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D C Han

Publications and source records attributed to D C Han.

At least 55 records · Page 3Linked to original sources
PubMed1992

Subcutaneously implanted catheters reduce the incidence of peritonitis during CAPD by eliminating infection by periluminal route.

UNLABELLED: Recent experiences with Y-connectors suggest that the flush-before-fill effectively reduces intraluminal infection. Periluminal infection, however, remains an important route of peritonitis (P). We have recently reported reduced P incidence with the introduction of a new access technique as described by Moncrief in which the external segment of peritoneal catheter is left implanted subcutaneously for 6 weeks before exteriorization and bag exchanges. P developed once every 14.0 patient-mos with the new access while the incidence was one episode per 10.7 mos with conventional access. Significantly fewer patients with the new access compared to those with conventional access experienced P during the observation period (p < 0.01). Although the overall incidence of exit-site infection (ESI) was not different, there were significantly fewer episodes of simultaneous P and ESI with the new access (2P in 47 episodes of ESI) than with conventional access (36P in 126 ESI). While 10 of the 36 episodes of simultaneous infection in the conventional technique were caused by same organisms, none of the 2 episodes with the new access technique was caused by same organisms. CONCLUSION: The results of this study suggest that the new access technique reduces P incidence by virtually eliminating infection by the periluminal route.

Adolescent↗
PubMed1992

Effects of erythropoietin-induced hemopoiesis on peritoneal transport and on in vitro T cell response in CAPD.

UNLABELLED: In order to investigate the therapeutic efficacy of subcutaneously administered erythropoietin (rHuEPO) and the effects of rHuEPO-induced hemopoiesis on peritoneal transport and on cellular immune responses, we performed standardized peritoneal equilibration tests and measured T cell subsets and phytohemagglutinin (PHA)-induced interleukin-2 receptor (IL-2R) expression of PBMC by flow cytometry before and after subcutaneous rHuEPO (Eprex-, Cilag), 4000 U twice weekly, in 13 stable CAPD patients. Hct increased from 21.3 +/- 3.4% to 30.0 +/- 4.8% after 1 mo and to 32.7 +/- 4.9% after 2 mon of rHuEPO. Drained volume after 4 hrs of dwell with 4.25% dialysate increased from 2,675 +/- 204 ml to 2,807 +/- 174 ml (P < 0.05). D4/P4 creatinine increased from 0.68 +/- 0.07 to 0.71 +/- 0.06 (P < 0.05) and creatinine clearance from 7.57 +/- 0.71 to 8.03 +/- 0.63 ml/min (P < 0.05). The number of total circulating lymphocytes, T4,T8, T4/T8 with or without PHA did not change after rHuEPO. PHA-induced IL-2R expression by PBMC as expressed by mean channel of fluorescence intensity increased from 149.8 +/- 6.7 to 156.8 +/- 6.1 (P < 0.05). CONCLUSION: Subcutaneous rHuEPO is effective in correcting anemia in CAPD patients. rHuEPO-induced hemopoiesis is associated with increase in peritoneal creatinine and water transport and also with PHA-induced IL-2R expression.

Adult↗
PubMed1991

Metabolic correlates of adenosine formation in stimulated guinea pig heart.

Adenosine release into epicardial fluid and coronary effluent of isolated isovolumic guinea pig hearts was examined at baseline and after stimulation with norepinephrine (30 nM) during 31P-nuclear magnetic resonance spectroscopy to monitor myocardial metabolism. At baseline flow (9.6 +/- 0.3 ml.min-1.g-1), epicardial and venous adenosine concentrations were 154 +/- 40 and 17 +/- 5 nM, respectively. The phosphorylation potential (log[ATP]/[ADP][Pi]) and the phosphocreatine-inorganic phosphate ratio ([PCr]/[Pi]) were 5.26 +/- 0.04 and 8.5 +/- 0.7, respectively. Norepinephrine increased left ventricular pressure, heart rate, and myocardial O2 consumption rate by approximately 21, 70, and 45%, respectively, and increased epicardial and venous adenosine to 496 +/- 74 and 461 +/- 94 nM, respectively. Log-[ATP]/[ADP][Pi] and [PCr]/[Pi] declined to 4.57 +/- 0.06 and 1.9 +/- 0.3, respectively. Epicardial [AMP] increased from 54 +/- 13 to 123 +/- 24 nM. AMP was not detectable in the venous effluent. Coronary resistance correlated with epicardial and venous [adenosine] (r = 0.86 and 0.90). Epicardial and venous [adenosine] correlated with log[ATP]/[ADP][Pi], [PCr]/[Pi], and cytosolic [AMP]. Hence, interstitial adenosine is linked to cytosolic metabolism and may regulate coronary vascular resistance. Venous adenosine underestimates epicardial adenosine at baseline but more closely approximates epicardial adenosine during norepinephrine infusion.

