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Biomedical subjects

J D Lee

Publications and source records attributed to J D Lee.

At least 109 records · Page 6Linked to original sources
PubMed1998

[Echocardiographic and hematological variables as a risk factor for stroke in chronic nonvalvular atrial fibrillation].

The relationship between echocardiographic variables and the incidence of ischemic stroke in patients with atrial fibrillation was investigated by transthoracic and transesophageal echocardiography in 67 patients with chronic nonvalvular atrial fibrillation. Hematologic variables were also measured simultaneously, including plasma levels of D-dimer and thrombin-antithrombin III complex in these patients. There was a prior history of ischemic stroke in 13 patients (stroke group), but not in the other 54 patients (nonstroke group). There were no significant differences in age, sex, left ventricular ejection fraction, left ventricular end-diastolic diameter, left atrial diameter or hematologic parameters between the groups. The left atrial appendage emptying flow velocity was lower in the stroke group than in the nonstroke group (21 +/- 5 vs 32 +/- 3 cm/sec, p < 0.05), and the incidence of left atrial spontaneous echo contrast was significantly higher in the stroke group than in the nonstroke group (69% vs 26%, p < 0.01). There was no significant difference in the incidence of left atrial thrombi between the groups (23% vs 12%). These findings suggest that transesophageal echocardiographic variables are correlated with the risk of ischemic stroke in patients with chronic nonvalvular atrial fibrillation.

Adult↗
PubMed1998

Lhermitte-Duclos disease: first report in Taiwan.

We report a case of Lhermitte-Duclos disease (dysplastic gangliocytoma of the cerebellum), an uncommon disorder of uncertain pathogenesis characterized by disarrangement of the normal cerebellar laminar cytoarchitecture. A 40-year-old man was admitted because of vomiting and syncope of a few days' duration, and a 2-month history of intermittent headaches and unsteady gait. A computed tomographic scan of the patient's head showed obstructive hydrocephalus due to displacement of the fourth ventricle by a large, nonenhancing cerebellar mass. The magnetic resonance images of the brain also revealed a space-occupying lesion within the right cerebellum with unusual septation. After surgery, the histologic examination confirmed the diagnosis of Lhermitte-Duclos disease. This is the first report of Lhermitte-Duclos disease in Taiwan.

Adult↗
PubMed1998

Crossed cerebellar diaschisis due to intracranial hematoma in basal ganglia or thalamus.

UNLABELLED: The purpose of our study was to evaluate the remote effects on the cerebellum and cerebral cortex from subcortical hematoma without cortical structural abnormality. METHODS: Our study included 23 patients with hematoma, strictly confined either to the basal ganglia (n = 12) or thalamus (n = 11) without cortical abnormality on CT or MRI. Twenty psychiatric patients without structural abnormality on MRI were selected as control subjects. Technetium-ethyl cysteinate dimer brain SPECT was performed in patients and control subjects. Regional cerebral blood flow (rCBF) was visually and semiquantitatively assessed. Asymmetry index (AI) was determined using data from regions of interest at the basal ganglia, thalamus, cerebellum, frontal, parietal and temporal cortex to support the semiquantitative analysis. The criteria for defining hypoperfusion that reflected diaschisis was based on an AI > the mean + 2 s.d. of AI in control subjects. RESULTS: In the basal ganglia hematoma, rCBF was reduced significantly in the contralateral cerebellum (10/12), ipsilateral thalamus (12/12), ipsilateral frontal (6/12), parietal (12/12) and temporal cortex (10/12). As for thalamic hematoma, significantly reduced perfusion was seen in the contralateral cerebellum (10/11), ipsilateral basal ganglia (7/11), ipsilateral frontal (5/11), parietal (11/ 11) and temporal cortex (3/11). CONCLUSION: Crossed cerebellar diaschisis (CCD) and cortical diaschisis frequently were observed in patients with subcortical hematoma without cortical structural abnormality. This suggested that CCD can develop regardless of interruption of the corticopontocerebellar tract, which is the principal pathway of CCD.

Adult↗
PubMed1997

BMK1/ERK5 regulates serum-induced early gene expression through transcription factor MEF2C.

