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Biomedical subjects

H H Kim

Publications and source records attributed to H H Kim.

At least 55 records · Page 3Linked to original sources

Laparoscopic nephrectomy for nonfunctioning tuberculous kidney.

BACKGROUND AND PURPOSE: Although laparoscopic nephrectomy for benign renal disease has been widely accepted, use of the operation for tubercular pyelonephritic kidney is relatively contraindicated because of difficulties in dissecting the dense fibrotic adhesions and the risk of spillage of caseous materials with subsequent dissemination of the disease. However, with the accumulation of experience, laparoscopic surgery is expanding its applications. In this study, we tried to evaluate the efficacy and safety of the laparoscopic nephrectomy for renal tuberculosis. PATIENTS AND METHODS: At three centers, 13 laparoscopic nephrectomies were performed between April 1996 and March 1999. The patients consisted of eight men and five women with a mean age of 44.8 years (range 37-51 years). All patients had known renal tuberculosis with a nonfunctioning kidney and underwent nephrectomy after at least 3 months of chemotherapy with four antituberculous drugs. Nine patients underwent the transperitoneal approach and four patients, the retroperitoneal approach. The follow-up was from 2 to 35 months with a mean of 15.8 months. RESULTS: Kidneys were removed laparoscopically in 12 patients (92%). The mean operative time was 268 minutes (range 190-500 minutes), and the mean estimated blood loss was 227 mL. Although there had been some difficulties releasing the adhesions, no significant intraoperative and postoperative complications were observed. Conversion to open surgery was needed in only one patient. The mean hospital stay was 4 days, and the patients returned to normal activity within 10 days. Neither local recurrence nor distant dissemination of the disease was observed during the follow-up period. CONCLUSION: Laparoscopic nephrectomy for renal tuberculosis was safe and effective with minor complications. Therefore, tuberculosis should not be a contraindication to a laparoscopic approach.

Adult↗

The value of CT-guided percutaneous needle aspiration in immunocompromised patients with suspected pulmonary infection.

OBJECTIVE: We evaluated the diagnostic efficacy of CT-guided percutaneous needle aspiration in immunocompromised patients with suspected pulmonary infection. SUBJECTS AND METHODS: We reviewed the findings and yields of 24 CT-guided percutaneous needle aspirations in 21 immunocompromised patients. Cytologic evaluation and culture for aerobes, anaerobes, Mycobacterium species, and fungus were performed in all aspirates. RESULTS: We identified one or more etiologic microorganisms in 19 (79.2%) of 24 CT-guided percutaneous needle aspirations. Of 19 aspirates with positive findings, single causal microorganisms were identified in 18. Staphylococcus aureus was found in four aspirates, and Aspergillus fumigatus in seven; these microorganisms were the principal bacterial (4/11) and fungal (7/9) causative organisms. One of the 19 aspirates with positive findings yielded two microorganisms. In the remaining five aspirates, no microorganisms were identified and cytologic examination revealed nonspecific inflammatory cells. No major complications were observed during or after the procedure. CONCLUSION: CT-guided percutaneous needle aspiration is a safe and useful diagnostic method for the identification of specific microorganisms in immunocompromised patients with suspected pulmonary infection.

Adult↗

Activation of c-Jun N-terminal kinase and activator protein 1 by receptor activator of nuclear factor kappaB.

Receptor activator of nuclear factor kappaB (RANK), a lately identified member of the tumor necrosis factor receptor superfamily, plays important roles both in osteoclastogenesis and in lymph node development. Previously, we and others showed that RANK could stimulate the activity of c-Jun N-terminal kinase (JNK). In this study, we investigated the mechanism by which RANK activates JNK. We found that N-terminal deletion mutants of tumor necrosis factor receptor-associated factor 2 and 6 were inhibitory to RANK activation of JNK. The JNK activation by RANK was also reduced by cotransfection of kinase-inactive mutants of apoptosis signal-regulating kinase 1, MAPK/ERK kinase kinase 1, and nuclear factor kappaB-inducing kinase. In addition, dominant negative mutants of Rac and Ras decreased the RANK stimulation of JNK activity. Furthermore, we determined whether the RANK engagement of JNK signaling pathways could lead to the activation of the activator protein 1 (AP-1) transcription factor, one of the potential downstream targets of activated JNK. RANK was found to activate AP-1 in a manner dependent on the signaling molecules involved in the JNK activation by this receptor. Furthermore, the activation of JNK and ERK, but not that of p38, appeared to be involved in the AP-1 activation by RANK. Thus, RANK may use both JNK and ERK pathways to signal to the AP-1 transcription factor.