Adenosine↗
PubMed1990

Inhibition of 125I organification and thyroid hormone release by interleukin-1, tumor necrosis factor-alpha, and interferon-gamma in human thyrocytes in suspension culture.

To elucidate the mechanism of decreased 131I uptake by the thyroid gland in patients with subacute thyroiditis and painless thyroiditis, human thyroid follicles were cultured with interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF alpha), and/or interferon-gamma (IFN gamma), and the effects of these cytokines on thyroid function were studied in vitro. When human thyrocytes were cultured in RPMI-1640 medium containing 0.5% fetal calf serum and TSH for 5-8 days, the cells incorporated 125I, synthesized de novo [125I]iodotyrosines and [125I]iodothyronines, and secreted [125I]T4 and [125I]T3 into the medium. IL-1 alpha and IL-1 beta inhibited 125I incorporation and [125I]iodothyronine release in a concentration-dependent manner. The minimal inhibitory effect was detected at 10 pg/ml. Electron microscopic examination revealed a marked decrease in lysosome formation in IL-1-treated thyrocytes. TNF alpha and IFN gamma also inhibited thyroid function in a concentration-dependent manner. Furthermore, when thyrocytes were cultured with IL-1, TNF alpha and IFN gamma, these cytokines more than additively inhibited thyroid function. Although the main mechanism of 131I uptake suppression in the thyroid gland in subacute thyroiditis is due to cellular damage and suppression of TSH release, our present findings suggest that IL-1, TNF alpha, and IFN gamma produced in the inflammatory process within the thyroid gland further inhibit iodine incorporation and at least partly account for the decreased 131I uptake by the thyroid gland in destruction-induced hyperthyroidism.

Cells, Cultured↗
PubMed1988

Dimethylsulfoxide maintains human thyroid cells in suspension culture, facilitating synthesis and release of thyroid hormone.

Usually, human thyrocytes in primary culture rapidly lose their thyroid function and fail to synthesize or release thyroid hormone after 3-5 days of culture. By culturing thyroid follicles obtained from patients with Graves' disease in medium supplemented with TSH and a low concentration of fetal calf serum (1%), thyrocytes can maintain thyroid function for several days. We have found that the addition of dimethylsulfoxide to culture medium (1.7%) furthermore enhanced and maintained thyroid function (de novo synthesis and release of [125I] thyroxine) for more than 13 days, probably by inhibiting dedifferentiation of thyrocytes. The present bioassay will be also useful for detecting thyroid stimulating immunoglobulin in patients with Graves' disease.

Cell Survival↗
PubMed1988

Effects of tumor necrosis factor-alpha/cachectin on thyroid hormone metabolism in mice.

