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Biomedical subjects

S Kim

Publications and source records attributed to S Kim.

At least 487 records · Page 27Linked to original sources
PubMed2000

Effect of denture cleansers, surface finish, and temperature on Molloplast B resilient liner color, hardness, and texture.

PURPOSE: The purpose of this study was to compare color, texture, and Shore A hardness of a resilient silicone denture liner with as-polymerized, roughened, or pumiced surfaces after treatment with perborate-, persulfate-, or hypochlorite-containing denture cleansers at 25 degrees or 55 degrees. MATERIALS AND METHODS: Fifty-eight specimens that each exhibited an as-polymerized, a roughened, and a pumiced area were exposed to 5 different commercially available perborate-, persulfate-, or hypochlorite-containing denture cleansers at 25 degrees or 55 degrees continuously for 4 (1/2) months. The solutions were replaced twice a day. Control specimens were soaked in water with no cleanser. Before and after the 4 (1/2) -month cleaning regimen, the color, hardness, and texture of resilient liner surfaces were evaluated using a color densitometer, a Shore A durometer (Shore Instrument & Mfg Co, Freeport, NY), and a surface profilometer, respectively. Differences among groups after the cleanser treatment were determined using a repeated measures analysis of variance (alpha = 0.05) and a Tukey's Honestly Significant Difference post hoc test. RESULTS: Roughened specimen surfaces after 25 degrees or 55 degrees cleanser treatment exhibited significant color loss with some perborate-containing cleansers compared with the control. Roughened specimens treated at 55 degrees with perborate-containing cleansers also exhibited significantly greater color loss than those treated with the persulfate-containing cleanser. With roughened surfaces, significantly greater hardness was found with some perborate-containing cleanser compared with a hypochlorite-containing cleanser after treatment at 25 degrees. No differences were observed in surface texture based upon cleanser treatment. CONCLUSION: After silicone resilient denture liner treatment with certain perborate-containing denture cleansers, a greater amount of components could leach from the liner leading to a loss of color if the liner surface is rough.

Analysis of Variance↗
PubMed2000

[MN/CA IX antigen as a potential target for renal cell carcinoma].

MN/CA IX is considered as a carbonic anhydrase isoenzyme expressed in the normal alimentary tract in a tissue-specific manner. This antigen is activated in the majority of renal cell carcinomas (RCC) but not in the normal kidney tissues. Our previous study revealed that increase of malignant potential is related to down-regulation of MN/CA9. To investigate the mechanism of MN activation in RCC, we examined the methylation status of this gene (MN/CA9) in RCC cell lines (SKRC-1, 6, 10, 12, 14, 44, 59). Moreover, we analyzed the circulating blood of patients for the presence of RCC cells by RT-PCR, to determine whether detection of circulating RCC cells could be useful as a biomarker. CpG methylation was investigated at 7 CpG sites in the MN/CA9 5' region. Clear mRNA signals were observed in 5 cell lines (SKRC-1, 6, 10, 44, 59), e.g., MN/CA9 positive. These 5 MN-positive cell lines showed hypomethylation in the 5' region. In contrast, all CpG sites were methylated in the remaining 2 lines and 3 normal kidney tissue samples. These results suggest that hypomethylation in the 5' region may play an important role in the expression of MN/CA9 in RCC. RT-PCR analysis of blood samples from RCC patients revealed the presence of circulating MN-positive cancer cells in the blood. Although a significant correlation with tumor stage and grade was not observed, the analysis of blood samples from patients with metastases resulted in a high detection rate of 82%. These findings suggest the usefulness of MN/CA IX as a potential diagnostic marker for detection of RCC.

Antigens, Neoplasm↗
PubMed2000

Global nursing leadership: a professional imperative.

Globalization is an inevitable trend in the modern world, as our communities become both closer and more diverse. Globalization is examined in this report as a key factor in recognizing the intersection of health and development. Nurse leaders face the crucial need to understand and take initiatives in responding to this radically changing world. The transformation of nursing requires active participation and leadership in practice, education, research, and policy arenas. To participate in shaping the public understanding of health and development, nurse leaders must be included in the multinational and multidisciplinary decision processes that shape health care at home and abroad.