Animals↗

SKP-450 inhibits migration and DNA synthesis stimulated by oxidized low density lipoprotein in smooth muscle cells.

This study was carried out to examine the inhibitory effects of SKP-450 (2-[2"(1", 3"-dioxolone)-2-methyl]-4-(2'-oxo-1'-pyrrolidinyl)-6-nitro-2H-1-be nzo pyran), a potassium channel opener, on the proliferation and migration stimulated by oxidized low density lipoprotein (LDL) of cultured smooth muscle cells of Wistar Kyoto rat aorta. SKP-450 (10(-7) and 10(-6) M) as well as probucol (10(-7)-10(-5) M) reduced the production of thiobarbituric acid reactive substances from LDL submitted to CuSO(4) (10 microM). The increased [3H]thymidine incorporation and migration (chemotactic and wound-edge) of the cultured smooth muscle cells in association with increased production of platelet-derived growth factor (PDGF)-BB-like immunoreactivity stimulated by oxidized LDL were significantly reduced by SKP-450 (10(-7)-10(-6) M). Inhibition by SKP-450 of the oxidized LDL-stimulated [3H]thymidine incorporation was antagonized by iberiotoxin (10(-7) M), but not by glibenclamide (10(-6) M), suggestive of mediation of Ca(2+)-activated K(+) channel opening in the action of SKP-450. Taken together, SKP-450 inhibited the proliferation and migration of the smooth muscle cells as well as PDGF production stimulated by oxidized LDL, accompanying with its antiperoxidative action.

Animals↗

Receptor activator of NF-kappaB recruits multiple TRAF family adaptors and activates c-Jun N-terminal kinase.

Receptor activator of NF-kappaB (RANK) is a recently cloned member of the tumor necrosis factor receptor (TNFR) superfamily, and its function has been implicated in osteoclast differentiation and dendritic cell survival. Many of the TNFR family receptors recruit various members of the TNF receptor-associated factor (TRAF) family for transduction of their signals to NF-kappaB and c-Jun N-terminal kinase. In this study, the involvement of TRAF family members and the activation of the JNK pathway in signal transduction by RANK were investigated. TRAF1, 2, 3, 5, and 6 were found to bind RANK in vitro. Association of RANK with each of these TRAF proteins was also detected in vivo. Expression of RANK in cultured cells also induced the activation of JNK, which was blocked by a dominant-negative form of JNK. Furthermore, by employing various C-terminal deletion mutants of RANK, the regions responsible for TRAF interaction and JNK activation were identified. TRAF5 was determined to bind to the C-terminal 11 amino acids and the other TRAF members to a region N-terminal to the TRAF5 binding site. The domain responsible for JNK activation was localized to the same region where TRAF1, 2, 3, and 6 bound, which suggests that these TRAF molecules might mediate the RANK-induced JNK activation.

Amino Acid Sequence↗

Characterization of the NF-kappaB activation induced by TR8, an osteoclastogenic tumor necrosis factor receptor family member.

TR8 is a recently identified member of the tumor necrosis factor (TNF) receptor superfamily. TR8 seems to play important roles in bone metabolism as stimulation of this receptor with its ligand, TL8 or osteoclast differentiation factor (ODF), induced the differentiation and activation of osteoclasts. Despite its important biological functions, the biochemical events ensuing from TR8 activation have not been revealed in detail. Most of TNF receptor family proteins provoke the activation of the NF-kappaB transcription factor. In the present study, we examined the signaling potential of TR8 to induce NF-B activation. When overexpressed in a human embryonic kidney cell line by transient transfection, TR8 caused a strong activation of NF-kappaB, which was further increased upon stimulation with TL8. The TR8-induced NF-B activation was abrogated by the co-expression of the TRAF6 mutant lacking the Ring and zinc finger domains and that of the kinase-inactive mutant NIK. Taken together, our study suggests that the presence of intact TRAF6 and the kinase activity of NIK may be essential for TR8 to induce NF-kappaB activation.

Carrier Proteins↗

Altered distribution of Pneumocystis carinii pneumonia during radiation therapy.