To elucidate the mechanism by which low T3 and low T4 syndrome occurs in patients with acute or chronic infection or malignancy, recombinant human tumor necrosis factor-alpha (TNF-alpha)/cachectin (TNF) was administered ip to mice and thyroid hormone metabolism was studied. Since administration of TNF caused a decrease in food intake and body weight, all experiments were performed using pair-fed control (PFC) mice. Administration of TNF at a dose of 1-100 micrograms/day for 3 days decreased serum T4, T3, and rT3 concentrations in a dose-dependent manner. In PFC mice, serum T4 and T3 also decreased, but rT3 was significantly increased. T3/T4 ratio was greater in TNF-treated mice than in PFC mice. Type I iodothyronine-5'-deiodinating activity in the liver was significantly decreased in PFC mice but not in TNF-treated mice. The effect of TNF was reversible and could be abolished by boiling the cytokine. Furthermore, T3 and T4 response to TSH was greatly diminished in TNF-treated mice in comparison with PFC mice. These findings suggest that TNF directly inhibited the effect of TSH on the thyroid gland and decreased the serum concentrations of T4 and T3. Although TNF decreased food intake and body weight in TNF-treated mice, it did not decrease type I 5'-deiodinating activity in the liver, resulting in a greater T3/T4 ratio and lower serum rT3 concentration than those in PFC mice. We speculate that TNF is at least partly involved in the altered thyroid hormone metabolism (decreased serum T4, T3, and rT3 concentrations) caused by infections in mice.

Animals↗
PubMed1988

3,3',5'-Triiodothyronine inhibits ontogenetic development of iodothyronine-5'-deiodinase in the liver of the neonatal mouse.

To elucidate the effect of rT3 on iodothyronine-5'-deiodinating activity (I-5'-DA) in the liver of neonatal mice, rT3 was injected sc on the 5-8th day after birth and I-5'-DA in the liver was determined. A single injection of rT3 (0.01-1 microgram/g) inhibited the ontogenetically developing I-5'-DA in a dose- and time-dependent manner. The inhibitory effect was reversible and specific for I-5'-DA. Lineweaver-Burk analysis revealed that the time- and dose-dependent decrease in the enzyme activity was due to a decrease in Vmax with no alteration in Km values (5 x 10(-8) mol/l). The maximal inhibitory effect was observed at a dose of 1 microgram rT3/g, whereas the inhibitory effect was diminished at greater doses (4-10 micrograms/g), probably owing to a contamination with T4 of the rT3 preparation administered. Furthermore, consistent with our previous in vitro findings, rT3 inhibited the I-5'-DA induced by T3 in the liver of neonatal mice. These findings suggest that rT3 inhibited I-5'-DA in the liver of neonatal mice by decreasing the amount of enzyme available to the substrate and that rT3 also elicited an antagonistic effect against T3 in the induction of I-5'-DA in vivo.

Animals↗
PubMed1988

Stimulation of alkaline phosphatase activity by thyroid hormone in mouse osteoblast-like cells (MC3T3-E1): a possible mechanism of hyperalkaline phosphatasia in hyperthyroidism.

In order to elucidate the mechanism of increased alkaline phosphatase (AI-P) activity of bone origin in serum of patients with hyperthyroidism, the effects of thyroid hormone on mouse osteoblast-like cells (MC3T3-E1) were studied in vitro. Triiodo-L-thyronine (T3) and thyroxine (T4) produced a dose-dependent increase in AI-P activity in the cells at minimum concentrations of 10(-10)M T3 (free T3, 5 x 10(-12) M) and 10(-8) M T4 (free T4, 8 x 10(-11) M), respectively. Scatchard analysis revealed that MC3T3-E1 cells contained nuclear binding sites specific for T3 with an apparent Kd of 120 pM (maximum number of binding sites, approximately 2500 per cell). When cells were cultured with T3 in alpha-minimal essential medium (alpha-MEM) for a prolonged period, AI-P activity also became detectable in the conditioned medium. In contrast to rat osteosarcoma cells (ROS 17/2.8), MC3T3-E1 cell growth was inhibited by T4 in a concentration-dependent manner. These findings suggest that thyroid hormone inhibits proliferation and stimulates differentiation of mouse osteoblast-like cells. Since T3 and T4 stimulate AI-P activity not only in the cells but also in the medium, we speculate that the hyper-alkaline phosphatasia frequently seen in patients with hyperthyroid Graves' disease is partly due to a direct effect of thyroid hormone on osteoblasts or osteoblast-like cells.

