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Biomedical subjects

H C Kim

Publications and source records attributed to H C Kim.

At least 271 records · Page 15Linked to original sources
PubMed1990

A moving-actuator type electromechanical total artificial heart--Part II: Circular type and animal experiment.

A new type of electromechanical total artificial heart (TAH) based on circular rolling-cylinder mechanism was developed to overcome critical problems in motor-driven artificial hearts such as large size and difficulties in fitting the heart to atrial remnants and arterial vessels. Its performance and reliability were evaluated in mock circulation and in an animal implant experiment. The total weight and volume of the pump is 650 g and 600 mL, respectively. This new pump was implanted in a calf for total heart replacement and 96 h of survival was achieved. The whole system, including pump, controller, and control algorithm performed well enough to improve the prospect of eventual clinical application of our TAH system.

Animals↗
PubMed1990

Clinical experience of a new monoclonal antibody purified factor IX: half-life, recovery, and safety in patients with hemophilia B.

Highly purified factor IX, produced by a monoclonal antibody immunoaffinity technique, contains a high concentration of factor IX with negligible amounts of other vitamin K-dependent coagulation factors. When infused in patients with hemophilia B, monoclonal factor IX concentrate yielded a mean half-life of 34.6 +/- 13.1 (+/- SD) hours and in vivo recovery of 0.67 +/- 0.14 U/dL rise per each U/kg of factor IX infused. Unlike prothrombin complex concentrate (PCC) infusion, monoclonal IX infusion was not associated with rises in factors II, VII, and X, but achieved in vivo recovery and half-life at least comparable to PCC. Long-term use of monoclonal IX as a home-care product provided excellent response in the control of bleeding episodes and was equivalent to previous patient experience with PCC. The results indicate that monoclonal IX concentrate raises factor IX levels effectively, while avoiding extraneous thrombogenic components.

Adult↗
PubMed1989

Binding of tissue plasminogen activator to vascular grafts.

Tissue plasminogen activator labeled with radioactive iodine (125I-tPA) was immobilized on vascular prostheses chemically modified with a thin coating of water-insoluble surfactant, tridodecylmethylammonium chloride (TDMAC). Surfactant-treated Dacron, polytetrafluoroethylene (PTFE), silastic, polyethylene and polyurethane bound appreciable amounts of 125I-tPA (5-30 micrograms 125I-tPA/cm2). Upon exposure to human plasma, the amount of 125I-tPA bound to the surface shows an initial drop during the first hour of incubation, followed by a slower, roughly exponential release with a t 1/2 of approximately 75 hours. Prostheses containing bound tPA show fibrinolytic activity as measured both by lysis of clots formed in vitro, and by hydrolysis of a synthetic polypeptide substrate. Prior to incubation in plasma, tPA bound to a polymer surface has an enzymic activity similar, if not identical to that of the native enzyme in buffered solution. However, exposure to plasma causes a decrease in the fibrinolytic activity of both bound tPA and enzyme released from the surface of the polymer. These data demonstrate that surfactant-treated prostheses can bind tPA, and that these chemically modified devices can act as a slow-release drug delivery system with the potential for reducing prosthesis-induced thromboembolism.

Antigens↗
PubMed1989

Plasma cell malignancy in the acquired immune deficiency syndrome. Association with Epstein-Barr virus.

The development of high-grade, malignant B-cell lymphoma is a well-recognized complication of human immunodeficiency virus (HIV) infection. Plasma cell neoplasms, however, have been rarely encountered in HIV-infected people. This study presents the morphologic and immunologic features of an unusual plasma cell tumor occurring in a 31-year-old HIV-antibody-positive male. The malignancy was characterized by widespread dissemination and hypercalcemia at presentation and a clinically aggressive course. Immunoperoxidase staining of tumor tissue obtained from biopsy and at autopsy had positive results for IgM and lambda. In the patient's serum, only an IgG kappa paraprotein was detected, indicating that the tumor was nonsecretory. DNA analysis of autopsy-derived tumor tissues demonstrated clonal rearrangements of the immunoglobulin (Ig) heavy chain gene locus and rearrangements in both kappa and lambda light chain gene loci. Furthermore, DNA hybridization studies revealed the presence of Epstein-Barr virus (EBV) genomes in tumor tissue but not in nontumor tissue from this patient.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Differentiation of bone and bone marrow infarcts from osteomyelitis in sickle cell disorders.

