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Biomedical subjects

E S Kang

Publications and source records attributed to E S Kang.

At least 19 recordsLinked to original sources
PubMed1992

Potential for hepatic and renal dysfunction during influenza B infection, convalescence, and after induction of secondary viremia.

Whether infection with influenza B virus alters hepatic function was examined in the ferret. Also, the possibility that viral-specific antibodies (Ab) could be produced well before their detection in serum was explored. During the febrile period of influenza, reductions in the serum potassium, anion gap, ammonia, albumin and CPK and elevations of the BUN, creatinine and the GGTP levels occurred. With convalescence, the electrolytes, BUN and creatinine normalized, FFA, SGPT and CPK levels rose and the serum GGTP rose even further. Hepatic fatty acid (FA) oxidation, ornithine transcarbamylase (OTC) and carnitine palmitoyltransferase (CPT) activities were minimally altered and liver ATP and total lipid content remained normal. Following experimental secondary viremia, serum FFA continued to rise, TG decreased and CPK remained elevated while SGPT and GGTP levels normalized. In the liver, FA oxidation and OTC rates remained unchanged but CPT activity was inhibited and the liver content of ATP was significantly reduced. Immune complex (IC) protein recovered from postmicrosomal supernatant fractions by polyethylene glycol precipitation was progressively increased in livers from convalescent and viremic animals. While the amount of IC protein recovered in the spleen also increases during convalescence, this is not the case after viremia when the IC formed seem to be processed largely by the liver. By SDS/PAGE, the major proteins identified in the IC were IgM and other viral proteins. However, the viral proteins could not be validated by immunoblot with Ab produced against purified influenza B hemagglutinin (HA) and neuraminidase (NA) most probably due to phagocytic alterations of glycoprotein immunodeterminants. These findings indicate that during influenza, convalescence and post viremia changes in the concentrations of several serum and liver components occur that reflect hepatic involvement. Also, antiviral Ab, largely IgM, appears to be produced early, complexes with Ag and can be found sequestered in both the liver and spleen at a time when Ab is not detectable in the serum.

Adenosine Triphosphate↗
PubMed1991

Fatty acid composition of hepatic triglycerides in Reye's syndrome: implications for hepatic desaturase abnormalities.

Serum NEFA profiles in Reye's syndrome are reportedly unique with a disproportionate percent made up of polyunsaturated fatty acids some of which are not ordinarily found in the serum. This pattern is also reflected in the serum triglyceride composition as well. As the liver is probably the sole source of the serum triglyceride in Rye's syndrome because patients are vomiting or in coma, the fatty acid acid composition of the liver triglyceride was examined for insight regarding the lipid abnormalities in this disease. Palmitic acid (16:0) and the sum of all the saturated fatty acids in the liver triglycerides were significantly decreased whereas the sum of the monoenoic fatty acids and the products of delta 9 desaturase activity were increased in Reye's samples. When these data were compared to the fatty acid composition of the serum triglyceride from a separate cohort of Reye's and control subjects, certain inferences regarding hepatic delta 9, delta 6, delta 5, and delta 4 desaturase activities and the elongases can be drawn from the liver and serum triglyceride fatty acid profiles which are unique. Collectively, these data reflect considerable intrahepatic fatty acid desaturation and elongation activity and/or acyl transfer from lipid to lipid of various polyunsaturated fatty acids in Reye's syndrome.

Adolescent↗
PubMed1991

An experimental intraarticular implantation of woven carbon fiber pad into osteochondral defect of the femoral condyle in rabbit.

