Search PubMed⌕ Search

Biomedical subjects

H D Kim

Publications and source records attributed to H D Kim.

At least 91 records · Page 5Linked to original sources
PubMed1996

Thin-section CT findings of the lungs: experimentally induced bronchial and pulmonary artery obstruction in pigs.

OBJECTIVE: The purpose of this study was to investigate whether a mosaic pattern of lung attenuation, or lobular low attenuation, is revealed on CT imaging after induction of bronchial and pulmonary artery obstruction in pigs. MATERIALS AND METHODS: Eight anesthetized and ventilated pigs, four for bronchial obstruction and four for pulmonary artery obstruction, were examined with thin-section CT. Bronchial obstruction was induced at the subsegmental level using 2- to 3-mm radiopaque silicon spheres at 14 sites. Pulmonary artery obstruction was induced at 11 sites by dislodging 2- to 3-mm silicon spheres at the level of the superior vena cava. CT scans were obtained at end expiration immediately after the obstruction in all pigs (n = 8) and after 1 day (n = 3), 3 days (n = 5), 7 days (n = 4), 14 days (n = 4), and 28 days (n = 3). RESULTS: Of the 14 sites of bronchial obstruction, six sites (43%) on the immediate scans showed a lobular distribution of low attenuation distal to the spheres, which changed to atelectasis, consolidation, or normal on follow-up CT. Of the four sites that did not show changes in lung attenuation on immediate CT scans, two sites showed lobular low attenuation after 1 day. The mean attenuation value +/- SD for the lobular low attenuation was -737 H +/- 122 and that of the adjacent lung was -522 H +/- 53 (p = .0077). None of the pulmonary artery obstruction sites showed visible change in lung attenuation, and mean attenuation values for obstructed sites and unobstructed sites did not show significant differences when scanned as many as 28 days after the immediate scans. CONCLUSION: Lobular low attenuation on thin-section CT was induced by bronchial obstruction, but we found no change in lung attenuation due to obstruction of the pulmonary arteries as many as 28 days after the immediate scans.

Animals↗
PubMed1995

Controlled release of platelet-derived growth factor using ethylene vinyl acetate copolymer (EVAc) coated on stainless-steel wires.

Controlled delivery of bioactive molecules to modulate or control biological processes has a number of clinical applications. The present study reports a delivery system which was designed to deliver growth factors locally to a fracture site. Ethylene vinyl acetate copolymer (EVAc), bovine serum albumin (BSA) and platelet-derived growth factor (PDGF-BB) were combined and coated onto a stainless-steel Kirschner wire (K-wire). A K-wire can be used as an intramedullary nail in small animal fractures, such as the rat. PDGF-BB stimulates thymidine uptake in human bone cell cultures when released from the K-wire delivery system. BSA release was modified by providing a final coating on the K-wire of 10% pure EVAc at the end of the fabrication. Electron microscopic examination of the surface of the rods revealed different surface pores on the K-wires coated with pure EVAc. Differences in porosity and tortuosity may account, in part, for the different release kinetics observed.

Animals↗
PubMed1995

Doppler sonography in experimentally induced acute renal failure in rabbits. Resistive index versus serum creatinine levels.

RATIONALE AND OBJECTIVES: The purpose of this study is to investigate the temporal relation between the change in the resistive index (RI) from renal Doppler sonography and that of serum creatinine values in the course of experimentally induced reversible acute renal failure (ARF) in rabbits. METHODS: Reversible ARF was induced in 10 New Zealand white rabbits by injecting a glycerol solution (6.0 mL/kg) into the thigh muscle. Doppler sonography was performed before injection, and 6, 12, and 24 hours, and 3, 5, 7, and 14 days after injection of glycerol. Blood samples for measuring serum creatinine levels were obtained in the same time sequence. Three rabbits, which died during the course of the experiment, were excluded from the study group. RESULTS: The RI elevated rapidly after glycerol injection, peaked at 12 hours, and then decreased to normal values by 7 days. Conversely, serum creatinine values were elevated and peaked at 1 day and then decreased to normal by 14 days. The change in the RI preceded the change in serum creatinine levels in the course of reversible ARF. There was a weak linear correlation between RI and serum creatinine levels, with a correlation coefficient of 0.33. CONCLUSION: Doppler sonography with measurement of resistive index may be useful in predicting the course of ARF.