Education, Nursing↗
PubMed2000

Factors affecting the stability of the performance of ambient fine-particle concentrators.

This article describes a systematic evaluation of factors affecting the stability of the performance of Harvard ambient fine-particle concentrators, an essential requirement for controlled animal and human exposure studies that utilize these technologies. Phenomenological problems during the operation of the concentrator, including pressure drop increase and decrease in concentration enrichment, were statistically correlated with ambient air parameters such as temperature, relative humidity, PM2.5 mass concentration, and mass median diameter. The normalized hourly pressure drop across the concentrator was strongly associated (R2 = .81) with the product of ambient PM2.5 mass concentration and the difference between the vapor pressure downstream of the impactor nozzle and the saturation vapor pressure at the adiabatic expansion temperature (i.e., the temperature of the aerosol immediately downstream of the virtual impactors). From multiple regression analysis, the average enrichment factor was predicted reasonably well (R2 = .67) by aerosol mass median diameter and the normalized hourly pressure drop. Based on these results, we can anticipate in any given day whether an exposure study can be conducted without a considerable increase in the concentrator pressure drop, which might lead to an abrupt or premature termination of the exposure. As particle mass concentration and ambient dewpoint are the two main parameters responsible for raising the pressure drop across the concentrator, efforts should be made to either desiccate the ambient aerosol at days of high dewpoints, or to dilute the ambient PM at days of high concentrations, prior to drawing the aerosol through the virtual impactors. The latter approach is recommended on days of severe ambient pollution conditions because it is simpler and also makes it possible to maintain the appropriate concentration level delivered to the exposure chamber.

Air Pollutants↗
PubMed2000

Enhanced expression of constitutive and inducible forms of nitric oxide synthase in autoimmune encephalomyelitis.

To elucidate the role of nitric oxide synthase (NOS) in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), we analyzed the expression of constitutive neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS) in the spinal cords of rats with EAE. We further examined the structural interaction between apoptotic cells and spinal cord cells including neurons and astrocytes, which are potent cell types of nitric oxide (NO) production in the brain. Western blot analysis showed that three forms of NOS significantly increased in the spinal cords of rats at the peak stage of EAE, while small amounts of these enzymes were identified in the spinal cords of rats without EAE. Immunohistochemical study showed that the expression of either nNOS or eNOS increased in the brain cells including neurons and astrocytes during the peak and recovery stages of EAE, while the expression of iNOS was found mainly in the inflammatory macrophages in the perivascular EAE lesions. Double labeling showed that apoptotic cells had intimate contacts with either neurons or astrocytes, which are major cell types to express nNOS and eNOS constitutively. Our results suggest that the three NOS may play an important role in the recovery of EAE.

Animals↗
PubMed1999

Characterization of millisecond time-scale dynamics in the molten globule state of alpha-lactalbumin by NMR.

The motional dynamics of the molten globule (MG) state of alpha-lactalbumin have been characterized using (15)N transverse relaxation rates (R2). A modified version of the Carr-Purcell-Meiboom-Gill (CPMG) R2 pulse sequence is proposed in order to overcome the loss of sensitivity that arises from extreme line broadening due to complex dynamics on the millisecond time-scale. Using this pulse sequence, chemical exchange rates were extracted by examining the (15)N transverse relaxation rates as a function of CPMG delay values. The results clearly illustrate that pervasive conformational exchange of 0.2-0.5 ms in the (15)N backbone resonances of the molten globule state of alpha-lactalbumin. The temperature dependence of the conformational exchange rates display standard Arrhenius kinetic behavior between 10 and 30 degrees C. Estimates of the activation energies range from 0.8 to 4. 4 kcal/mol, indicating a low energetic barrier to conformational fluctuations relative to native state proteins. The fluctuations and low energetic barriers may be critical for directing the search for contacts that will result in the transition from the MG state to the native state.

