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Biomedical subjects

K H Hsieh

Publications and source records attributed to K H Hsieh.

At least 145 records · Page 8Linked to original sources
PubMed1982

Immunologic evaluation of patients with polychlorinated biphenyl poisoning: evaluation of delayed-type skin hypersensitive response and its relation to clinical studies.

Polychlorinated biphenyl (PCB) poisoning causes many physiological abnormalities including immune suppression. Cellular immunity was studied in 30 PCB-poisoned patients and 50 normal human subjects. PCB poisoning caused suppression of cellular immunity such as the delayed-type skin response to streptokinase and streptodornase. The suppression of cellular immunity was correlated with the severity of the disease. Thus evaluation of the immune function may be helpful for the diagnosis of PCB poisoning.

Adolescent↗
PubMed1982

Interferon-induced suppression of in vitro IgE biosynthesis in asthmatic children.

The effect of interferon on the in vitro IgE biosynthesis was studied in 22 asthmatic children. Peripheral blood mononuclear cells, T cells and B cells were treated with 400 IU human fibroblast interferon for six hours, washed, cultured for one week and the supernatant IgE concentrations were determined. The results showed (1) B cells were the targets for interferon effect as interferon-treated B cells produced much less IgE than did the untreated B cells and (2) the presence of normal T cells could protect the B cells from interferon-induced suppression of IgE synthesis. The results obtained in this study can be used to explain the depressed IgE levels after viral infections.

Asthma↗
PubMed1982

Study of T-cell subpopulations defined by monoclonal antibodies in asthmatic children with or without atopic eczema and normals.

The distributions of OKT4+ cells (helper/inducer T cells) and OKT8+ cells (suppressor/cytotoxic T cells) were studied in 47 house dust sensitive asthmatic children with or without atopic eczema and 26 normals. When purified T cell population was studied, the percentage of OKT4+ cells was lower in patients than that in normals before allergen challenge but this difference disappeared after antigen stimulation. In addition, the percentage of OKT4+ cells was decreased in patients with atopic eczema. In contrast, when unfractionated mononuclear cells were studied, no difference in OKT4+ cells and OKT8+ cells was found between patients and normals, irrespective of antigenic stimulation, but the OKT8+ cells were markedly increased in both normals and patients after allergen challenge. The immunopathogenic implication of decreased OKT4+ cells in allergic patients is discussed.

Adolescent↗
PubMed1982

Study of immunological changes after hyposensitization in house dust sensitive asthmatic children.

The working mechanisms of hyposensitization were studied in 22 asthmatic children who had completed an one-year course of immunotherapy with house dust. Several immunological parameters were followed every four months during the study period. The results showed: (1) There was no significant change in the distribution of total T, active T and B lymphocytes. (2) While the numbers of Tmu and Tgamma cells remained unchanged, their capability to increase after allergen challenge was lost four months after immunotherapy. (3) No change could be found in the total serum IgE, specific IgE and IgG antibodies. Surprisingly enough, the specific IgG antibody, and thus the specific IgG/IgE antibody ratio, decreased in patients who often developed immediate-type asthmatic reactions after allergen shots. (4) The lymphoproliferative response to house dust started to decrease four months after treatment while the mitogenic response to phytohemagglutinin remained the same. (5) The mean percentages of polymorphonuclear leukocytes with Fc and complement receptors were lower than those for normals throughout the study period but the sensitivity of receptor functions to allergen challenge began to decline four months after immunotherapy. Thus this study shows that hyposensitization is able to specifically correct some of the immunological aberrations of the atopic individuals and provides the rationale for the hyposensitization in the treatment of allergic diseases.

Adolescent↗
PubMed1982

Further study on the role of active T lymphocytes in human immunity to tuberculous infection.

Lymphocytes from healthy tuberculin reactors, but not those from patients with active pulmonary tuberculosis and positive tuberculin skin test, were able to respond drastically to the in vitro purified protein derivative (PPD) stimulation with a marked increase in active T lymphocytes. Furthermore, the active T lymphocytes, but not late T lymphocytes, from normals were able to secrete a soluble factor (lymphokine)which was capable of activating in vitro the active T lymphocytes of the patients.

Adult↗
PubMed1982

[Development of serum IgE and house dust-specific IgE antibodies in normal Chinese from birth to adult and its clinical usefulness in the diagnosis and treatment of childhood asthma (author's transl)].