Acute Kidney Injury↗
PubMed1995

Relation between ischemic preconditioning and the duration of sustained ischemia.

It has been reported that repetitive brief periods of ischemia and reperfusion (ischemic preconditioning, IP) cause a significant reduction in the extent of myocardial necrosis or in the incidence of reperfusion arrhythmias in rat heart. However, recent reports have stated that IP effect is diminished or lost in the canine or bovine heart if ischemia (mostly regional) is sustained for 40 min or longer. The main objective of this study is to assess whether IP provides myocardial protection in prolonged sustained ischemia under the condition of global ischemia in isolated rabbit heart. The hearts were subjected to 10-60 min sustained ischemia (SI) followed by 60 min reperfusion with (IP heart) or without IP (ISCH heart). IP was induced by 4 cycles of 5 min global ischemia and 5 min reperfusion. Left ventricular function (LVF), extent of infarction (EI) and ultrastructural changes were examined. As a whole, the LVF began to recover on reperfusion but there was no significant difference in the functional parameters. However, extracellular Ca2+ concentration was lower in the ISCH hearts (p < 0.05) and the EI was significantly different between the hearts which had received 60 min SI (67% in the ISCH versus 32% in the IP heart, p < 0.01). Ultrastructural changes were homogeneous in the ISCH hearts and became irreversible in accordance with increase of the duration of ischemia, while these changes were heterogeneous and restricted in the IP heart. These results suggest that IP does not attenuate the postischemic dysfunction in prolonged ischemia but it can provide an infarct size-limiting effect and delay ultrastructural changes. This cardioprotective effect may be related to calcium homeostasis.

Animals↗
PubMed1995

Intracellular Ca2+ pool depletion is linked to the induction of nitric oxide synthesis in murine peritoneal macrophages.

The ability of putative Ca(2+)-ATPase inhibitor of endoplasmic reticulum (ER), thapsigargin (TG), to induce nitric oxide (NO) synthesis in murine peritoneal macrophages was examined. TG alone had small effect on NO synthesis, whereas TG in combination with LPS markedly increased NO synthesis in a dose dependent manner. This increase in NO synthesis was reflected as increased amount of inducible NO synthase (iNOS) mRNA by Northern blotting. In addition, the ability of TG on NO synthesis could be mimicked by another chemically unrelated inhibitor of Ca(2+)-ATPase, 2,5-DI-(t-butyl)-1, 4-benzohydroquinone (tBuBHQ). Adding EGTA, a calcium chelator, to the incubation medium significantly reduced the ability of macrophages to induce NO synthesis in response to the optimal stimulation of TG or TG plus LPS. These results therefore demonstrate that intracellular Ca2+ pool depletion is linked to the induction of NO synthesis in murine peritoneal macrophages and further suggest that it is also related with interferon-gamma (IFN-gamma)-induced signaling.

Animals↗
PubMed1994

Quantitative study on the relation between structural and functional properties of the hearts from three different mammals.

The ultrastructural quantitative composition of left ventricular cardiac myocytes from isolated Langendorff-perfused hearts was studied in three different mammals (rabbit, guinea pig, and rat). Volume densities of mitochondria, myofibrils, and unspecified cytoplasm were determined using morphometry and were compared to functional parameters including left ventricular developed pressure (LVDP), contractility (dP/dt), heart rate, TTI (tension-time index, an index of oxygen consumption), and relative heart mass (H/B) obtained from these hearts. Each of the mammals was found to possess a very specific and characteristic quantitative composition of cardiac myocyte. Cardiac myocytes contained 26.8% mitochondria and 56.3% myofibrils in rabbits, 25.8% mitochondria and 60.9% myofibrils in guinea pigs, and 27.7% mitochondria and 58.1% myofibrils in rats. The LVDP, contractility, heart rate, and TTI were quite different among species. However, there were close correlations between the mitochondrial volume density and the LVDP (p < 0.05), and between the mitochondrial volume density and the TTI (p < 0.05), in any group of the animals. It is concluded that the mitochondrial volume density is a good indirect indicator of function of cardiac muscle related to oxidative capacity.