To determine whether imaging techniques can differentiate osteomyelitis from bone infarction in sickle cell disorders, 39 sets of bone scans (BS) and bone marrow scans (BMS) were performed on 31 patients with sickling disorders and bone pain. In addition, three patients who had either a BS or a BMS were included. Results were analyzed according to whether scans were performed three days or less (Period 1), four to six days (Period 2), or seven or more days (Period 3) after the onset of pain. Regardless of the period, all but five BMS for 34 episodes of assumed infarction showed decreased uptake. BS findings varied depending on the time interval, with none of the ten in Period 1 showing increased uptake, but all 11 in Period 3 showing increased uptake. However, in Period 2, about half of the 13 BS showed increased uptake. All three patients with osteomyelitis in Period 3 had increased uptake on BS. The BMS done in one of these patients showed decreased uptake. Three patients with cellulitis had normal BS and BMS. One patient with septic arthritis had normal BMS, but slightly increased uptake on BS. Although typical imaging patterns are present in early and late infarction (Periods 1 and 3), the patterns for late infarction may not differ from those of advanced osteomyelitis. Therefore, imaging studies are only of value in differentiating infarction from osteomyelitis when both BS and BMS are performed soon after the appearance of symptoms.

Adolescent↗
PubMed1989

Transglutaminase expression in rat parotid gland after isoproterenol stimulation.

Transglutaminases (E.C. 2.3.2.13) are calcium-dependent enzymes that catalyze the covalent cross-linking of proteins, and occur in multiple molecular forms in a variety of tissues. Distribution of each form of transglutaminase varies with different tissues. Studies were undertaken to characterize the form of transglutaminase expressed in rat parotid gland, and to examine a possible physiological role for the enzyme. It was found that chronic treatment of rats with the beta-adrenergic agonist isoproterenol (IPR) resulted in the induction of parotid transglutaminase activity. The properties of this transglutaminase appeared to be distinct from those of the well-characterized guinea pig liver cytosol transglutaminase (TGase C). The findings that protein polymerization (observed on SDS-PAGE) and incorporation of radioactive putrescine, a polyamine, into protein occur in the presence of exogenous transglutaminase and calcium indicated that certain rat parotid salivary proteins are or could be substrates for this enzyme. Analysis of proteolytic digests of rat parotid salivary proteins on an amino acid analyzer and by high-performance liquid chromatography also indicated that these salivary proteins contain gamma-glutamyl derivatives of primary amines (e.g., polyamines or lysine), post-translational products of transglutaminase catalysis. The possible physiological function of this enzyme in the oral cavity might be stabilization of proteinaceous structures during normal oral homeostasis and/or woundhealing.

Animals↗
PubMed1989

Human immunodeficiency virus (HIV) infection in haemophiliacs: long-term prognostic significance of the HIV serologic pattern.

To identify markers of prognostic value in the course of HIV disease, immunologic parameters and profiles of HIV antibodies and antigen were studied in 60 haemophiliacs. The 43 HIV-seropositive subjects were followed prospectively over a 4 year period with a retrospective analysis as well of their frozen plasma for HIV markers. This group had a significant decrease in number of helper/inducer T lymphocytes as compared with 17 HIV seronegative subjects. The degree of changes correlated with the stage of disease, with the most severe depletion of CD4 cells in those who developed AIDS. Counts of B cells and platelets were also lower in HIV-infected haemophiliacs. Ten out of 12 AIDS patients had undetectable antibodies to HIV p24 antigen; low levels of p24 antibody were also seen in six out of 15 subjects with lymphadenopathy (CDC stage III), but in only two out of 16 asymptomatic subjects (CDC stage II). Sustained HIV p24 antigenaemia (greater than 30 pg/ml) was seen in 10 AIDS patients, in five subjects with lymphadenopathy and in two asymptomatic haemophiliacs. Initial HIV serologic profiles, obtained when all patients were asymptomatic, were highly predictive for progression of the HIV infection: the initial pattern of low anti-p24 antibody and positive p24 antigenaemia conferred the worst prognosis, with all patients in this group developing ARC or AIDS within 36 months, whereas an initial high level of anti-p24 without p24 antigenaemia was associated with relatively the best prognosis. Of such subjects, 58% have remained clinically asymptomatic after 48 months of the study (P less than 0.00001). The serologic profile of HIV antibody pattern and HIV antigen in haemophilic patients thus already provides important prognostic information at an early stage of HIV infection.

AIDS Serodiagnosis↗
PubMed1989

Immune thrombocytopenia in hemophiliacs infected with human immunodeficiency virus and their response to splenectomy.