Total serum IgE and house dust-specific IgE antibodies were checked in 217 healthy subjects aged from birth to 39 years and 67 newly diagnosed asthmatic children in order to study their developmental patterns in normal Chinese and evaluate their clinical usefulness in the diagnosis and treatment of bronchial asthma. The serum IgG concentrations were determined by using Phadebas IgE PRIST kits and specific IgE antibodies by Phadebas RAST kits purchased from Pharmacia, Sweden. The results showed: 1) The serum IgE increased gradually after birth, approached adult level at 3-4 years of age, continued to rise to peak at 14-16 years of age and then declined to the adult level; 2) The house dust-specific IgE antibodies increased after birth, peaked at 5-6 years of age and then declined; 3) The serum IgE was increased (greater than mean + 2SD) in 64.2% (43/67) of asthmatic children and house dust-specific IgE antibody in 62.7% (42/67) and 4) While in asthmatic children, there was a positive correlation (r = + 0.67) between serum IgE concentrations and house dust specific IgE antibodies, no such relation was found for healthy children. It is, therefore, concluded that determinations of serum IgE and house dust-specific IgE antibody are of help in the diagnosis and treatment of childhood asthma.

Adolescent↗
PubMed1982

[Humoral and cell-mediated immunities in epileptic patients (author's transl)].

Humoral and cell-mediated immunities were studied in 50 epileptic patients receiving phenytoin treatment and in 20 normals. The mean serum concentrations of IgG, IgA and IgM showed no significant difference between these two groups; however, abnormally low serum IgA (less than 125 mg/dl) was found in 10 patients (10/50, 20%) and in one of them serum IgA was less than 50 mg/dl (1/50, 2%). The serum IgA was related neither to the duration of phenytoin therapy nor to the serum concentration of the drug. The mean serum C3 value was lower in the patient group than in the normals. The mean percentages of T cells, Tmu cells, T gamma cells and monocytes were also lower in the patients, especially in those with serum level of phenytoin over 20 micrograms/ml. These data indicate that phenytoin can suppress the cell-mediated immunity, whereas certain genetic factors, in addition to the effect of phenytoin, may contribute to the change of serum immunoglobulin levels in the epileptics. The incidence of positive antinuclear antibody among the epileptics was 18%, which was much higher than that in the general population. The occurrence of autoantibody did not correlate with the serum concentration of phenytoin.

Adolescent↗
PubMed1981

Fine specificity of genetic regulation of guinea pig T lymphocyte responses to angiotensin II and related peptides.

Guinea pig T lymphocyte responses to the octapeptide antigen angiotensin II (NH(2)-Asp(1)-Arg(2)-Val(3)-Tyr(4)-Ile(5)-His(6)-Pro(7)-Phe(8)-OH; AII) were examined using various synthetic peptide analogues and homologues. Each peptide antigen was assessed for immunogenicity and antigenicity in strain 2 and strain 13 guinea pigs as determined by in vitro T cell proliferative responses. The genetic control of T cell responses to these peptides was found to be highly specific and capable of distinguishing subtle differences in the antigens. For example, strain 2 guinea pigs responded to AII and were low responders to [Val(5)]-AII, whereas strain 13 animals responded to [Val(5)]-AII but not to AII. The genetic control in this case involved the difference of one methyl group between Val(5) and Ile(5). Differences in T cell responsiveness by strain 2 and strain 13 guinea pigs were also observed with analogues involving para substitutions on the phenyl ring of Tyr(4) and of Phe(8). However, the genetic regulation of T cell responses did not seem to be based on a single peptide residue. For example, removal of Asp(1) allowed strain 13 animals to respond to the Ile(5)-containing analogue, but eliminated responsiveness to the Val(5)-containing analogue. Thus, the first and fifth AII residues are both involved in the regulation of strain 13 T cell responses. Substitutions for Tyr(4) and Phe(8) suggested that the same residue may serve to alter the specificity of T cell responses in one strain, and determine responsiveness or unresponsiveness in the other strain. One of the most striking observations is that T cell responsiveness to the various AII analogues and homologues randomly fluctuates between strain 2 and strain 13 guinea pigs, and in general neither strain responds to the same peptide antigens. This suggests that strain 2 and strain 13 T cell responses are rarely directed against the same antigenic determinants, and that the T cell antigen-combining diversity is usually exclusive between these two strains. These results are discussed with respect to the specificity of Ir gene control and the relationship between Ir gene function and antigen recognition by T cells. Note added in proof: More recent experiments using a new lot of [Val(5)]- AII have indicated that [Val(5)]-AII-immune strain 2 T cells show significant stimulation with AII but remain relatively low responders with [Val(5)]-AII, as shown in Table I. The difference in priming for cross-reactivity for AII with the different lots of [Val(5)]-AII is at present unknown.