Alkaline Phosphatase↗
PubMed1987

Thyroid hormone stimulates alkaline phosphatase activity in cultured rat osteoblastic cells (ROS 17/2.8) through 3,5,3'-triiodo-L-thyronine nuclear receptors.

To investigate the increased alkaline phosphatase activity of bone origin in patients with hyperthyroidism, we studied the thyroid hormone effects on alkaline phosphatase activity in a clonal rat osteoblastic cell line (ROS 17/2.8). T4 and T3 increased alkaline phosphatase activity in ROS 17/2.8 cells in a dose-dependent manner. The minimal effective T4 and T3 concentrations in medium containing 10% thyroid hormone-depleted fetal calf serum were 10(-8) M (free T4, 8 X 10(-11) M) and 10(-9) M (free T3, 4 X 10(-11) M), respectively. ROS 17/2.8 cells possessed high affinity, low capacity nuclear receptors specific for T3 [dissociation constant (Kd) approximately 150 pM; maximal binding capacity, approximately 2000 T3 binding sites per nucleus]. The relative affinity of T3, T4, rT3, MIT, and DIT were in good agreement with their biological activity. These findings suggest that rat osteoblast-like cells contain T3 nuclear receptors and that alkaline phosphatase activity is stimulated by thyroid hormone via a nuclear receptor-mediated process at free thyroid hormone concentrations attainable in patients with Graves' disease.

Alkaline Phosphatase↗
PubMed1987

A highly sensitive bioassay for PTH using ROS 17/2.8 subclonal cells.

A highly sensitive bioassay for PTH was developed by using rat osteosarcoma cells (ROS 17/2.8). By limiting dilution, ROS cells were subcloned and the subclonal cell line (ROS 17/2.8-5) most responsive to PTH was selected. When subconfluent ROS 17/2.8-5 cells were treated with hydrocortisone for 3 days and then incubated with PTH, the cAMP response was significant at 10-40 ng/l hPTH (1-34) (4 approximately 16 X 10(-12) mol/l). Osteoclast activating factors such as human interleukin 1 alpha and beta, and tumour necrosis factor alpha did not stimulate cAMP production, whereas a conditioned medium of oesophageal carcinoma cells established from a patient with humoral hypercalcaemia stimulated cAMP production. By selecting PTH-responsive subclonal cells and treating them with hydrocortisone, the sensitivity for detecting PTH was improved approximately 15 times. This method will be useful in the characterization and purification of PTH-like factors produced by malignant tumours from hypercalcaemic patients.

Animals↗
PubMed1986

Production of bone-resorbing activity and colony-stimulating activity in vivo and in vitro by a human squamous cell carcinoma associated with hypercalcemia and leukocytosis.

A squamous cell carcinoma of 33-yr-old patient who developed marked leukocytosis and hypercalcemia was transplanted into nude mice in which more marked leukocytosis and hypercalcemia also developed. This tumor (LJC-1-JCK) produced a colony-stimulating factor (CSF) and formed a cyst in the tumor from which a CSF-producing cell line (T3M-1) was established. The CSF causes predominantly formation of granulocytic colonies in addition to macrophage colonies. Bone-resorbing activity (BRA) was detected in the cystic fluid and was eluted as two separate peaks with proteins of an apparent molecular weight of 30,000-50,000 and 10,000-20,000. Colony-stimulating activity (CSA) was eluted at an apparent 30,000 mol wt. The conditioned medium of the T3M-1 cells also contained a BRA with an apparent 14,000 mol wt, whereas CSA eluted at an apparent 30,000 mol wt. PTH, epidermal growth factor, transforming growth factor-alpha, prostaglandin Es, and vitamin D could not account for the powerful BRA. In contrast to CSA, BRA was not inactivated by trypsin and more stable at 70 degrees C. When T3M-1 cells were transplanted into nude mice, marked hypercalcemia developed in addition to granulocytosis. Our findings suggest that the tumor produces and secretes a powerful BRA in vivo and in vitro, which is different from CSA in terms of molecular weight, heat stability, and trypsin treatment. We speculate that the synergistic action of CSF that stimulates macrophage colony formation and recruits osteoclast precursors, and BRA, which stimulates mononuclear phagocytes and/or osteoclasts were responsible for a marked increase in osteoclastic bone resorption and humoral hypercalcemia in the patient.