Big MAP kinase 1 (BMK1), also known as ERK5, is a mitogen-activated protein (MAP) kinase member whose biological role is largely undefined. We have shown previously that the activity of BMK1 in rat smooth muscle cells is up-regulated by oxidants. Here, we describe a constitutively active form of the MAP kinase kinase, MEK5(D), which selectively activates BMK1 but not other MAP kinases in vivo. Through utilization of MEK5(D), we have determined that a member of the MEF2 transcription factor family, MEF2C, is a protein substrate of BMK1. BMK1 dramatically enhances the transactivation activity of MEF2C by phosphorylating a serine residue at amino acid position 387 in this transcription factor. Serum is also a potent stimulator of BMK1-induced MEF2C phosphorylation, since a dominant-negative form of BMK1 specifically inhibits serum-induced activation of MEF2C. One consequence of MEF2C activation is increased transcription of the c-jun gene. Taken together, these results strongly suggest that in some cell types the MEK5/BMK1 MAP kinase signaling pathway regulates serum-induced early gene expression through the transcription factor MEF2C.

3T3 Cells↗
PubMed1997

Genetic alterations of p16INK4a and p53 genes in sporadic dysplastic nevus.

It is still unclear whether the sporadic form of dysplastic nevi (SDN) represents a premalignant lesion of malignant melanoma and whether genetic alterations are involved in the development of SDN. To determine whether p16INK4a and p53 genetic abnormalities could be associated with development of SDN, nevus cell nests were procured selectively from H & E-stained slide sections by using a modified microdissection technique and were screened for the presence of mutations and loss of heterozygosity (LOH) of p16INK4a and p53 genes using a polymerase chain reaction-based LOH, single-strand conformation polymorphism, and direct DNA sequencing analyses. Hemizygous deletion was detected in 9 of 12 informative cases (75%) for 9p21-22 (p16INK4a) at one or more loci and 60% (6/10) for 17p13 (p53). As for mutation, we found 3 missense mutations and 1 mutation in the first intron in p16INK4a and 2 missense mutations in p53. Among these mutations in p16INK4a and p53, 5 of 6 mutations were of the C:G to T:A transitional type; this is known to be related to ultraviolet radiation as previously confirmed in other skin cancers. This indicates that p16INK4a and p53 genetic alterations may play an important role in the evolution of SDN and may represent an early event in the development of malignant melanoma. Furthermore, ultraviolet radiation might be the predominant etiologic agent in the development of SDN.

Amino Acid Sequence↗
PubMed1997

c-Src is required for oxidative stress-mediated activation of big mitogen-activated protein kinase 1.

Big mitogen-activated kinase 1 (BMK1) or extracellular signal-regulated kinase-5 (ERK5) has recently been identified as a new member of the mitogen-activated protein kinase family. We have shown that BMK1 is activated to a greater extent by H2O2 than growth factors, suggesting that in comparison with other mitogen-activated protein kinase family members, BMK1 is a redox-sensitive kinase. Previous investigations indicate that the tyrosine kinase c-Src mediates signal transduction by reactive oxygen species, including H2O2. Therefore, the role of Src kinase family members (c-Src and Fyn) in activation of the BMK1 by H2O2 in mouse fibroblasts was studied. An essential role for c-Src was suggested by four experiments. First, H2O2 stimulated c-Src activity rapidly in fibroblasts (peak at 5 min), which preceded peak activity of BMK1 (20 min). Second, specific Src family tyrosine kinase inhibitors (herbimycin A and CP-118,556) blocked BMK1 activation by H2O2 in a concentration-dependent manner. Third, BMK1 activation in the response to H2O2 was completely inhibited in cells derived from mice deficient in c-Src, but not Fyn. Finally, BMK1 activity was much greater in v-Src-transformed NIH-3T3 cells than wild type cells. These results demonstrate an essential role for c-Src in H2O2-mediated activation of BMK1 and suggest that redox-sensitive regulation of BMK1 is a new function for c-Src.

Animals↗
PubMed1997

Phagocytosis of gram-negative bacteria by a unique CD14-dependent mechanism.