The defects of the articular cartilage structure are not replaced unless the subchondral plate has been breached. However, following the creation of a defect in the subchondral plate, the area is filled in with a fibrous tissue which gradually transforms to hyaline cartilage. The porous nontoxic materials of both biologic and synthetic origin have reportedly been used as matrices for repairing bone and cartilage. Following implantation, carbon fibre, chemically inert and well-tolerated by the body, induces a proliferation of ordered fibrous tissue. We implanted carbon fiber pads in osteochondral defects in rabbits. Those repairs were compared to control holes with no implants. The pads appeared to induce the gross appearance of a restored joint surface, mechanically strong to loading for periods from 2 to 6 weeks. Also, carbon fiber pads promoted the healing of the osteochondral defects in the rabbit femoral condyle, supplying well-organized cartilagenous tissue over repaired subchondral bone. The use of carbon fiber pads as implant material is suggested for the restoration of articular surface in osteoarthritis and osteochondritis dissecans.

Animals↗
PubMed1991

Ossifying fibroma.

Our experience includes seven cases of ossifying fibroma. The condition also appears in the literature under diagnostic names such as congenital fibrous dysplasia, congenital osteitis fibrosa, congenital fibrous defect of the tibia, and osteofibrous dysplasia of the tibia and fibula. The lesions develop in childhood and are located in the diaphysis of the tibia, or fibula. Of seven patients, we performed wide excision with free vascularized fibular graft in five cases, wide resection of the distal one-third of the fibula in one case, and curettage and bone graft in one case. Two of the patients who had wide excision with free vascularized fibular graft had recurrence. One case of recurrence occurred where incomplete wide excision with free-vascularized fibular graft was performed because the lesion was too close to the distal epiphysis of the tibia. One of the patients who had curettage and bone graft also had recurrence. It was concluded that children who have an ossifying fibroma requiring surgery can safely be treated with wide excision with or without free-vascularized fibular graft.

Adolescent↗
PubMed1991

Acute alterations in the regulation of lipid metabolism after intravascular reexposure to a single bolus of homologous virus during influenza B infection in ferrets: possible model of epiphenomena associated with influenza.

Metabolic responses occurring 24 h following the secondary haematogenous dissemination of influenza B virus during convalescence from infection were examined in the ferret as a possible model for epiphenomena which can occur following infection with influenza. Among the major changes found were a further rise in the mean fasting serum free fatty acid (FFA) level to three times the control mean value and a 50% drop in the mean serum triglyceride (TG) concentration after the intravascular administration of a single bolus of virus compared to levels found in uninfected or convalescent animals. In adipose tissue, hormone-sensitive and lipoprotein lipase activities were increased six and three-fold, respectively, over mean control values, probably accounting for the changes that were observed in serum lipid concentrations. In the liver, total carnitine palmitoyltransferase (CPT) activity was affected only slightly and the total lipid content of the liver remained unchanged. These findings indicate that 24 h after the intravascular dissemination of homologous virus in a single bolus during convalescence from influenza B infection, major distortions in the regulation of lipid metabolism occur in the ferret. Loss of the synchronous regulation of the two adipose tissue lipases is a significant consequence leading to the mobilization of a large amount of FFA during fasting from both adipose tissue and the circulating plasma TG stores.

Adipose Tissue↗
PubMed1990

Modulation of natural killer cell activity by surface phosphorylation reactions.

To determine whether phosphorylation of cell surface proteins is involved in NK cell activity, the phosphorylation patterns of a rat NK cell line (RNK-16) incubated with 12.5 microM [gamma-32P]ATP were characterized before and after exposure to YAC-1 cells, which serve as targets for killing, and K562 cells, which are not killed by RNK-16 cells. By 51Cr release assays, the inhibitory effect of ATP on RNK-16 killing activity previously reported was corroborated. RNK-16 cells prelabeled with 12.5 microM ATP show enhanced labeling of a 70- to 72,000-Da protein after exposure to unlabeled target YAC-1 cells but not after exposure to K562 cells. A protein of similar apparent molecular size is also labeled upon exposure of RNK-16 cells to OX-34, an antibody which binds and inhibits killing, as well as upon exposure to OX-18, which also binds but does not inhibit NK activity. These findings are indicative of the activation of a kinase with high affinity for [gamma-32P]ATP, which phosphorylates an endogenous surface substrate of 70-72,000 Da upon binding of macromolecules to the RNK-16 cells. RNK-16 cells, previously labeled with micromolars [gamma-32P]ATP and subsequently treated with millimolars unlabeled ATP, showed loss of label from a 110,000-Da protein component, indicative of the rapid turnover of a phosphate group on a surface protein. Thus, extracellular ATP enhances the phosphorylation of a 70- to 72,000-Da component upon binding of RNK-16 cells to target cells or upon binding of antibodies at micromolar concentrations of ATP and catalyzes the loss of phosphate from a 110,000-Da component at millimolar concentrations of ATP. These findings reflect a complex repertoire of surface phosphorylation changes which occur in RNK-16 cells.