Lactalbumin↗
PubMed1999

Function of the c-Myc oncogenic transcription factor.

The c-myc gene and the expression of the c-Myc protein are frequently altered in human cancers. The c-myc gene encodes the transcription factor c-Myc, which heterodimerizes with a partner protein, termed Max, to regulate gene expression. Max also heterodimerizes with the Mad family of proteins to repress transcription, antagonize c-Myc, and promote cellular differentiation. The constitutive activation of c-myc expression is key to the genesis of many cancers, and hence the understanding of c-Myc function depends on our understanding of its target genes. In this review, we attempt to place the putative target genes of c-Myc in the context of c-Myc-mediated phenotypes. From this perspective, c-Myc emerges as an oncogenic transcription factor that integrates the cell cycle machinery with cell adhesion, cellular metabolism, and the apoptotic pathways.

Basic Helix-Loop-Helix Leucine Zipper Transcriptio↗
PubMed1999

Different upstream transcriptional activators have distinct coactivator requirements.

Activated transcription by RNA polymerase II (Pol II) requires coactivators, one of which is the SRB/mediator. Whereas Srb4, an essential subunit of the SRB/mediator, is broadly required for Pol II transcription in yeast, we have shown that it is dispensable for the transcriptional activation of some genes. Here, we show that transcriptional activation by different natural activators, and by artificial recruitment of various transcription factors, have very different degrees of Srb4 independence. These data, and the analysis of an rgr1 mutant, point to an Rgr1 subcomplex of the SRB/mediator as the mechanistic route of activation by Srb4-independent activators in vivo.

Carrier Proteins↗
PubMed1999

Control of transferrin receptor expression via nitric oxide-mediated modulation of iron-regulatory protein 2.

Cellular iron storage and uptake are coordinately regulated post-transcriptionally by cytoplasmic factors, iron-regulatory proteins 1 and 2 (IRP-1 and IRP-2). When iron in the intracellular transit pool is scarce, IRPs bind to iron-responsive elements (IREs) in the 5'-untranslated region of the ferritin mRNA and 3'-untranslated region of the transferrin receptor (TfR) mRNA. Such binding inhibits translation of ferritin mRNA and stabilizes the mRNA for TfR, whereas the opposite scenario develops when iron in the transit pool is plentiful. However, we (Richardson, D. R., Neumannova, V., Nagy, E., and Ponka, P. (1995) Blood 86, 3211-3219) and others reported that the binding of IRPs to IREs can also be modulated by nitric oxide (NO). In this study, we showed that a short exposure of RAW 264.7 cells (a murine macrophage cell line) to the NO(+) donor, sodium nitroprusside (SNP), caused a significant decrease in IRP-2 binding to the IREs followed by IRP-2 degradation and that these changes occurred without affecting IRP-1 binding. The SNP-mediated degradation of IRP-2 in RAW 264.7 cells could be prevented by MG-132 or lactacystin, known inhibitors of proteasome-dependent protein degradation. A SNP-mediated decrease in IRP-2 binding and levels was associated with a dramatic decrease in TfR mRNA levels and an increase in ferritin synthesis. Importantly, the proteasome inhibitor MG-132 prevented the SNP-mediated decrease in TfR mRNA levels. These observations suggest that IRP-2 can play an important role in controlling transferrin receptor expression.

Animals↗
PubMed1999

Circadian rhythm of motor restlessness and sensory symptoms in the idiopathic restless legs syndrome.

