgroup with hyperlactatemia (r = 0.69, p < 0.01). Pulmonary lactate flux was not related to arterial lactate levels (r = 0.25). CONCLUSION: In patients with acute lung injury and hyperlactatemia, the lung is a major source of lactate and lactate flux correlates with LIS. This lactate flux could explain some of the hyperlactatemia seen in sepsis.

Adult↗

High-resolution CT of the lung: determination of the usefulness of CT scans obtained with the patient prone based on plain radiographic findings.

OBJECTIVE: We assessed the usefulness of chest radiographs for predicting whether high-resolution CT scans obtained with the patient prone would be valuable in assessing suspected diffuse lung disease. MATERIALS AND METHODS: In 100 consecutive patients undergoing high-resolution CT, findings on plain chest radiographs were classified as normal, possibly abnormal, or abnormal. CT scans obtained with the patient supine were assessed for the presence and distribution of lung abnormalities without knowledge of the plain radiographic classification. A second review of the CT scans was done with equal numbers of scans obtained with the patient prone and with the patient supine. The usefulness of the CT scans obtained with the patient prone for detecting lung disease was determined and related to the plain radiographic classifications. RESULTS: High-resolution CT scans obtained with patients prone were helpful in excluding or confirming posterior lung abnormalities in 10 (28%) of 36 patients who had normal findings on chest radiographs, five (28%) of 18 patients who had possibly abnormal findings on chest radiographs, and only two (4%) of 46 patients who had abnormal findings on chest radiographs. The proportion of patients who benefited from high-resolution CT scans obtained with the patient prone was significantly lower among the patients with abnormal findings on chest radiographs than among the patients with normal (p = .008) or possibly abnormal (p = .02) findings on chest radiographs. The two patients with abnormal findings on radiographs in whom CT scans obtained with the patient prone were helpful had minimal radiographic abnormalities. CONCLUSION: In patients with suspected diffuse lung disease, obtaining high-resolution CT scans with the patient prone may be useful when chest radiographs show normal findings, possibly abnormal findings, or minimal abnormalities indicative of diffuse lung disease. However, such scans are of little value in patients whose radiographs show abnormalities indicative of diffuse lung disease.

Adolescent↗

Perception of a border defined by rapidly reversing luminance contrast.

We report a new visual illusion of a perceptual boundary visible between two contiguous regions of equal luminance when the intensity is modulated with a temporal frequency that is higher than the critical fusion rate. Measurements of the luminance threshold of the perceptual border with various slopes of the luminance gradient yielded a function suggestive of the range of ocular instability. These findings raise the possibility that this new border illusion may be influenced by involuntary ocular motion during fixation.

Adult↗

P53, MDM-2, BAX and BCL-2 and drug resistance in chronic lymphocytic leukemia.

Most antitumor agents exert their cytotoxic effect through the induction of apoptosis, and this process may be mediated through an elevation in p53 protein, with a subsequent increase in bax and decrease in bcl-2. p53 also increases mdm-2 expression and mdm-2 may then bind and inactivate p53. Cells from 31 patients with chronic lymphocytic leukemia (CLL) were treated in vitro with 2-chlorodeoxyadenosine (CdA), arabinosyl-2-fluoroadenine (F-ara-A), or chlorambucil (CLB) and drug sensitivity measured using the MTT assay. The protein levels of bax and bcl-2 were measured in CLL cells from 25 patients, and were found to be higher in leukemic cells than in normal B cells. The bcl-2 levels varied three-fold, the bax levels fifteen-fold, and the bax:bcl-2 ratios ranged from 0.44 to 2.91. The expression of mdm-2 mRNA was measured in CLL cells from 28 patients and was found to vary twenty-fold. However, no correlation was observed between drug sensitivity to CdA, F-ara-A, or CLB and the cellular levels of mdm-2 mRNA, or the protein levels of bax or bcl-2, or the bax:bcl-2 ratio. Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA. This was not observed in cells having a p53 mutation, and these cells were highly resistant to both CLB and the nucleoside analogs. In contrast to the nucleoside analogs and CLB, dexamethasone and vincristine had no effect on mdm-2 mRNA levels. Treatment of CLL cells containing a wild type p53 gene with CdA, F-ara-A, or CLB, did not produce any consistent changes in bax or bcl-2. Thus, CdA, F-ara-A and CLB appear to act in CLL cells through a p53-dependent pathway, whereas this does not occur with dexamethasone or vincristine. The cellular levels of mdm-2, bcl-2, bax or the bax:bcl-2 ratios are not predictive indicators of clinical sensitivity in CLL, but an increase in mdm-2 levels after drug treatment is indicative of p53 function in these cells.

Adult↗

Congenital deficiency of the fibula with ipsilateral iliac horn and absence of the kidney.