THP-1-derived cell lines were stably transfected with constructs encoding glycophosphatidylinositol (GPI)-anchored or transmembrane forms of human CD14. CD14 expression was associated with enhanced phagocytosis of serum (heat-inactivated)-opsonized Escherichia coli (opEc). Both the GPI-anchored and transmembrane forms of CD14 supported phagocytosis of opEc equally well. Lipopolysaccharide-binding protein (LBP) played a role in CD14-dependent phagocytosis as evidenced by inhibition of CD14-dependent phagocytosis of opEc with anti-LBP monoclonal antibody (mAb) and by enhanced phagocytosis of E. coli opsonized with purified LBP. CD14-dependent phagocytosis was inhibited by a phosphatidylinositol (PI) 3-kinase inhibitor (wortmannin) and a protein tyrosine kinase inhibitor (tyrphostin 23) but not a protein kinase C inhibitor (bisindolyl-maleimide) or a divalent cation chelator (ethylenediaminetetraacetate). Anti-LBP mAb 18G4 and anti-CD14 mAb 18E12 were used to differentiate between the pathways involved in CD14-dependent phagocytosis and CD14-dependent cell activation. F(ab')2 fragments of 18G4, a mAb to LBP that does not block cell activation, inhibited ingestion of opEc by THP1-wtCD14 cells. 18E12 (an anti-CD14 mAb that does not block LPS binding to CD14 but does inhibit CD14-dependent cell activation) did not inhibit phagocytosis of LBP-opEc by THP1-wtCD14 cells. Furthermore, CD14-dependent phagocytosis was not inhibited by anti-CD18 (CR3 and CR4 beta-chain) or anti-Fcgamma receptor mAb.

Cell Line↗
PubMed1997

Delayed enhancement of myocardial FDG uptake on glucose loading FDG-PET in NIDDM patient.

We report a case of delayed enhancement of myocardial FDG uptake in NIDDM patient after oral glucose loading. A 65-year-old man who had a past history of NIDDM received FDG-PET examination during fasting and glucose loading. In neither condition, was an accumulation of FDG in the myocardium, and myocardial blood flow was normal. An oral glucose tolerance test (OGTT) was performed to find the best time for FDG injection and 3 hours after loading, the serum insulin concentration was increased significantly. When the interval between glucose loading and the injection of FDG was set at 3 hours, enhancement of myocardial FDG uptake was demonstrated. To know the best time for the FDG injection in advance is thought to be important in obtaining better image quality and interpreting the myocardial viability when FDG-PET examination during glucose loading is performed in NIDDM patients.

Aged↗
PubMed1997

Primary cultured chondrocytes of different origins respond differently to bFGF and TGF-beta.

Responses of rib and ear chondrocytes to basic fibroblast growth factor (bFGF) and transforming growth factor-beta (TGF-beta) were investigated using high density primary culture isolated from the same rabbit. Degrees of tritiated thymidine, leucine, and proline incorporation were used as indicators of DNA, protein and collagen syntheses, respectively. 10 ng/ml bFGF increased thymidine, proline, and leucine incorporation into rib, but not ear, chondrocytes. 1 ng/ml TGF-beta enhanced thymidine incorporation into both chondrocytes but did not affect proline or leucine incorporation into the ear cells. When both growth factors were added simultaneously, both cells showed rises in syntheses of DNA, protein and collagen. Incorporation of [35S]sulfate, used as indicator of proteoglycan synthesis, was elevated by TGF-beta but was reduced by bFGF especially in the rib cells. This inhibitory effect of bFGF was not reversed by cotreatment with TGF-beta in both cell types. Thus, the origin and cellular differentiation states of chondrocytes seem to cause different responses to these growth factors.

Animals↗
PubMed1997

Overexpression of cyclin D1 correlates with early recurrence in superficial bladder cancers.