The radiographic findings of Pneumocystis carinii pneumonia (PCP) are various. The typical findings are diffuse, bilateral, symmetric, finely granular, or reticular infiltrates. In patients taking aerosol pentamidine, atypical findings may be the first manifestation. One interesting radiologic finding of PCP is that the pneumonia may spare the irradiated lung. We report PCP developed in a patient undergoing irradiation for lung cancer. High-resolution CT revealed diffuse, bilateral, and symmetric ground-glass opacities with septal thickening in both lungs; however, the radiation port was spared and appeared as the "photographic negative of post-radiation pneumonia." The distribution of the pneumonic infiltrates was altered by radiotherapy.

Adenocarcinoma↗

Microsurgical reconstruction of partial thumb defects.

We have reconstructed thumb defects using microsurgical techniques in 43 patients. The flap survival was 100% and functional improvement with near normal appearance was obtained in the reconstructed thumbs. In order to obtain satisfactory results, donor sites were confined to the great toe and its adjacent structures and adventitia was removed from the vascular pedicle, which was transferred by subcutaneous tunnelling to minimize scar formation in the reconstructed thumb. The width of transferred nail and pulp volume were matched to the defect in the thumb before transfer.

Adolescent↗

Electrochemical studies of a truncated laccase produced in Pichia pastoris.

The cDNA that encodes an isoform of laccase from Trametes versicolor (LCCI), as well as a truncated version (LCCIa), was subcloned and expressed by using the yeast Pichia pastoris as the heterologous host. The amino acid sequence of LCCIa is identical to that of LCCI except that the final 11 amino acids at the C terminus of LCCI are replaced with a single cysteine residue. This modification was introduced for the purpose of improving the kinetics of electron transfer between an electrode and the copper-containing active site of laccase. The two laccases (LCCI and LCCIa) are compared in terms of their relative activity with two substrates that have different redox potentials. Results from electrochemical studies on solutions containing LCCI and LCCIa indicate that the redox potential of the active site of LCCIa is shifted to more negative values (411 mV versus normal hydrogen electrode voltage) than that found in other fungal laccases. In addition, replacing the 11 codons at the C terminus of the laccase gene with a single cysteine codon (i.e., LCCI-->LCCIa) influences the rate of heterogeneous electron transfer between an electrode and the copper-containing active site (k(het) for LCCIa = 1.3 x 10(-4) cm s(-1)). These results demonstrate for the first time that the rate of electron transfer between an oxidoreductase and an electrode can be enhanced by changes to the primary structure of a protein via site-directed mutagenesis.

Amino Acid Sequence↗

Metabolism of cAMP to adenosine: role in vasodilation of rat pial artery in response to hypotension.

The purpose of this experiment was to examine whether the cAMP-adenosine pathway is implicated in the autoregulatory vasodilation in response to hypotension. Suffusion with cAMP (1-100 micromol/l) or adenosine (0.01-10 micromol/l) caused a sustained vasodilation of the resting pial arteries in a concentration-dependent manner. In contrast, N6,2'-O-dibutyryl-cAMP and 8-bromo-cAMP exerted a weak dilation at high concentration (100 micromol/l). The vasodilation to cAMP (1-100 micromol/l), adenosine (0.01-10 micromol/l), and hypotension was significantly reduced by pretreatment with 3,7-dimethyl-1-propargylxanthine (1 micromol/l), an A2 receptor antagonist, as well as 3-isobutyl-1-methylxanthine (3 micromol/l), an inhibitor of endo- and ectophosphodiesterase, 1, 3-dipropyl-8-p-sulfophenylxanthine (100 micromol/l), an inhibitor of ecto-5'-phosphodiesterase, or alpha,beta-methylene-adenosine 5'-diphosphate (100 micromol/l), an inhibitor of ecto-5'-nucleotidase. However, 8-cyclopentyltheophylline (1 micromol/l), an A1 antagonist, did not elicit a similar response. The increased release of adenosine when the cortical surface was suffused with cAMP (100 micromol/l) was significantly reduced by 3-isobutyl-1-methylxanthine, 1,3-dipropyl-8-p-sulfophenylxanthine, and alpha,beta-methylene-adenosine 5'-diphosphate (each 100 micromol/l). These results indicate that the cAMP-adenosine pathway as a viable metabolic mechanism is implicated in the production of adenosine in the rat pial artery and contributes to the regulation of vasodilation in response to hypotension.