Alkaline Phosphatase↗
PubMed1990

Autolysed antigen-extracted allogeneic bone for repair of diaphyseal bone defects in rabbits.

Autolysed antigen-extracted allogeneic bone (AAA bone) was used to bridge a large osteoperiosteal gap in the diaphysis of the radius of 50 rabbits. Periodic observations of the graft were made clinically, radiologically and histologically every week up to fourteen weeks. The continuity of the radius was evaluated macroscopically and histologically. The AAA bones were progressively resorbed and replaced by the new bone. The bone remodelled to the mature tubular bone and did not undergo absorption during the experimental period. The AAA bone proceeded to be an osteoinductive and osteoconductive material. There were no appreciable histologic signs of immune or foreign body reaction.

Animals↗
PubMed1990

An experimental study of healing of the partially severed flexor tendon in chickens.

There is a lack of clinical and experimental studies of the treatment of incompletely transected tendons. The controversy concerning the source of flexor tendon nutrients is of important clinical concern in healing of the injured tendon; thus, the flexor tendon blood supply has cited as a reason for using specific tendon suture techniques, and as a rationale for preserving the superficialis tendon and its vincula during tendon repair surgery. Our knowledge of the normal physiology of digital flexor tendons and the mechanism of their healing process is deficient. The aim of this study was to investigate the relative importance of the synovial fluid and the blood supply respectively for the healing of partially severed flexor tendons. We observed the sequential histological and vascular changes which occur in healing of the partial lacerations in the dorsal and plantar aspects of the tendons. We observed the vascularities of the two partially severed tendon groups after injection of microfil and india ink through the femoral artery. In the healing process there was no sequential histological difference between the dorsal and the plantar severed tendons. The vascularity patterns of the healing tendons were significantly increased and the hypervascularity of dorsal severed tendons was greater than that of plantar severed tendons. Partially severed tendons were completely healed without surgical repair with dense collagen fibers without adhesion in most cases. We concluded from this study that the blood vessels appeared to play a significant role in the healing of the severed flexor tendons. An intact synovial environment did not seem to be required for healing of the severed tendon. It is not necessary to surgically repair the partially severed tendon for prevention of rupture and adhesion.

Animals↗
PubMed1990

Hepatic steatosis during convalescence from influenza B infection in ferrets with postprandial hyperinsulinemia.