Congenital deficiency of the fibula is sometimes accompanied by femoral hypoplasia, genu valgum, patellar a/hypoplasia or dislocation, tibial bowing, foot deformity, and toe deficiency in the affected limb. 'Iliac horns' are bony projections extending posterolaterally from the ilium and considered to be pathognomonic of nail-patella syndrome. We report a 5-year-old Japanese girl with congenital complete deficiency of the left fibula, ipsilateral iliac horn and absence of the left kidney.

Female↗

Molecular recognition by cholesterol esterase of active site ligands: structure-reactivity effects for inhibition by aryl carbamates and subsequent carbamylenzyme turnover.

Interactions of mammalian pancreatic cholesterol esterases from pig and rat with a family of aryl carbamates CnH2n+1NHCOOAr [n = 4-9; Ar = phenyl, p-X-phenyl (X = acetamido, bromo, fluoro, nitro, trifluoromethyl), 2-naphthyl, 2-tetrahydronaphthyl, estronyl] have been investigated, with an aim of delineating the ligand structural features which lead to effective molecular recognition by the active site of the enzyme. These carbamates inhibit the catalytic activity of CEase by rapid carbamylation of the active site, a process that shows saturation kinetics. Subsequent slow decarbamylation usually leads to full restoration of activity, and therefore aryl carbamates are transient inhibitors, or pseudo-substrates, of CEase. Structural variation of carbamate inhibitors allowed molecular recognition in the fatty acid binding and steroid binding loci of the extended active site to be probed, and the electronic nature of the carbamylation transition state to be characterized. Optimal inhibitory activity is observed when the length of the carbamyl function is n = 6 and n = 7 for porcine and rat cholesterol esterases, respectively, equivalent to eight- and nine-carbon fatty acyl chains. In contrast, inhibitory activity increases progressively as the partial molecular volume of the aromatic fragment increases. Hammett plots for p-substituted phenyl-N-hexyl carbamates indicate that the rate-determining step for carbamate inhibition is phenolate anion expulsion. Effects of the bile salt activator taurocholate on the kinetically resolved phases of the pseudo-substrate turnover of aryl carbamates were also studied. Taurocholate increases the affinity of the carbamate for the active site of cholesterol esterase in the reversible, noncovalent complex that precedes carbamylation and increases the rate constants of the serial carbamylation and decarbamylation steps. Structural variation of the N-alkyl chain and of the aryl fused-ring system provides an accounting of bile salt modulation of the fatty acid and steroid binding sites, respectively. In that pseudo-substrate turnover of aryl carbamates proceeds by a three-step mechanism that is analogous to that for rapid turnover of lipid ester substrates, these investigations illuminate details of ligand recognition by the extended active site of cholesterol esterase that are prominent determinants of the substrate specificity and catalytic power of the enzyme.

Animals↗

The influx of Ca2+ and the release of noradrenaline evoked by the stimulation of presynaptic nicotinic receptors of chick sympathetic neurons in culture are not mediated via L-, N-, or P-type calcium channels.

We have shown earlier that nicotinic agonists induce the release of noradrenaline from chick sympathetic neurons in culture in two ways: (a) by activating the postsynaptic nicotinic receptors on nerve cell bodies, giving rise to spreading electrical activity and opening of voltage operated calcium channels in neuronal processes; (b) by activating the presynaptic nicotinic receptors on neuronal processes. In the present work, we investigated the contribution of various pathways to the observed Ca2+ influx and subsequent noradrenaline release. Sympathetic neurons in culture were stimulated either by the nicotinic agonist dimethylphenylpiperazinium or electrically, in the presence or absence of tetrodotoxin and of specific blockers of calcium or nicotinic channels, and the effects on [Ca2+]i in the area of neuronal processes and on noradrenaline release were measured. Under control conditions, the N-type channel blocker omega-conotoxin (0.1 mumol/l) diminished the release of noradrenaline and the increase of intraterminal Ca2+ by 48% and 55%, respectively, whereas the L-type channel blocker (+)Bay k 8644 (1 mumol/l) diminished the release of noradrenaline by 25% and the increase of [Ca2+]i by 39%. The P-type channel blocker omega-agatoxin (0.3 mumol/l) had no effect. The effects of the L-type channel ligands were complex and could only be explained on the assumption that, at high concentrations, these drugs also act as nicotinic antagonists. Tetrodotoxin blocked the Ca2+ response evoked by electrical stimulation whereas DMPP applied in the presence of tetrodotoxin still evoked an increase of [Ca2+]i and the release of noradrenaline (27% and 30% of control without tetrodotoxin, respectively). These residual responses were not blocked by any of the calcium channel blockers used or by their combination. Apparently, a substantial part of the influx of Ca2+ induced by the activation of presynaptic nicotinic receptors is not carried by the N-, L- or P-type channels and probably occurs directly via the open channels of nicotinic receptors.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