Animals↗
PubMed1994

Human osteoblast response to PTFE surfaces.

Recently, expanded polytetrafluoroethylene (ePTFE, Gortex) vascular grafts have been rolled and used for interpositional arthroplasties of the carpus in the wrist. Little data, however, are available on the response of human osteoblasts to ePTFE. In-vitro cell culture is a useful method to determine initial cell-biomaterial interactions. The present study explores the morphological and mitogenic response of human bone cells cultured on vascular grade ePTFE grafts. The present findings suggest that neither the inner nor the outer surface of ePTFE, in its present form, support osteoblast growth. PTFE may be a suitable material to act as a space filler for carpal bone interpositional arthroplasties.

Arthroplasty↗
PubMed1994

Contrast enhancement of brain tumors at different MR field strengths: comparison of 0.5 T and 2.0 T.

PURPOSE: To compare the degree of MR contrast enhancement of 0.5 T and 2.0 T in various brain tumors. METHODS: MR images were studied prospectively in each of 31 patients with brain tumors (11 gliomas, 6 meningiomas, 6 neurinomas, and 8 others) before and after intravenous injection of gadopentetate dimeglumine. In every patient, both 0.5-T and 2.0-T MR studies were done within 1 week. Each patient received an initial standard dose (0.1 mmol/kg) of gadopentetate dimeglumine, followed by a subsequent 0.1-mmol/kg dose (total, double dose) in MR of each field strength. MR was done before and after each injection of the contrast agent. Degree of contrast enhancement in the lesions was assessed both visually and quantitatively. RESULTS: With standard-dose study, the tumor enhancement was visually stronger at 2.0 T than at 0.5 T in 9 gliomas. In extraaxial tumors there was visually no or minimal difference between 0.5 T and 2.0 T. Overall mean contrast-enhancement ratio and tumor and brain contrast-to-noise ratio were higher at 2.0 T than at 0.5 T by 53% and 108%, respectively. The double-dose study showed higher contrast-enhancement ratio and contrast-to-noise ratio than the standard-dose study at both field strengths, and the differences between 0.5 T and 2.0 T were almost similar to those of the standard-dose study. The degree of contrast enhancement with the standard dose at 2.0 T was comparable to that of the double dose at 0.5 T in most intraaxial tumors. CONCLUSION: The results suggest that effect of contrast enhancement increases with the field strength. Therefore, reevaluation of optimal doses of contrast media may be needed in a variety of brain lesions at each field strength.

Adolescent↗
PubMed1993

Rapid induction of mouse virus-like (VL30) element transcripts by erythropoietin in murine erythroid progenitor cells.

We examined the activation of genes induced by erythropoietin (Epo) in erythroid progenitor cells that were isolated from the spleens of mice infected with anemia-inducing strain of the Friend virus. These erythroid progenitor cells, termed FVA cells, undergo in vitro differentiation to erythrocytes under the influence of Epo within 2 to 3 days. We used a differential hybridization procedure to screen a cDNA library constructed from FVA cells that were treated with Epo 2U/mL in the absence of serum for 2 hours. Of 20,000 recombinant phages, 47 plaques hybridized preferentially to cDNA probe prepared from Epo-stimulated cells. We found at least three different Epo-responsive genes (ERGs) and one of them corresponds to the mouse virus-like (VL30) element, similar to already reported BVL-1. The induction of VL30, which was evident within 30 minutes after Epo exposure, reached a maximum by 1 hour and remained stable for up to 4 hours. The treatment of FVA cells with cycloheximide (CHX) 10 micrograms/mL, which in itself activates the expression of VL30 caused a superinduction of the Epo signal. Changes in intracellular Ca2+ concentrations, either raised by ionomycin or depleted by EGTA, had no effect on the Epo-induced VL30 expression. In addition, protein kinase C (PKC) inhibitors such as staurosporine (3 mumol/L) or H7 (20 mumol/L) and a tyrosine kinase inhibitor, genistein (200 mumol/L), did not inhibit the Epo-induced expression of VL30. TPA (100 ng/mL), a PKC agonist, did not induce VL30 expression. Although the physiologic role of VL30 in the differentiation of erythroid progenitor cells is not known, our findings demonstrate that VL30 is an early ERG, and may be a useful indicator of the initial molecular actions of Epo.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Manganese exposure to PC-12 cells alters triacylglycerol metabolism and promotes neurite outgrowth.