The possibility that postprandial hyperinsulinemia could play a role in the development of hepatic lipid disturbances during convalescence from influenza B infection was explored in the ferret as a possible model of the steatosis of Reye's syndrome. Postprandial hyperinsulinemia was produced by feeding young ferrets glucose/water and a regular diet (glucose-treated group), as reflected by the mean serum insulin levels attained, which were 57 and 135 microU/ml during control and postinfluenza periods, respectively. By comparison, ferrets fed water and a regular diet (untreated group) had mean insulin levels of 19 and 22 microU/ml, while postprandial glucose levels were comparable in the two groups of animals for each period. In contrast to untreated animals, grossly visible fatty livers were found in glucose-treated ferrets during convalescence. The total lipid content of these livers had doubled compared with preinfection samples and compared with livers of untreated ferrets. By electron microscopy hepatic mitochondria showed striking changes with diminution of matrix density and reduction in cristae surface area only in convalescent samples from glucose-treated animals. Serum free fatty acid (FFA) levels were considerably higher in the glucose-treated animals during fasting before influenza and also after feeding during convalescence. Serum triglyceride (TG) levels were also high during convalescence in the glucose-treated group. Adipose tissue lipoprotein lipase activities were similar between groups, but hormone-sensitive lipase activity was twelvefold higher in glucose-treated ferrets before and after influenza B. These findings indicate that for a given stimulus, glucose-treated ferrets would mobilize more FFA than untreated ferrets. The total capacity for beta-oxidation of FA by the mitochondrial pathway was identical in all groups of animals. Total carnitine palmitoyl transferase (CPT) activity was the same in both control groups, but was significantly diminished in glucose-treated animals during convalescence. As CPT regulates the entry of FA into the mitochondrial matrix, its reduction in response to higher insulin concentrations would limit the oxidation of FA and stimulate TG accumulation. Therefore, the accumulation of lipid in the liver in this model is regarded to have been caused by the simultaneous occurrence of increased lipolysis and increased hepatic TG synthesis owing, in part, to diversion of activated FA by CPT, which is reduced in activity due to the regulatory action of insulin. These findings may have pathophysiologic relevance for the lipid changes that occur in Reye's syndrome and to fatty liver formation in hyperinsulinemic states.

Adipose Tissue↗
PubMed1989

Serum lipolytic activity in Reye's syndrome.

High levels of the serum free fatty acids (FFA) are found in Reye's syndrome (RS). While this is attributed to enhanced adipose tissue lipolysis, the possibility that intravascular lipolysis could augment this process was investigated by measuring lipase activity in sera from RS and other subjects. Ordinarily, lipolytic activity is not detectable in serum from unheparinized subjects. Significant lipolytic activities ranging from 1-3 mumol/ml serum per hour were detected in sera from 5 of the 7 RS patients studied. Similar activities were also found in sera from two other subjects one of whom was a long-term survivor of RS and the other who had recurrent bouts of biliary obstruction and encephalopathy. Lipase activity was negligible in the serum from 2 other RS patients, 4 other long-term survivors of RS, 2 siblings, one RS parent and in 20 disease controls including patients with influenza, diabetic ketoacidosis and cerebral edema, meningitis and febrile infections with diarrhea and vomiting. None of these individuals had received heparin. An inverse relationship was found between LPL and hepatic lipase (HL) activities. Glucose levels tended to correlate directly with LPL and inversely with HL activity. The basis for the presence of LPL activity in RS sera is not known but the presence of serum lipase activity in unheparinized patients supports the notion that the TG in the circulating lipoprotein particles probably also serve as another source of FFA in the sera of RS patients.

Child↗
PubMed1989

Effects of in vitro prepared immune complexes on rat adipose tissue lipoprotein lipase.

The possibility that circulating immune complexes (IC) could modify lipoprotein lipase (LPL) activity or release was explored in in vitro systems. IC were precipitated at antibody-Ag equivalence by using specific rabbit antisera and Ag from inactivated rubella virus and hemagglutinins from purified whole virions from three prototype strains of influenza (A/Brazil, A/Bangkok, and B/Singapore) as well as from a combined diphtheria and tetanus toxoid adsorbed with inactivated pertussis. After resolubilization, these IC were exposed to delipidated homogenates of rat epididymal fat pads before assay for LPL activity. LPL activity was stimulated two- to three-fold by the presence of 20 to 40 micrograms IC protein. This effect is not caused by the individual components of the IC because neither the specific Ag nor the individual antisera had any significant effect on LPL activity. With the rubella IC, a greater stimulatory effect was seen with increase in IC protein. With the influenza and diphtheria, pertussis, tetanus (DPT) IC, however, inhibition occurred when IC protein exceeded the amount of protein used for the LPL assay. C did not appear to be involved because IC prepared with heated antisera had similar effects. When intact rat epididymal fat pads were exposed to the rubella, influenza, or DPT IC, LPL activity recovered in the suspension medium was increased in each instance compared with pads exposed to a comparable amount of albumin. These findings may have implications for specific lipid changes that may occur during the immediate post-infectious period following rubella, influenza, or infections with the several bacteria whose Ag were present in the DPT IC used in these studies.