Adenosine↗

Low dose dobutamine echocardiography in the assessment of contractile reserve to predict the outcome of valve replacement for chronic aortic regurgitation.

BACKGROUND: When to perform surgery for aortic regurgitation is a difficult clinical decision. Occult left ventricular (LV) dysfunction may be present in patients with minimal or no symptoms, and in some patients LV dysfunction may persist after valvular replacement. OBJECTIVES: To examine the role of preoperative low dose dobutamine echocardiography (LDDE) in predicting postoperative outcome in patients who had aortic valve replacement for aortic regurgitation. PATIENTS AND METHODS: The study group comprised 16 patients (15 men, aged 48 +/- 15 years) undergoing elective surgery for aortic regurgitation. Preoperative echocardiograms were obtained in the resting state and during dobutamine infusion at 7.5 micrograms/kg/min. Complete recovery was defined by normalization of LV size and function, and the absence of symptoms at the six-month follow-up visit. Patients with complete recovery (group 1) and without complete recovery (group 2) were compared in relation to their echocardiographic parameters at rest and during LDDE. RESULTS: Of 16 patients in the study, nine were in group 1 and seven were in group 2. Age, functional class and LV end-diastolic dimensions were similar between the two groups. Group 1 patients had a smaller preoperative LV end-systolic dimension index (22.4 +/- 3.3 versus 29.9 +/- 5.9 mm/m2, P < 0.05) and a higher preoperative ejection fraction (53 +/- 8% versus 37 +/- 13%, P < 0.01). Dobutamine infusion augmented the difference in ventricular size and function between patients in group 1 and those in group 2 (LV end-systolic dimension index 18.9 +/- 3.9 mm/m2 versus 28.8 +/- 7.1 mm/m2, P < 0.01; ejection fraction 61 +/- 7% versus 41 +/- 12%, P < 0.01). CONCLUSIONS: Dobutamine accentuates differences in ventricular size and function between those with and without subsequent complete recovery following valve surgery. Because preoperative ejection fraction during LDDE is highly predictive of postoperative ejection fraction, LDDE may have a role in predicting the clinical outcome of patients following aortic valve replacement for aortic regurgitation.

Adult↗

Malignant ectopic thymoma in the neck: a case report.

We report a case of malignant ectopic thymoma in the neck. Contrast-enhanced CT of the neck showed a well-defined inhomogeneously enhancing mass in the left jugulodigastric chain. One year after surgery, the mass had metastasized to the tongue base, and CT of the neck showed an ill-defined densely enhancing mass with lymphadenopathy.

Aged↗

A prospective transesophageal echocardiographic study to assess a new type of left atrial spontaneous contrast at rest and during respiratory manoeuvres.

BACKGROUND: Recent observations suggest that a spontaneous echocardiographic contrast with fast motion (FEC) mimicking intravenous contrast can be seen in the left atrium in the absence of intravenous contrast injection. OBJECTIVE: To assess the incidence of FEC and to evaluate the differentiating features between FEC and injected saline contrast. STUDY DESIGN: Prospective cohort study. SETTING: Tertiary referral centre. PATIENTS AND METHODS: Transesophageal echocardiography was performed in 91 consecutive patients with a mean age of 58+/-15 years. Patients with mechanical valves and congenital heart disease were excluded. Images of the right atrium, left atrium and pulmonary veins were obtained in the absence of an intravenous catheter during quiet respiration, cough and the Valsalva manoeuvre. The same procedure was repeated during injection with agitated saline after venous cannulation. RESULTS: In the absence of intravenous cannulation, FEC was detected in eight patients (9%) during quiet respiration, 36 patients (40%) during cough and 55 patients (60%) during the Valsalva manoeuvre. During the Valsalva manoeuvre, FEC was detected in the right atrium in 41 patients (45%) and in the left atrium in 33 patients (36%) (P=0.15). FEC was not related to a history of embolic event, left atrial smoke or patent foramen ovale. Intra- and interobserver agreements in the detection of FEC were 96% and 90%, respectively. CONCLUSIONS: FEC can be observed frequently in the left atrium during cough or the Valsalva manoeuvre, and awareness of FEC is important to avoid the erroneous diagnosis of patent foramen ovale.

Contrast Media↗

Inhibitory effect of rebamipide on the neutrophil adherence stimulated by conditioned media from Helicobacter pylori-infected gastric epithelial cells.