Exposure of PC-12 cells to MnCl2 (10-100 microM for 1 to 3 days) resulted in both morphological and metabolic changes as indicated by promotion of neurite outgrowth and an increased incorporation of labeled fatty acids (14:0, 18:1 and 20:4) into triacylglycerols (TG). Cells prelabeled with [14C]arachidonic acid (AA) showed a time-dependent decrease in labeled TG, and the rate of decline was inhibited by Mn (100 microM). In the pulse-chase type of study, the decrease in the proportion of labeled TG as well as labeled phosphatidylcholine (PC) was marked by an increase in labeled phosphatidylinositol and phosphatidylethanolamine. These results support previous notion that TG plays an important role in channeling the fatty acid nutrients for biosynthesis of membrane phospholipids. Thus, the Mn-induced inhibition of the ability to transfer TG fatty acids to other lipids in PC-12 cells may be an underlying cause for the observed morphological changes.

Animals↗
PubMed1992

Human fetal heart development after mid-term: morphometry and ultrastructural study.

A total of 44 normally developed human fetal hearts aged from 17 to 40 weeks gestation were provided for routine ultrastructural and morphometric studies. For morphometric analysis, the maximal thicknesses of the anterior, lateral and posterior wall of both ventricles and that of interventricular septum were measured and the left-to-right thickness ratios calculated. The cross-sectional areas of both ventricles in the plane of the greatest heart diameter were measured with computerized image analysis system. Data were analyzed using linear regression and one-way analysis of variance. Myofibril formation occurred by attachment of thin filaments into amorphous Z materials which were presented in sarcolemmal plaques, sarcoplasmic condensations, desmosomes and in Z lines. From these Z centers, myofibrils radiated many directions and branched and anastomosed with further development. This pattern of myofibrillar development continued throughout the whole fetal period. A transverse tubule system was clearly evident in later fetal development. It occurred by invagination of sarcolemma into myocardial cells and formation of subsarcolemmal caveolae. Mitochondria, well-developed Golgi complexes, glycogen granules and well-developed microvessels were found throughout the whole fetal period. Binucleated myocytes appeared by 32 weeks gestation and this suggests that myocyte hyperplasia may cease before birth in humans. The growth of both ventricular walls, the interventricular septum and that of both ventricular cross-sectional areas showed linear regression, and the left-to-right wall thickness ratios were nearly constant. Also, there were no differences in morphometric data between the left and right ventricles. In conclusion, development of the myocyte is an ongoing process which may be continued in the post-natal period in humans, and our statistical results do not support the theory of the right ventricular dominance during the fetal period.

Cell Differentiation↗
PubMed1991

Metabolic adaptation during erythropoietin-mediated terminal differentiation of mouse erythroid cells.