Animals↗
PubMed1986

3,3',5'-Triiodothyronine inhibits iodothyronine-5'-deiodinating activity induced by 3,5,3'-triiodothyronine at equimolar concentrations in cultured fetal mouse liver.

To investigate the rT3 effect on iodothyronine-5'-deiodinating activity (I-5'-DA) in cultured fetal mouse liver, liver on the 19th day of gestation, in which little or no I-5'-DA was detected and, therefore, rT3 was very stable, was cultured in medium containing thyroid hormone-depleted fetal calf serum supplemented with cortisol, insulin, and various concentrations of iodothyronines. After 4-15 days of culture, I-5'-DA in the homogenate was assessed by the amount of iodide released from outer ring-labeled rT3 and expressed as picomoles of 127I- per mg protein/min. I-5'-DA was induced by T3 (10(-9)-10(-8) M) and T4 (10(-7) M). In contrast, rT3 could not induce I-5'-DA at 10(-8)-10(-6) M. Furthermore, rT3 significantly decreased I-5'-DA induced by T3 (10(-8) M) at almost equimolar concentrations (1-5 X 10(-8) M). The inhibitory action of rT3 was reversible and was specific for I-5'-DA; no alteration in malic enzyme activity or intracellular glutathione concentration was detected. The inhibitory effect of rT3 on I-5'-DA was dose dependent, and the enzyme activity decreased with a half-life of 16 h in the presence of 10(-6) M rT3. The inhibitory effect was not due to contaminating rT3 in the liver homogenates. Lineweaver-Burk analysis revealed that the decrease in I-5'-DA was due to a decrease in the maximum velocity, whereas no alteration in Km was detected, suggesting that rT3 decreases the amount of 5'-deiodinase induced by T3. The minimal free rT3 concentration capable of inhibiting the induction of iodothyronine-5'-deiodinase was approximately 10(-10) M, which may be attainable in vivo, as in amnionic fluid. In summary, we have demonstrated that rT3 exerts a strong antagonistic effect against T3 in inducing I-5'-DA in cultured fetal mouse liver.

Animals↗
PubMed1985

Graves' disease with neutropenia and marked splenomegaly: autoimmune neutropenia due to propylthiouracil.

A 38-year-old man with Graves' disease taking propylthiouracil (PTU) for 6 years developed neutropenia and marked splenomegaly. After subtotal thyroidectomy with discontinuance of PTU the patient remained asymptomatic for the last two and half years. The serum obtained during the period of neutropenia demonstrated opsonic activity to neutrophils of the patient as well as of normal volunteers. This opsonic antineutrophil activity was located in the IgG fraction of the serum. Furthermore, PTU at the concentration (0.1-1.0 micrograms/ml) attainable in the patient's serum significantly stimulated [3H] thymidine incorporation in the patient's lymphocytes. These findings indicate that the patient developed autoimmune neutropenia by producing opsonic antineutrophil antibodies in association with the PTU therapy.

Adult↗
PubMed1985

Primary aldosteronism with normal aldosterone levels in blood and urine.

A 47 year old women examined for hypertension (200/100 mmHg) was normokalaemic, and had low plasma renin activity (PRA) (0.1 ng/ml X h) and normal aldosterone levels in both plasma (7-13 ng/dl) and urine (4.7-7.4 micrograms/day). Computed tomography (CT) and scintiscan indicated an adenoma on the right adrenal gland, which was then removed. The histology of the adenoma and analysis of the aldosterone content were compatible with the criteria for an aldosterone-producing adenoma. Three months after surgery, her hypertension had improved, serum potassium levels had increased slightly, and PRA had normalized. This was an unusual form of primary aldosteronism which showed normal levels of aldosterone in both blood and urine.

Adenoma↗
PubMed1984

Ontogenesis of iodothyronine-5'-deiodinase. Induction of 5'-deiodinating activity by insulin, glucocorticoid, and thyroxine in cultured fetal mouse liver.