STUDY OBJECTIVES: To determine if motor restlessness in the Restless Legs Syndrome (RLS) shows a circadian rhythm with maximum at night, as previously found for subjective discomfort and periodic limb movements (PLMs), and to correlate RLS peak intensity with the core temperature cycle. DESIGN: Subjects underwent two days of normally timed wakefulness and sleep followed by a night and subsequent day of sleep deprivation. Activity was standardized through modified suggested immobilization tests (mSITs). SETTING: The study was conducted in a laboratory environment with a bedroom equipped for polysomnography during sleep and the mSITs. PATIENTS: Nine patients (mean age 59.8+/-11.3 years [range: 33-72]; 4 males, 5 females) with clinically severe idiopathic RLS. INTERVENTIONS: Patients were monitored with continuous ambulatory activity and core temperature recording. The mSITs were performed every three hours while subjects were awake. During the mSITs, subjective discomfort was measured every 15 minutes while motor restlessness was assessed through activity monitoring. MEASUREMENTS AND RESULTS: Subjective discomfort and motor restlessness increased from a trough in the morning to a maximum at night in the hours following midnight. Peak intensity was found on the falling phase of the core temperature cycle, whose circadian rhythm appeared to be within the normal range for age. CONCLUSIONS: An independent circadian factor modulates the intensity of RLS, which seems to peak on the falling phase of the core temperature cycle. Therefore, the diagnostic criteria that RLS occurs with rest and during the night have independent bases. Furthermore, RLS may be partially controlled by some process or substance whose level varies with the normal circadian rhythm.

Adult↗
PubMed1999

Effect of all-trans-retinoic acid on c-fms proto-oncogene [colony-stimulating factor 1 (CSF-1) receptor] expression and CSF-1-induced invasion and anchorage-independent growth of human breast carcinoma cells.

Abnormal expression of c-fms proto-oncogene, which encodes for the macrophage colony-stimulating factor-1 (CSF-1) receptor, has been observed in a variety of carcinomas of epithelial origin, including those of the breast. Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. We have demonstrated that all-trans-RA (atRA) significantly increases levels of c-fms transcripts in the estrogen receptor-negative but RA receptor alpha-positive breast carcinoma cell lines BT20 and SKBR3. The atRA-induced increase in fms transcript levels was completely abolished by RO41-5253, a synthetic RA receptor alpha antagonist. Our results indicate that atRA could enhance fms expression by up-regulating the activity of the first promoter of the fms gene. DNase I protection, mobility shift, and mutational analysis revealed that a potential activator protein 1 (AP-1) site in the first fms promoter sequence could mediate the observed atRA effect on fms transcription. Our results also showed that atRA, by itself and in the presence of CSF-1, can increase the ability of breast carcinoma cells to invade in vitro. Furthermore, we demonstrated that atRA is able to abolish the CSF-1-induced increase in anchorage-independent growth of breast carcinoma cells without affecting the anchorage-dependent growth. In summary, our findings suggest that retinoids may play conflicting roles throughout breast cancer progression, depending on the stage of cancer development. Although retinoids might suppress growth at the early stages of tumor formation, they might promote malignant transformation at later stages by stimulating the invasive capacity of certain cell variants in the breast tumor population.

Antineoplastic Agents↗
PubMed1999

Activation of monocytes, T-lymphocytes and plasma inflammatory markers in angina patients.

Inflammation and activation of immune cells have important roles in the pathogenesis of atherosclerosis. We analyzed the plasma levels of inflammatory markers and the degree of activation of peripheral blood monocytes and T-lymphocytes isolated from 12 unstable angina, 12 stable angina, and 12 normal subjects. In 20%-33% of patients, monocytes expressed high basal levels of IL-8, tissue factor, IL-1beta, and monocyte chemoattractant protein-1 mRNA. Furthermore, basal mRNA levels of these cytokines showed strong correlation with each other (p < 0.01 in all combination) but not with tumor necrosis factor-alpha or transforming growth factor-beta1. Plasma level of C-reactive protein was highest in the unstable angina patients (1.63+/-0.70 mg/l) and lowest in the control subjects (0.22+/-0.08 mg/l) (P = 0.03). We also observed a high correlation between C-reactive protein level and the occurrence of minor and major coronary events during 6 months of follow-up. Activation status of T-cells, assessed by the percentage of HLA-DR positive cells, was highest in the unstable angina patients (26.8+/-1.4%) compared with that in the control (14.7+/-1.2%) (P = 0.0053). Our data represent the first case showing that the circulating monocytes in angina patients are activated to a state express numerous proatherogenic cytokines. These results may help to diagnose angina patients according to the inflammatory markers and evaluate the prognosis of the disease.