Metabolic development was examined in erythroid precursor cells, which were isolated from the spleens of mice infected with the anemia-inducing strain of Friend virus (FVA cells). FVA cells undergo differentiation in vitro from the proerythroblast stage through the reticulocyte stage over a 48-hour period in the presence of erythropoietin. Concomitant with marked decreases in cellular size and energy demand, metabolic capacities of both glycolysis and oxygen consumption diminish after 48 hours in culture by 7- and 18-fold, respectively. Because the oxidative capacity decreases more than glycolytic ability does, the metabolic machinery increasingly shifts toward anaerobic metabolism. During the 48-hour period of differentiation, the 2,3-diphosphoglyceric acid (DPG) content per cell and 2,3-DPG mutase activity per cell increased eightfold and threefold, respectively. Freshly harvested FVA cells have adenosine triphosphate (ATP) levels of 7.23 +/- 2.52 mumol/10(10) cells or 3.76 +/- 1.31 mumol/mL cell water which are 12- or 2.3-fold higher, respectively, than the ATP levels of mature red blood cells. In the course of FVA cell differentiation, ATP content per cell decreases by fourfold, but ATP concentration in cell water remains unchanged because of a corresponding decrease in cellular size and water content during differentiation. These studies show that in the face of dramatic decreases in cell size and cellular energy demand, terminally differentiating erythroid cells maintain a constant ATP level by undergoing an involution of their glycolytic machinery as well as by losing their aerobic metabolic capacity.

2,3-Diphosphoglycerate↗
PubMed1991

Effects of adenosine receptor agonists on volume-activated ion transport in pig red cells.

Swelling of pig red cells leads to an increase in a chloride-dependent K flux which can be potentiated by cAMP, whereas cell shrinking causes a selective increase in Na movement which is mediated by a Na/H exchanger. We examined the influence of adenosine and adenosine receptor agonists on the volume-sensitive, ouabain-resistant, chloride-dependent K flux, referred to as Rb flux and volume-activated Na/H exchange pathway. It was found that adenosine and adenosine receptor agonists inhibited the Rb flux. N6-cyclohexyl adenosine (CHA) has been found to be the most potent inhibitor with EC50 of approximately 4.5 microM followed by 2-chloroadenosine (Cl-ado) with EC50 of approximately 27 microM and 5'-(N-ethyl)-carboxamido-adenosine (NECA) with EC50 of approximately 185 microM. CHA also inhibits the cAMP-stimulated Rb flux. However, CHA does not alter the basal intracellular cAMP level nor the intracellular cAMP content raised by exogenously added cAMP. In contrast to the adenosine agonist action on the Rb flux, Na/H exchange, which is activated upon cell shrinkage, exhibits a slight stimulation in response to CHA. These findings suggest that the presence of A1 adenosine receptors on the surface of red cells influences the regulation of volume-activated ion transport.

2-Chloroadenosine↗
PubMed1991

Regulation of calcium-activated potassium efflux by neurotensin and other agents in HT-29 cells.

Neurotensin receptors have been shown previously to be coupled to polyphosphoinositide turnover and intracellular Ca2+ ([Ca2+]i) mobilization in HT-29 colonic epithelial cells (Bozou et al. Biochem. J. 264: 871, 1989; Turner et al. J. Pharmacol. Exp. Ther. 253: 1049, 1990). In this study, neurotensin was found to enhance dramatically the Ba2(+)- and tetraethylammonium chloride-sensitive K(+)-efflux rate (measured with 86Rb+) in the presence of ouabain and bumetanide, with basal efflux increasing 4.5 +/- 0.5-fold with 10 nM neurotensin. The K(+)-efflux rate, which was partially dependent on the extracellular Ca2+ concentration, was also increased by carbachol and ATP, two other [Ca2+]i-mobilizing agonists in HT-29 cells, as well as by the Ca2+ ionophores ionomycin and A23187, suggesting that the efflux was through Ca2(+)-activated K+ channels. Pretreatment of cells with neurotensin, carbachol, or ATP desensitized subsequent neurotensin-stimulated efflux by 82, 57, and 63%, respectively, confirming our previous results which indicated homologous and heterologous desensitization of the neurotensin receptor-signal transduction pathway. Pretreatment of cells with the protein kinase C activators phorbol 12-myristate 13-acetate (PMA) and mezerein did not affect [Ca2+]i mobilization or K+ efflux directly but desensitized neurotensin-stimulated efflux by greater than 80%. Pretreatment (2 h) with PMA also decreased K+ efflux in response to ionomycin by 59%, although ionomycin-induced [Ca2+]i mobilization was not inhibited. Downregulation of protein kinase C by overnight pretreatment with PMA resulted in recovery of ionomycin-stimulated efflux. These results suggest that agonist-stimulated Ca2(+)-activated K+ channels in HT-29 cells are regulated at multiple steps in the signal transduction pathway.