Angiotensin II↗
PubMed1981

Imbalances in T-cell subpopulations in myasthenia gravis.

Distributions of peripheral blood lymphocyte subpopulations and T-cell subsets were studied in 38 patients with myasthenia gravis (MG) and 23 healthy controls. T cells were detected by rosette formation with sheep red blood cells and B cells with erythrocyte-antibody-complement (EAC) complexes. T mu cells were identified by rosette formation of T cells with Ox RBC-IgM complexes, and T gamma cells with Ox RBC-IgG complexes. The means of total lymphocyte count and active T cell percentage were marginally significantly lower in MG patients than in normal controls (0.05 less than P less than 0.1). The mean percentage of T mu cells was higher in MG patients than in controls (50.2 +/- 11.8% vs. 38.5 +/- 15.3%, P less than 0.01), whereas that of T gamma cells in the former was lower than that in the latter (20.4 +/- 7.1% vs. 27.6 +/- 6.2%, P less than 0.001). Thus, the loss of regulatory suppressor T cells and the increase of helper T cells in the patients are in favour of regarding MG as an autoimmune disease. The fact that the percentage of T gamma cells was significantly decreased in MG patients after autologus serum incubation, and that no such a phenomenon was seen in normal controls, may suggest a possible role of serum factors in the pathogenesis of MG.

Adolescent↗
PubMed1981

Fibrin Polymerization. 1. Alkylating peptide inhibitors of fibrin polymerization.

A series of analogues relating to the NH2-terminal region of the fibrin alpha chain, i.e., Gly-Pro-Arg-Pro, were prepared by stepwise solid-phase synthesis, and their abilities to inhibit fibrin polymerization and to prolong thrombin-initiated clotting time were evaluated. Among the analogues systematically modified at different positions, replacement of the NH2-terminal three residues of Gly-Pro-Arg-Pro by either chlorambucil, p-nitrophenyl-L-alanine, or p-aminophenyl-L-alanine gave inactive compounds in the thrombin time assay, whereas similar substitution or extension of the COOH terminus produced the highly active analogues Gly-Pro-Arg-Phe(4-NH2), 22%; Gly-Pro-Arg-Pro-Phe(4-NO2), and Gly-Pro-Arg-Pro-Phe(4-NH2), 105%; relative to Gly-Pro-Arg-Pro = 100% in the fibrin polymerization inhibitory assay. As potential photoaffinity labeling probes, analogues containing a nitrophenylalanine residue in position 4 or 5 underwent photolysis under the experimental photoactivation conditions. As a potential alkylating probe, Chl-Pro-Arg-Pro was selectively effective in inhibiting thrombin amidolysis and fibrin polymerization. In the latter assay, Chl-Pro-Arg-Pro was approximately 20 times more potent than Gly-Pro-Arg-Pro in inhibiting fibrin aggregation.

Alkylation↗
PubMed1981

Synthesis of fluorine-containing peptides. Analogues of angiotensin II containing hexafluorovaline.

Gamma, gammma, gammma, gammma', gamma', gammma'-Hexafluorovaline and derivatives have been prepared and incorporated into angiotensin II by fragment condensation and solid-phase peptide synthesis. Hexafluorovaline derivatives showed general resistance toward various enzymatic digestions and the tendency to racemize extensively upon carboxyl activation. When the angiotensin II analogues were assayed on rat uterus, [Hfv5]AII had 133% activity, [D-Hfv5]AII was inactive, and [Ac-Asn1,DL-Hfv8]AII was a potent inhibitor of angiotensin II in vitro and in vivo.

Angiotensin II↗
PubMed1981

The effects of histamine, antihistamines, isoproterenol and theophylline on the Fc and complement receptor functions of polymorphonuclear leukocytes in asthmatic children.

The effects of histamine, antihistamines, isoproterenol and theophylline on the expressions of Fc and complement (C') receptors on the polymorphonuclear leukocytes (PMN's) were studied in 40 asthmatic children. Histamine in concentrations of 10(-13) to 10(-3), isoproterenol in 10(-5) to 10(-3) and theophylline in 5 X 10(-6) to 10(-4) were all capable of causing a dose-related suppression of Fc and C' receptor functions of PMN's. Either diphenhydramine or cimetidine alone could partially block the histamine-induced suppressive effect but combination of H1 and H2 receptor antagonists were required for complete abolishment.

Adolescent↗