Cyclin D1 is a cell cycle regulator essential for G1 phase progression and is frequently overexpressed in several human tumour types as a consequence of gene amplification or chromosomal rearrangements. We analysed the expression of cyclin D1 in 75 patients with transitional cell carcinoma (TCC) to investigate the possible relationship between its expression and clinical outcome as well as histopathological findings using the immunohistochemical method. We observed strong staining (++, > 50% positive cells) for cyclin D1 in 19 cases (25.3%) and weak staining (+, 5-50% positive cells) in 19 cases (25.3%). Overexpression of cyclin D1 was not associated with tumour invasion. No significant association was found between overexpression of cyclin D1 and tumour grade (P > 0.05). We assessed the differences of disease-free interval in superficial tumours and actuarial survival probability in invasive tumours according to the status of cyclin D1 expression. Tumours with (++) staining for cyclin D1 recurred much more rapidly than (-) and/or (+) staining tumours (P < 0.01 for - vs ++; P < 0.05 for + vs ++). However, overexpression of cyclin D1 was not associated with a shortened overall survival of patients with invasive tumours (P < 0.1). These results suggest that genetic alteration of cyclin D1 appears to be an early event in the tumorigenesis of bladder TCC and is associated with early recurrence in superficial tumours.

Adult↗
PubMed1997

The small GTPase Cdc42 initiates an apoptotic signaling pathway in Jurkat T lymphocytes.

Apoptosis plays an important role in regulating development and homeostasis of the immune system, yet the elements of the signaling pathways that control cell death have not been well defined. When expressed in Jurkat T cells, an activated form of the small GTPase Cdc42 induces cell death exhibiting the characteristics of apoptosis. The death response induced by Cdc42 is mediated by activation of a protein kinase cascade leading to stimulation of c-Jun amino terminal kinase (JNK). Apoptosis initiated by Cdc42 is inhibited by dominant negative components of the JNK cascade and by reagents that block activity of the ICE protease (caspase) family, suggesting that stimulation of the JNK kinase cascade can lead to caspase activation. The sequence of morphological events observed typically in apoptotic cells is modified in the presence of activated Cdc42, suggesting that this GTPase may account for some aspects of cytoskeletal regulation during the apoptotic program. These data suggest a means through which the biochemical and morphological events occurring during apoptosis may be coordinately regulated.

Apoptosis↗
PubMed1997

Atomic force microscope analysis of chromatin volumes in human sperm with head-shape abnormalities.

We used the atomic force microscope to perform volume measurements on individual human sperm nuclei under ambient conditions. Data obtained for normal sperm and for sperm from seven of the nine classes of head-shape abnormality revealed that the nuclear volumes were essentially identical for sperm in each headshape class, even though the projected areas and shapes of the nuclei have were shown to vary widely. These results indicate that the abnormal sperm head morphologies found at a rate of 25-40% in fertile males are not caused by factors that affect the volume of sperm chromatin, such as the DNA content of the sperm nucleus, differences in chromatin organization, or the extent of DNA compaction.

Cell Nucleus↗
PubMed1997

Sequential Tc-99m MDP bone scans after cementless total hip arthroplasty in asymptomatic patients.

PURPOSE: To evaluate the distribution and degree of radioactivity on sequential Tc-99m methylene diphosphonate (Tc-99m MDP) scans in the diagnosis of postoperative loosening in asymptomatic patients who underwent cementless total hip replacement. MATERIAL AND METHODS: Tc-99m MDP scans were obtained every three months where possible, for one year in those patients who underwent total hip replacement using a Harris Galante cementless prosthesis. Eighty-three scans from 45 patients were obtained. Uptake was assessed within the five periprosthetic zones (zone 1: greater trochanter; 2: lateral stem of the prosthesis; 3: tip of the prosthesis; 4: medial stem of the prosthesis; and 5: lesser trochanter) using an arbitrary 5-point grading system. Grade 1 indicated normal uptake and Grade 5 indicated highest uptake. The grade of uptake within each zone was then analyzed against their postoperative ages. RESULTS: The radioactivity regressed to Grade 1 or 2 from Grade 4 or 5 within 12 months after cementless total hip replacement in 87.5% and 93.8% of patients in zones 2 and 4, respectively. Even though the radioactivity within zones 1, 3, and 5 tended to decrease, persistent elevation of activity (over grade 2) lasted up to 12 months after surgery in 31% or 37% of the patients. CONCLUSION: The radioactivity after cementless total hip replacement tended to regress in proportion to the postimplant age. The regression rate varied depending on the periprosthetic zones.

Bone Cements↗