Adenocarcinoma↗
PubMed1991

Myocardial glucose utilization. Failure of adenosine to alter it and inhibition by the adenosine analogue N6-(L-2-phenylisopropyl)adenosine.

The effects of adenosine and the nonmetabolizable adenosine analogue N6-(L-2-phenylisopropyl)adenosine (PIA) on glucose transport or metabolism were determined in purified myocardial sarcolemmal vesicles, isolated cardiocytes, and perfused hearts. Adenosine (100 microM) did not affect hexose transport in myocytes. Also, adenosine deaminase, added to metabolize adenosine to inosine, did not alter transport of hexose into myocytes regardless of whether or not insulin was present. In contrast, PIA effectively inhibited 3-O-methyl-D-glucose uptake in myocytes even during insulin stimulation. PIA inhibited D-glucose-specific transport in both rat and bovine cardiac sarcolemmal vesicles (Ki = 26 microM at [D-glucose] = 5 mM). However, insulin did not affect glucose transport in sarcolemmal vesicles, which implies that receptor-coupled processes probably are not intact in this preparation. Thus, inhibition of PIA may not be receptor mediated. Also, PIA inhibited binding of cytochalasin B to bovine cardiac sarcolemmal vesicles, which supports the idea that PIA inhibits glucose flux by binding to the glucose transporter. To determine if adenosine altered glucose metabolism rather than transport, we measured the rate of 3H2O production from metabolism of D-[2-3H]glucose in paced rat hearts ([D-glucose] = 5.5 mM, [pyruvate] = 0.2 mM) perfused with a range of PIA or adenosine concentrations with or without 0.01 microM insulin. Adenosine (0.01-100 microM) in the presence or absence of insulin increased coronary flow but did not change glycolytic rates. Similar results were obtained with PIA (no insulin) rather than adenosine in the perfusate. However, with glucose as the only exogenous substrate, 100 microM PIA inhibited glycolysis by approximately 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Is adenosine a second metabolic substrate for human red blood cells?

Adenosine is present in the micromolar range in human plasma. In this study, metabolism of adenosine, which was maintained between 0.62 +/- 0.03 and 2.92 +/- 0.43 microM by means of a continuous infusion using a Harvard infusion pump, was investigated in human red blood cells. It was found that lactate production increases linearly as the adenosine concentration was raised. Cells infused with an average adenosine concentration of 2 microM produced lactate comparable to that produced by 5 mM glucose. The extent to which ATP concentration is maintained by adenosine also depends on its concentration. After a 4 h infusion with an average adenosine concentration of 0.7 microM, ATP content amounts to 75% of the glucose control. Raising the adenosine infusion concentration to 1.5 microM results in a full maintenance of ATP levels and at concentrations higher than 1.5 microM, adenosine produces a net synthesis of ATP. A net synthesis of ATP also occurs with adenosine concentration below 1.5 microM, if supplemented with glucose. In contrast, inosine infusion provides only a partial support of ATP and fails to produce a net synthesis of ATP in the presence of glucose. In addition, the presence of purine nucleoside and glucose together influence the metabolism of each other, depending on inorganic phosphate content (Pi). At a Pi concentration of 1 mM, the glucose consumption rate is reduced by approx. 25% by purine nucleoside infusion and vice versa. In sharp contrast, glucose consumption at 16 mM Pi is potentiated by adenosine. These findings suggest that plasma adenosine contributes significantly to human red cell energetics, even though it is present at a concentration several orders of magnitude lower than glucose.

Adenosine↗