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Y H Chang

Publications and source records attributed to Y H Chang.

At least 163 records · Page 9Linked to original sources
PubMed1989

Molecular cloning and sequencing of genomic DNA encoding aminopeptidase I from Saccharomyces cerevisiae.

Yeast aminopeptidase I is a vacuolar enzyme, which catalyzes the removal of amino acids from the NH2 terminus of peptides and proteins (Frey, J., and Rohm, K-H. (1978) Biochim. Biophys. Acta 527, 31-41). A yeast genomic DNA encoding aminopeptidase I was cloned from a yeast EMBL3A library and sequenced. The DNA sequence encodes a precursor protein containing 514 amino acid residues. The "mature" protein, whose NH2-terminal sequence was confirmed by automated Edman degradation, consists, based only on the DNA sequence, of 469 amino acids. A 45-residue presequence contains positively and negatively charged as well as hydrophobic residues, and its NH2-terminal residues could be arrayed in an amphiphilic alpha-helix. This presequence differs from the signal sequences which direct proteins across bacterial plasma membranes and endoplasmic reticulum or into mitochondria. It remains to be established how this unique presequence targets aminopeptidase I to yeast vacuoles and how this sorting utilizes classical protein secretory pathways. Further, the aminopeptidase I gene, localized previously by genetic mapping to yeast chromosome XI and called the LAP4 gene (Trumbly, R. J., and Bradley, G. (1983) J. Bacteriol. 156, 36-48), was determined by DNA blot analyses to be a single copy gene located on chromosome XI.

Amino Acid Sequence↗
PubMed1989

Effects of moxibustion on cellular immunocompetence of gamma-irradiated mice.

The effects of moxibustion on cellular immunocompetence of gamma-irradiated mice were investigated in this study. A total of 240 male young mice (ICR strain), 6-8 weeks of age, were chosen and divided into three groups. Group A was the normal control. Group B, the experimental control, was treated with 400 rad whole body gamma-irradiation. Group C, the experimental group, was treated with moxibustion (MT) after being exposed to gamma-irradiation. Six to eight mice from each group were sacrificed on days 1, 5, 12, 19, 26 and 33 post-irradiation. The body and splenic weights of mice in each group were measured. The cellular immunocompetence was measured by 3H-thymidine uptake in each experimental mouse. The results revealed that 400 rad of gamma-ray irradiation inhibited the increase of body and splenic weights, and exerted a pronounced inhibitory effect on the incorporative rates of 3H-thymidine after being stimulated by mitogens such as PHA, PWM, Con A and LPS in the splenic lymphoid cells. MT seemed to help the recovery of the cellular immunocompetence in the gamma-ray irradiated mice.

Animals↗
PubMed1989

[Experience in using modified HM-3 Dornier lithotripter to treat urinary tract stones].

Low pressure generator has been developed mainly to reduce pain and kidney injury while at the same time maintain an equally effective stone-free rate. Our experience in using Modified HM-3 Dornier lithotripter to treat urinary tract stones has given an average of stone-free rate (58.88%) quite similar to what the conventional one can give. Compared with the conventional intervention, the modified one might increase by 52.07% (2281 vs 1500 pulses) in the average frequency of shock wave and by 26.52% (38.40 vs 30.35 minutes) in average operation time. However, low pressure may contribute to less complications and overall smoother procedure under oral analgesic use.

Adolescent↗
PubMed1988

Effects of hemorrhagic serum on interleukin-2 generation and utilization.

Exposure of normal peripheral blood mononuclear cells (PBMCs) to serum obtained from hemorrhaged animals produces marked depression of mitogen-induced cellular proliferation. In order to examine the mechanism which underlies its suppressive action, the effects of hemorrhagic serum on the production and utilization of interleukin-2 (IL-2) by PBMCs in mitogen-stimulated cultures were investigated. The production of IL-2 by PBMCs obtained from normal animals was reduced by approximately 90% after these cells were washed with hemorrhagic serum for 60 sec at 0 degrees C. Cells cultured in hemorrhagic serum showed greater than 30% reduction in proliferative response to phytohemagglutinin, and no significant change in the degree of suppression was produced by adding recombinant IL-2 to the cell cultures. PBMCs cultured with recombinant IL-2 and hemorrhagic serum, but not mitogen, proliferated significantly less than did cells cultured with IL-2 and normal serum. These findings suggest that although hemorrhagic serum produces a marked decrease in IL-2 generation, the suppressive effects of hemorrhagic serum on mitogen-induced lymphocyte proliferation are not due to this decrease in IL-2 production.

Animals↗
PubMed1988

Generation of functionally active suppressor cells by haemorrhage and haemorrhagic serum.

Mitogen (PHA)-induced proliferation of peripheral blood mononuclear cells (PBMC) was reduced by more than 70% 2 h after the haemorrhage of 30% of blood volume. Experiments using isolated macrophages and lymphocytes showed that post-haemorrhage macrophages were functionally normal and that lymphocytes were responsible for the observed haemorrhage-induced depression of proliferative response. Surface marker determinations showed that at least some, if not all, of the haemorrhage-induced suppressor cells are of the OX8+ phenotype. Exposure of PBMCs to serum from bled animals also brought about activation of OX8+ suppressor T cells. These results suggest that the depressed proliferative response of PBMCs induced by haemorrhage or by exposing the cells to haemorrhagic serum (serum from bled animals) is due to the activation of OX8+ suppressor T cells.

Animals↗
PubMed1988

Effects of hemorrhage on interleukin-1 production.