Aged↗
PubMed1999

Overexpression of phospholipase C-gamma1 suppresses UVC-induced apoptosis through inhibition of c-fos accumulation and c-Jun N-terminal kinase activation in PC12 cells.

Ultraviolet-C (UVC) irradiation induces DNA damage and UVC-irradiated cells undergo cell growth arrest to repair the damaged DNA or the induction of apoptosis to prevent the risk of neoplastic transformation. Phospholipase C-gamma1 (PLC-gamma1) is a mediator of growth factor induced-signal cascade, catalyzing the hydrolysis of phosphatidyl 4,5-bisphosphate to generate second messengers, diacylglycerol and inositol 1,4,5-trisphosphate (IP(3)). PLC-gamma1 is activated by phosphorylation of tyrosine residues upon occupation of cell surface receptors by growth factors and plays an important role in controlling cellular proliferation and differentiation. In this study, we found that PLC-gamma1 was tyrosine phosphorylated within 2.5 min after UVC irradiation. To investigate the role of UVC-induced tyrosine phosphorylation of PLC-gamma1, we compared the effect of UVC between PLC-gamma1 overexpressing cells and empty vector transfected cells. Overexpression of PLC-gamma1 inhibited UVC-induced sub-diploid peak and DNA fragmentation. Northern blot analysis revealed that UVC-induced c-fos mRNA accumulation was inhibited in PLC-gamma1 overexpressing cells, while c-jun expression was not affected. In addition, UVC-induced activation of c-Jun N-terminal kinase (JNK) was significantly suppressed in PLC-gamma1 overexpressing cells. These results suggest that PLC-gamma1 may associate with the protective function against the UVC-induced cell death progression via the inhibition of accumulation of c-fos mRNA and the inhibition of JNK kinase activity.

Animals↗
PubMed1999

Engraftment of hematopoietic progenitor cells transduced with the Fanconi anemia group C gene (FANCC).

Fanconi anemia (FA) is an autosomal recessive disorder that leads to aplastic anemia. Mutations in the FANCC gene account for 10-15% of cases. FA cells are abnormally sensitive to DNA-damaging agents such as mitomycin C (MMC). Transfection of normal FANCC into mutant cells corrects this hypersensitivity and improves their viability in vitro. Four FA patients, representing the three major FANCC mutation subgroups, were entered into a clinical trial of gene transduction aimed at correction of the hematopoietic defect. Three patients received three or four cycles of gene transfer, each consisting of one or two infusions of autologous hematopoietic progenitor cells that had been transduced ex vivo with a retroviral vector carrying the normal FANCC gene. Prior to infusion, the FANCC transgene was demonstrated in transduced CD34-enriched progenitor cells. After infusion, FANCC was also present transiently in peripheral blood (PB) and bone marrow (BM) cells. Function of the normal FANCC transgene was suggested by a marked increase in hematopoietic colonies measured by in vitro cultures, including colonies grown in the presence of MMC, after successive gene therapy cycles in all patients. Transient improvement in BM cellularity coincided with this expansion of hematopoietic progenitors. A fourth patient, who received a single infusion of transduced CD34-enriched BM cells, was given radiation therapy for a concurrent gynecologic malignancy. The FANCC transgene was detected in her PB and BM cells only after recovery from radiation-induced aplasia, suggesting that FANCC gene transduction confers a selective engraftment advantage. These experiments highlight both the potential and difficulties in applying gene therapy to FA.

Adolescent↗
PubMed1999

Up-regulation of human telomerase catalytic subunit during gastric carcinogenesis.