We studied five patients with hemophilia A in the age range of 18 to 64 years who were infected with human immunodeficiency virus and who developed immune thrombocytopenia. The clinical course of immune thrombocytopenia in relation to human immunodeficiency virus infection and the patients' responses to splenectomy and immune variables were determined. All five patients developed antibody to human immunodeficiency virus 6 to 60 months (median, 24 months) before the onset of thrombocytopenia, and two patients became human immunodeficiency virus antigenemic (one patient at the onset of immune thrombocytopenia and the other 60 months after the onset of immune thrombocytopenia [24 months after splenectomy]). All five patients had a strong platelet-associated immunoglobulin G and three patients also had a weak platelet-associated immunoglobulin M on their platelets. In four of five patients danazol therapy failed, and three patients required moderate doses of prednisone. Because of the progression of immune thrombocytopenia, four of the five patients underwent splenectomy with preoperative high-dose intravenous immune globulin. All four had an excellent immediate response to splenectomy, with a rise in platelet count to more than 300 x 10(9)/L and sustained remission during postsplenectomy follow-up of 6 to 45 months. There was no significant drop in CD4 and CD8 counts after splenectomy, and all four patients remained clinically well.

Adult↗
PubMed1988

Patients with prolonged bleeding time of undefined etiology, and their response to desmopressin.

Between 1981 and 1986, we evaluated 59 patients who presented with isolated prolongation of bleeding time with normal platelet counts, platelet aggregation and coagulation parameters (including von Willebrand's factor), and without evidence of liver or kidney disease, or exposure to anti-platelet agents. These patients, termed as vascular fragility syndrome (VFS), were analyzed to further characterize their bleeding patterns. The pattern of bleeding manifestations was similar to that of patients with platelet dysfunction, such as mucocutaneous bleeding or excessive post-operative bleeding. In 16 patients, desmopressin (1-desamino-8-d-arginine vasopressin, DDAVP) was infused to control active bleeding or as a part of pre-surgical evaluation. Bleeding time improved (pre-DDAVP bleeding time 15.3 +/- 3.4 min, mean +/- S.D.; post-DDAVP bleeding time 10.7 +/- 3.9 min; p less than 0.01) within 30 minutes following the DDAVP infusion with either satisfactory arrest of acute bleeding or good control of subsequent hemostasis with surgery. Side effects with DDAVP were transient and minor, i.e. facial flushing, or conjunctival erythema. These findings indicate that VFS with isolated prolongation of bleeding time is a frequently encountered bleeding disorder and that DDAVP is effective in achieving hemostasis for the management of acute bleeding and may be useful prior to surgical procedures.

Bleeding Time↗
PubMed1988

Epidermal and hair follicle transglutaminases. Partial characterization of soluble enzymes in newborn mouse skin.

Treatment of skins of newborn mice with the neutral protease Dispase in order to separate dermis and epidermis causes pronounced changes in the levels of transglutaminase activity in the epidermis. Two soluble transglutaminases, one anionic enzyme and one cationic enzyme, of Mr approximately 90,000 and approximately 50,000, respectively, are extracted from epidermis; and the activities of both enzymes increase as a function of the time of Dispase treatment of skin. When the anionic Mr approximately 90,000 enzyme is incubated with Dispase after its chromatographic isolation from epidermal extracts, it is converted to a lower molecular weight enzyme. Hair follicles isolated from dermis prepared by a 12-h Dispase treatment of the skin of newborn mice contain two soluble cationic transglutaminases, one of which is indistinguishable from that of epidermis and the other which is not seen in epidermis. Both of these hair follicle enzymes are of Mr approximately 50,000 and appear to exist in monomeric form. They have been partially purified. Based upon these findings, we suggest that transglutaminase processing and control occur during normal differentiation of keratinocytes in epidermis and of hair follicle epidermal cells in dermis and that production of the proper forms of the enzyme may be essential to the formation of mature cornified envelopes and hair shafts, respectively.

Animals↗
PubMed1988

Verapamil, diltiazem and nifedipine interactions with calmodulin stimulated (Ca2+ + Mg2+)-ATPase.

The functional interactions of the three prototype Ca2+ antagonists, verapamil, diltiazem and nifedipine, were examined in relation to the calmodulin regulated plasma membrane Ca2+ pump ATPase. For this we used low ionic strength derived, calmodulin depleted, human red cell ghost membranes. Exogenously added calmodulin activated basal (Ca2+ + Mg2+)-ATPase in a concentration-dependent manner. Half-maximal activation by 6 nM calmodulin was antagonized by 10(-3) M verapamil and 10(-3) M diltiazem 25.1 and 12.1% respectively. The inhibition appeared to be specific for calmodulin activation since basal activity was not affected by these agents. Nifedipine had no effects on basal or calmodulin stimulated (Ca2+ + Mg2+)-ATPase activity. Unlike dihydropyridine modulation of verapamil and diltiazem binding at high affinity channel sites, nifedipine in this system did not alter the inhibitory responses of verapamil and diltiazem. The calmodulin directed antagonism of the two drugs was shown to be strictly additive over a full range of calmodulin concentrations and appeared to change predominantly the Vmax and, to a lesser degree, the affinity of calmodulin for the (Ca2+ + Mg2+)-ATPase. It is concluded that this model system provides evidence for additional functional discrepancies among the various classes of Ca2+ antagonists.