To elucidate the regulatory mechanism of ontogenetic development of iodothyronine-5'-deiodinase in the fetal and neonatal period, fetal mouse liver of the 19th day of gestation, in which no iodothyronine-5'-deiodinating activity was detectable, was cultured in Dulbecco-Vogt medium supplemented with 10% thyroid hormone-depleted fetal calf serum, insulin, hydrocortisone, and thyroid hormones. Iodothyronine-5'-deiodinating activity of the homogenate was assessed by the amount of iodide released from outer-ring-labeled reverse T3 and expressed as picomoles of 127I- per milligram of protein per minute. The enzyme activity was induced in a dose-dependent manner; optimal concentrations for insulin, hydrocortisone, and thyroxine were 1 microgram/ml, 0.4 microgram/ml, and 10(-6) M, respectively. Without supplementation of either hydrocortisone or thyroxine, no 5'-deiodination was detected. The enzyme activity was observed after 3 d of culture, peaked at days 14-20, and then gradually decreased. Lineweaver-Burk analysis revealed that the increase in activity was primarily due to an increase in Vmax (day 3, 0.2 pmol/mg protein per min; day 20, 2.5 pmol/mg protein per min). Half maximal thyroxine (T4) and triiodothyronine (T3) concentrations were 1 X 10(-7) M (free T4: 4 X 10(-10) M), and 2 X 10(-9) M (free T3: 5.0 X 10(-11) M), respectively, whereas reverse T3 did not elicit any activity at 10(-8)-10(-6) M. These results suggest that ontogenetic development of iodothyronine-5'-deiodinase in the liver of the fetal and neonatal mouse is induced by physiological concentrations of glucocorticoid and thyroid hormones, and that insulin plays a permissive role in enhancing T3 formation from T4 in the liver.

Animals↗
PubMed1983

Rectal malacoplakia in a patient with Hodgkin's disease. Report of a case and review of the literature.

A 37-year-old man was found to have classic malacoplakia of the rectum after three courses of chemotherapy for stage IV Hodgkin's disease. Sigmoidoscopy with excisional biopsy was performed because of rectal bleeding. The biopsy specimen of the rectal lesion showed focal extensive granulomatous changes with large macrophages containing round, dense Michaelis-Gutmann bodies. Electromicroscopy demonstrated calcifying spheres with laminated concertric structures (Michaelis-Gutmann bodies) and coliform bacillus in the cytoplasm of macrophages (Von Hansemann bodies). Review of the literature revealed that association of malacoplakia with Hodgkin's disease has never been documented, although it has been reported to be associated with conditions such as malignancy, organ transplantation, collagen disease, and leukemia. The possible role of immune disturbance as an underlying cause of malacoplakia is discussed.

Adult↗
PubMedDate not supplied

Host recognition by the VirA, VirG two-component regulatory proteins of agrobacterium tumefaciens.

Agrobacterium tumefaciens contains about 25 vir genes localized on a 200-kb tumour-inducing (Ti) plasmid that direct a conjugation-like transfer of tumorigenic DNA from the bacterium to the nuclei of infected plant cells. These genes are strongly and coordinately induced during infection in response to three different classes of stimuli which are thought to be key chemical features of a typical wound site. These stimuli are (i) guaiacol and syringol derivatives such as acetosyringone, (ii) sugars such as glucose and glucuronic acid, and (iii) acidic pH. The sensing of these compounds is carried out by the VirA, VirG and ChvE proteins. VirA is a four-domain histidine protein kinase, while VirG is a transcriptional activator which is activated by VirA-mediated phosphorylation. ChvE is a chromosomally encoded periplasmic sugar binding protein which is required for sensing sugars but dispensable for sensing the other two stimuli. Here we will review the nature of these chemical stimuli, the structure and function of the three regulatory proteins, their similarity to sensors found in human and animal pathogens, the factors influencing their pool size, and their role in the host range of different strains of A. tumefaciens.

Agrobacterium tumefaciens↗