Depression of lymphocyte proliferative response occurs after trauma and hemorrhage. Because abnormalities in interleukin-1 (IL-1) production can result in depression of mitogen-induced lymphocyte proliferation, we investigated the effects of unanesthetized hemorrhage on IL-1 generation. The capacity of peripheral blood monocytes to produce IL-1 increased more than five fold by 2 h after loss of 30% of the total blood volume and returned to normal by 12 h after hemorrhage. Removal of 15% of total blood volume did not result in any alterations in IL-1 production. These results show that the diminished lymphocyte proliferative response which occurs after unanesthetized hemorrhage was not due to decreased IL-1 production. The increase in IL-1 generation which occurs shortly after severe hemorrhage may play a role in mediating the acute phase reaction which follows hemorrhage and trauma.

Animals↗
PubMed1986

Cellular and humoral bases of hemorrhage-induced depression of lymphocyte function.

Bacterial infection often occurs after trauma and hemorrhage and is believed to be a reflection of a compromised host defense system. In the present study, the effect of hemorrhage on phytohemagglutinin-induced lymphocyte proliferation was investigated. Lymphocytes obtained from rats 2 h after blood withdrawal in an amount equivalent to 30% of total blood volume showed a 48% reduction in proliferative response as compared to cells obtained from the same animal before bleeding. This depression in lymphocyte proliferative capacity appeared to be due to a serum factor or factors induced by hemorrhage. The hemorrhage-induced serum factor(s) is heat-stable, dialyzable, and has an apparent molecular weight between 13,000 and 23,000 on gel filtration chromatography. The hemorrhage-induced factor seems to suppress lymphocyte proliferation in a rapid and irreversible manner. This abnormality in host defense mechanisms may contribute to the increased incidence of sepsis present after trauma and hemorrhage.

Animals↗
PubMed1986

Lack of effect of exogenous recombinant interleukin-2 on trauma-induced abnormalities in lymphocyte proliferation.

Injury impairs cell-mediated immune function by depressing mitogen-induced lymphocyte proliferation and decreasing interleukin-2 (IL-2) production. In this study, we examined the ability of exogenous, recombinant IL-2 to restore lymphocyte proliferation after trauma. Recombinant IL-2 was added to cultures of phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells obtained from seven healthy volunteers and from 21 victims of accidental trauma. In comparison to the healthy group, lymphocyte proliferation was reduced approximately 20% in patients with minor and moderate injuries, and 50% in patients with severe injuries. The addition of recombinant IL-2 to PHA-stimulated lymphocytes from injured patients did not substantially improve cellular proliferation. These results suggest that the depressed response of lymphocytes to mitogen stimulation after trauma is not due to decreased IL-2 generation.

Adult↗
PubMed1986

The role of interleukin 2 in hemorrhage-induced abnormalities of lymphocyte proliferation.

Depression of lymphocyte proliferative response occurs after trauma and hemorrhage. Because abnormalities in production or utilization of interleukin 2 (IL-2) can result in depression of mitogen-induced lymphocyte proliferation, we investigated the effects of unanesthetized hemorrhage on the generation of IL-2 by rat peripheral blood lymphocytes and the response of these cells to exogenous IL-2. Two hours after loss of 30% of total blood volume, IL-2 production was reduced by greater than 90%. Return to normal levels of IL-2 generation occurred by 48 hr after hemorrhage. Addition of purified rat IL-2 to cultures of phytohemagglutin-stimulated peripheral blood lymphocytes obtained from normal animals resulted in suppression of the proliferative response. Exogenous IL-2 produced a similar degree of suppression in the proliferation of cells obtained from hemorrhaged animals. These results show a profound hemorrhage-induced suppression of IL-2 generation, but no benefits of exogenous IL-2 in improving the depressed lymphocyte proliferative response that exists after hemorrhage.

Animals↗
PubMed1985

The effects of hemorrhage on mitogen-induced lymphocyte proliferation.

Bacterial infection often occurs after trauma and hemorrhage and is believed to be a reflection of a compromised host defense system. In the present study, the effect of temporary loss of blood on lymphocyte proliferative capacity was investigated. Hemorrhage was induced in unanesthetized rats with chronically catheterized carotid arteries. Two hours after withdrawal of 30% of total blood volume, phytohemagglutinin-induced lymphocyte proliferation was almost completely suppressed; proliferation remained depressed for at least 24 hrs. The degree of suppression in lymphocyte proliferation was found to be dependent on the duration of hemorrhage. Mitogen-induced proliferation of lymphocytes was significantly reduced as early as 30 min after hemorrhage and became more depressed at 2.0 hr after hemorrhage. This abnormality in host defense mechanisms may contribute to the increased incidence of sepsis present after trauma and hemorrhage.

Animals↗
PubMed1984

Effects of hemorrhage on inflammatory response.

Bacterial infection often occurs after trauma and hemorrhage and is believed to be a reflection of a compromised host defense system. In the present study, we investigated the effect of the temporary loss of blood on the integrity of the inflammatory response. Hemorrhage was induced in rats that had long-term carotid artery catheterizations and the autologous blood was returned to the animals two hours later. The development of carrageenan-induced inflammation was suppressed after the temporary loss of blood in a volume-dependent manner. After the withdrawal of 30% of the total blood volume the inflammatory response was decreased 82%, and remained suppressed for at least 24 hours. The degree of depression of the inflammatory response also was found to be dependent on the time elapsed before retransfusion. Vasoconstriction induced by hypovolemic stress does not appear to be the cause of the posthemorrhage suppression in inflammatory response.

Animals↗