Adipose Tissue↗
PubMed1989

Procainamide N-acetyltransferase: modulation by clofibrate and a microsomal form.

1. Detoxification of procainamide by N-acetyltransferase which occurs primarily in the cytoplasmic fraction of the rat liver can be modulated by clofibrate treatment. 2. When the concentration of one of the substrates, procainamide, is 100 microM while the other, acetyl CoA, is 10 or 100 microM, the specific activity is reduced following clofibrate treatment. However, total activity is unchanged because of a 44% increase in cytoplasmic protein. 3. At more physiological levels of the two substrates (10 microM), total enzyme activity is increased from 9.5 +/- 1.5 to 14.0 +/- 1.8 pmol/mg/min, P less than 0.05. 4. A microsomal form of N-acetyltransferase activity is reported which is unaffected by the concentration of acetyl CoA in contrast to the cytoplasmic form.

Acecainide↗
PubMed1989

Dose effects of adenine on myocardial ATP content in the post-anoxic nonworking rat heart.

1. Tissue ATP levels were measured in Langendorff perfused nonworking rat hearts subjected to 50 min anoxia prior to reperfusion with Krebs-Ringer bicarbonate (KRB) buffer alone or supplemented with 50 microM or 1 mM adenine for 60 min. 2. ATP content was restored to the normoxic range in hearts reperfused with 50 microM adenine in KRB (20.82 +/- SEM 1.90 mumol/g dry weight vs 24.95 +/- 0.83 in normoxic hearts, P = NS). 3. Reperfusion with oxygenated KRB alone or buffer with 1 mM adenine failed to improve ATP levels (17.23 +/- 0.91 mumol/g dry weight for buffer alone, 15.60 +/- 0.46 with 1 mM adenine and 13.45 +/- 0.93 for anoxic hearts not reperfused). 4. These findings indicate that adenine at 50 microM dosage can restore ATP concentrations to the normoxic range after 60 in of anoxia in the nonworking rat heart while raising the adenine dose to 1 mM inhibited the tissue ATP content.

Adenine↗
PubMed1988

Differential effects of freezing on total hepatic peroxisomal fatty acid oxidation and on the rate-limiting enzyme, acyl-CoA oxidase.

Fatty acid oxidation defects can be acutely fatal, leading to the collection of tissues which are frozen for future analysis. Since peroxisomes can also oxidize long-chain fatty acids, differentiation of the contributions from the peroxisome as opposed to the mitochondria is important. We studied the effects of freezing and storage of rat livers on peroxisomal and mitochondrial beta-oxidation as measured by cyanide sensitivity of the oxidation of [1-14C]oleoyl-CoA to 14CO2 and acid-soluble labeled products. In addition, we examined the effects of freezing and storage on the rate-limiting enzyme for peroxisomal beta-oxidation, acyl-CoA oxidase, by the H2O2 generation method. Marked reduction in the oxidation of [1-14C]oleoyl-CoA was found for both peroxisomal and mitochondrial systems upon freezing at -18 or -70 degrees C for 2 days which declined further on storage at these temperatures for 12 weeks. Loss of activity after freezing was greater for the mitochondrial than the peroxisomal beta-oxidation system. By contrast, acyl-CoA oxidase activity was resistant to these changes, maintaining prefrozen activities despite storage for 12 weeks. The contribution of the peroxisomal system to beta-oxidation was 32% of the total rate of oxidation of [1-14C]oleoyl-CoA in the rat liver. These findings indicate that the contributions of the peroxisomal system to total fatty acid oxidation may be considerable, that freezing of the liver results in drastic reduction in enzyme activities of both peroxisomal as well as mitochondrial beta-oxidation, but that the rate-limiting enzyme of the peroxisomal system, acyl-CoA oxidase, retains full activity despite freezing and storage.