We investigated the mechanism or mechanisms by which rebamipide protects against the gastric mucosal inflammation associated with Helicobacter pylori. The production of interleukin (IL)-8 in association with expression of IL-8 mRNA was greatly increased in the H. pylori-infected Kato III cells in a concentration- and time-dependent manner, whereas the secretion of IL-6 and tumor necrosis factor-alpha was not detectable. The increased production of IL-8 and expression of IL-8 mRNA were significantly inhibited by rebamipide (100-1000 microM) in a concentration-dependent manner. Formyl-methionyl-leucyl-phenylalanine (1 nM), as well as conditioned medium (CM) that was produced from H. pylori-infected Kato III cells, caused an increase in surface expression of CD11b on human neutrophils and an increase in neutrophil adhesion to the human umbilical vein endothelial cells. Rebamipide also suppressed the adherence of neutrophils to endothelial cells as well as the expression of CD11b on neutrophils induced by formyl-methionyl-leucyl-phenylalanine and CM. Furthermore, CM-induced neutrophil adhesion to the endothelial cells was significantly inhibited by IL-8-neutralizing antibody, suggesting that IL-8 is implicated in the CM-induced neutrophil adhesion to the cultured human umbilical vein endothelial cells. It is concluded that rebamipide exerts its preventive effect against H. pylori-evoked gastric mucosal cell inflammation by inhibition of the neutrophil adherence to the endothelial cells as well as by suppressing the surface expression of CD11b on neutrophils and the production of proinflammatory cytokine such as IL-8 from gastric epithelial cells.

Alanine↗

Effects of the cys mutations on structure and function of the ATP-dependent HslVU protease in Escherichia coli. The Cys287 to Val mutation in HslU uncouples the ATP-dependent proteolysis by HslvU from ATP hydrolysis.

To define the role of the Cys residues in the ATP-dependent HslVU protease, mutagenesis was performed to replace either Cys261 or Cys287 in HslU with Val and Cys159 in HslV with Ser or Ala. Whereas HslU/C261V could hydrolyze ATP and support the ATP-dependent proteolytic activity of HslV as well as the wild-type HslU, HslU/C287V could not hydrolyze ATP. Nevertheless, HslU/C287V could support the HslV-mediated proteolysis by forming the HslVU complex in the presence of ATP but not its absence, indicating that ATP binding but not its hydrolysis is essential for proteolysis. Whereas treatment of N-ethylmaleimide (NEM) resulted in dissociation of the oligomeric HslU into monomers, the C261V mutation, but not C287V, prevented the NEM effect. These results suggest that Cys261 is involved in oligomerization and that Cys287 is related to the ATPase function of HslU. NEM also dissociated the dodecameric HslV into monomers, and this effect could be prevented by either the C159S or C159A mutation, suggesting the involvement of Cys159 in oligomerization of HslV. Moreover, either mutation abolished both the basal and HslU-activated proteolytic activity of HslV and its ability to activate the HslU ATPase and to form the HslVU complex, indicating that Cys159 is essential for the proteolytic activity of HslV and its interaction with HslU. These results suggest that the Cys residues play an important role in maintaining the structure and function of the HslVU protease.

ATP-Dependent Proteases↗

Signal transduction by epidermal growth factor and heregulin via the kinase-deficient ErbB3 protein.

The role of protein tyrosine kinase activity in ErbB3-mediated signal transduction was investigated. ErbB3 was phosphorylated in vivo in response to either heregulin (HRG) in cells expressing both ErbB3 and ErbB2, or epidermal growth factor (EGF) in cells expressing both ErbB3 and EGF receptor. A recombinant receptor protein (ErbB3-K/M, in which K/M stands for Lys-->Met amino acid substitution) containing an inactivating mutation in the putative ATP-binding site was also phosphorylated in response to HRG and EGF. Both the wild-type ErbB3 and mutant ErbB3-K/M proteins transduced signals to phosphatidylinositol 3-kinase, Shc and mitogen-activated protein kinases. Separate kinase-inactivating mutations in the EGF receptor and ErbB2 proteins abolished ErbB3 phosphorylation and signal transduction activated by EGF and HRG respectively. Hence the protein tyrosine kinase activity necessary for growth factor signalling via the ErbB3 protein seems to be provided by coexpressed EGF and ErbB2 receptor proteins.

3T3 Cells↗