BACKGROUND: Telomerase activation is thought to be essential for the stabilization of telomere length, through which immortalization and oncogenesis are achieved, but little is known about the regulation of telomerase in human gastric carcinoma cells. METHODS: A total of 27 primary gastric tumors, 29 cases of intestinal metaplasia, and 30 cases of normal mucosa, as well as 8 gastric carcinoma cell lines, were examined for the relation between telomerase activation and gastric carcinogenesis. Telomerase activity was detected by telomeric repeat amplification protocol, and the expression of each telomerase subunit was evaluated by Northern blot analysis or reverse transcriptase--polymerase chain reaction. RESULTS: Telomerase activity was found in all 8 gastric carcinoma cell lines and in 25 of 27 gastric carcinoma tissue samples (93%), and weakly observed in 11 of 29 gastric intestinal metaplasia samples (38%). None of 30 normal gastric tissue samples displayed telomerase activity. The mRNA expression of human telomerase catalytic subunit (hTERT) was up-regulated in 26 of 26 tumor tissue samples (100%) and in 19 of 24 intestinal metaplasia (79%) in which telomerase activity was weak or negative. Normal gastric mucosa expressed the telomerase gene, albeit at low levels. In contrast to hTERT, human telomerase RNA component and human telomerase-associated protein expression did not parallel telomerase activity, which was independent of tumor stage and histology. CONCLUSIONS: hTERT expression is up-regulated during an early stage in the carcinogenic process, and telomerase activation may be a critical step in gastric carcinogenesis.

Adult↗
PubMed1999

Human immunodeficiency virus type 1 protease inhibitor modulates activation of peripheral blood CD4(+) T cells and decreases their susceptibility to apoptosis in vitro and in vivo.

CD4(+) T cells from patients with human immunodeficiency virus (HIV) infection undergo apoptosis at an increased rate, which leads to their depletion during disease progression. Both the Fas-Receptor (Fas-R) and interleukin-1beta (IL-1beta)-converting enzyme (ICE; caspase 1) appear to play a role in the mechanism of apoptosis of CD4(+) lymphocytes. Although Fas-R is upregulated on both CD4(+) and CD8(+) cells in HIV-infected patients, results from our laboratory and others indicate that, in patients with advanced disease, CD4(+) cells preferentially express ICE. Protease inhibitors have successfully halted the progression of HIV disease and increased CD4(+) T counts. In this study, we examined the effect of protease inhibitors on Fas-R (CD95), ICE (caspase 1) expression, apoptosis, and cell death in CD4(+) T cells of (1) HIV-infected patients who were receiving protease inhibitors, and (2) normal and patient CD4(+) T cells cultured with a protease inhibitor in vitro. Fifteen patients with advanced HIV disease on treatment showed dramatically decreased CD4(+) T-cell ICE expression, diminished apoptosis, and increased numbers of CD4(+) cells within 6 weeks of institution of protease inhibitor therapy, and before down-modulation of Fas-R (CD95) expression was evident. To determine the role of HIV infection, we studied the effect of ritonavir, a protease inhibitor, on normal and patient cells in vitro. Stimulated and unstimulated normal CD4(+) T cells, cultured with protease inhibitor, demonstrated markedly decreased apoptosis and ICE expression (P =. 01). While Fas-R expression was not significantly altered during short-term culture by such treatment, Fas-Ligand (Fas-L) membrane expression of phytohemagglutinin (PHA)-stimulated blood lymphocytes was decreased by protease inhibitor. In the presence of ritonavir, CD4(+) T cells from HIV-infected patients showed similar changes in ICE intracellular levels without alteration of Fas expression. In conclusion, protease inhibitors appear to decrease CD4(+) T-cell ICE expression and apoptosis before they affect Fas-R expression in HIV-infected patients. This action was independent of HIV infection, as similar effects were seen in CD4(+) T cells from normal controls. Some of the benefit of protease inhibitors may be related to modification of programmed cell death, which increases CD4(+) T-cell number. Whether this is due to directly to the changes effected in the caspase system remains to be determined.

Apoptosis↗