Ca(2+) Mg(2+)-ATPase↗
PubMed1988

Adverse reactions to trimethoprim-sulfamethoxazole in hemophiliacs.

Adverse reactions to trimethoprim-sulfamethoxazole are very prevalent in patients with acquired immunodeficiency syndrome (AIDS). Recently we have observed severe toxicities associated with trimethoprim-sulfamethoxazole in three hemophiliacs, a group known to be at risk for developing AIDS. At the time of these reactions to the antibiotic, none of the patients had yet manifested any stigmata of AIDS per se. We advise caution in the use of trimethoprim-sulfamethoxazole in hemophiliacs and other patients at high risk for the development of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1988

DDAVP in the treatment of bleeding disorders.

Hemophilia A and von Willebrand's disease are hereditary disorders associated with qualitative and quantitative abnormalities of clotting factor VIII. A major clinical feature is excessive or abnormal bleeding often necessitating the use of transfusions of pooled blood products to achieve hemostasis. Exposure to blood products places the recipient at risk for infection by the hepatitis B virus or the human immunodeficiency virus. A synthetic analog of arginine vasopressin, 1-desamino-8-D-arginine vasopressin, has been shown to increase the plasma levels of factor VIII coagulant activity and von Willebrand's factor, and clinically to improve abnormal bleeding, obviating the need to use blood products.

Deamino Arginine Vasopressin↗
PubMed1988

Modulation of cellular transglutaminase: protease-induced activation.

Multiple molecular forms of transglutaminase are found in cells and each form is widely distributed. We find a 95 K dalton enzyme associated with membrane fractions. A 50 K dalton enzyme occurs primarily in epidermis and hair follicles. Cells after treatment with proteases show greater transglutaminase activity. The activated enzyme in rat chondrosarcoma cells is one of 95 K daltons, whereas mouse epidermal cells and rabbit endometrium cells after protease activation display enzymes of both 95 K daltons and 50 K daltons. The 95 K dalton enzyme, but not that of 80 K daltons, can be activated by proteases or sulfhydryl compounds after cell lysis. In cells that undergo terminal differentiation, e.g., reticulocytes, megakaryocytes, monocytes, chondrocytes, and epidermal cells, the forms of transglutaminase are modulated. Our findings suggest that these modulations in differentiating cells are the results of transglutaminase post-translational modifications that cause pronounced changes in catalytic activity.

Animals↗
PubMed1988

Impaired fibrinolytic response to exercise in type II diabetes: effects of exercise and physical training.

We studied the effects of exercise and physical training on coagulation parameters and fibrinolytic activity in 16 sedentary non-insulin-dependent diabetics and nine control subjects matched for prior physical activity. Parameters were measured at rest and after 30 minutes of bicycle exercise at 70% to 75% of maximal oxygen uptake before and after 6 weeks of thrice-weekly physical training. In the untrained state, fibrinolytic activity was impaired in diabetics compared with controls (1.26 +/- 0.19 v 2.20 +/- 0.34 U; P less than .03), and resting levels of plasma fibrinogen (329 +/- 21 v 266 +/- 17 mg/dL; P less than .01) and the prothrombin time (PT) maximal velocity (Vmax) (4.9 +/- 0.5 v 2.9 +/- 0.5; P less than .05) were increased. The activated partial thromboplastin time (APTT) Vmax was also increased but this did not reach statistical significance (3.6 +/- 0.2 v 2.3 +/- 0.5; P less than 0.10). Activation of fibrinolysis occurred following exercise in both groups but the peak activity and increment were less in diabetics. Physical training for 6 weeks had no effect on plasma fibrinogen levels but significantly improved the resting and postexercise APTT Vmax and resting fibrinolytic activity in diabetics. The exercise-induced increment in fibrinolytic activity following training remained depressed compared with normal controls. The changes in APTT Vmax correlated with changes in the indices of blood glucose control. The relevance of these findings to possible antiatherogenic effects of exercise and the mechanism by which exercise produces these effects remain to be established.

Adult↗