Acyl Coenzyme A↗
PubMed1986

Reye's syndrome. Salicylate metabolism, viral antibody levels, and other factors in surviving patients and unaffected family members.

To investigate possible etiologic factors for Reye's syndrome (RS), five survivors and their unaffected family members were studied. This study showed low salicylate levels among the patients with RS compared with siblings and parents when challenged with three doses of aspirin. Thus, the patients with RS, three to ten years after having had RS, exhibited normal or increased ability to metabolize aspirin. We found significantly higher antibody levels to influenza A and varicella among the patients with RS, further supporting the importance of these viral infections in the etiology of the syndrome.

Adolescent↗
PubMed1986

Characterization of the major phosphoprotein and its kinase on the surface of the rat adipocyte.

Intact rat fat cells exposed to 12.5 microM [gamma-32P]ATP incorporate label into specific proteins within minutes. By solubilizing the reaction mixture with SDS which by passes the subcellular fractionation steps, the labeled proteins can be identified in autoradiographs of SDS-PAGE gels. The most prominently labeled protein has an Mr of 42,000. Localization of this component to the cell surface can be made on the basis of inhibition of phosphorylation by addition of a protein derived from the rat brain with protein kinase inhibitory property, susceptibility of the phosphorylated protein to tryptic digestion, whereas the unphosphorylated protein is unaffected by digestion with trypsin (15 min), inhibition of phosphorylation of this protein after brief exposure to melittin, and the consistent observation that more label is associated with the 42,000 Mr band in homogenates and permeabilized cells than in comparable numbers of intact cells exposed to the same amount of label. A 42,000 Mr phosphoprotein is also present in mitochondria which is most likely the alpha subunit of pyruvate dehydrogenase. To rule out the possibility that the cell surface protein might be a mitochondrial contaminant from broken cells, 32Pi-labeled and [gamma-32P]ATP-labeled cells were solubilized with Triton and chromatographed on a rabbit anti-pyruvate dehydrogenase antibody-Sepharose 4B column. A single labeled peak was detected upon elution of the bound fraction only in the 32Pi-labeled sample, and not in the [gamma-32P]ATP-labeled sample. Subcellular fractionation studies of intact cells labeled with [gamma-32P]ATP showed differences in the recovery of phosphoproteins of 42,000 Mr depending on whether a continuous sucrose gradient (27.6-54.1%, g/ml) or a discontinuous sucrose gradient (16, 35 and 48%, g/ml) was used. Phosphoproteins of 42,000 Mr were located in the mitochondrial and membrane fractions collected by discontinuous sucrose gradient separation, whereas a phosphoprotein of 42,000 Mr was found primarily in the mitochondrial fraction after continuous sucrose gradient separation. By 5'-nucleotidase activity measurements, the latter approach appears to result in the isolation of a heavy fragment of the plasma membrane with the mitochondrial light fraction which is 42,000 in Mr and labeled. Finally, comparison of the autoradiographs of two-dimensional (2D) gels (isoelectric focusing followed by 10% SDS-PAGE) show different isoelectric points for 42,000 Mr components in [gamma-32P]ATP- and 32Pi-labeled cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗
PubMed1986

Total and peroxisomal fatty acid oxidation by liver homogenates from autopsied Reye's and control subjects.

To determine whether the accumulation of liver triglyceride in Reye's syndrome could be due to a block in beta-oxidation of the fatty acids, the ability of Reye's and control liver homogenates from samples obtained at autopsy to oxidize fatty acids was examined. Total fatty acid oxidation as measured by oxidation of [1-14C]oleoyl CoA, which mostly represents mitochondrial activity, was comparable between the groups. Peroxisomal fatty acid oxidation was, likewise, similar despite the reported increase in the numbers and sizes of these organelles. This disparity could not be explained by an artifactual dilution of product by accumulated endogenous substrate. Inference is made that active peroxisomal beta-oxidation may contribute to the increased short chain fatty CoA content of liver which was reported earlier.

Acyl Coenzyme A↗