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Biomedical subjects

J Tseng

Publications and source records attributed to J Tseng.

At least 55 records · Page 3Linked to original sources
PubMed1994

Induction of B cell IgA secretion by the culture supernatants of lipopolysaccharide-stimulated peritoneal macrophages.

The regulatory effects of peritoneal macrophage culture supernatant on B-cell growth and IgA secretion were demonstrated in this study. When the LPS-stimulated murine splenic B cells were cultured in medium containing 50% LPS-activated macrophage culture supernatant, both the cell growth and IgM secretion of B cells were suppressed by 64% and 50%, respectively, whereas the IgA secretion was increased 2.6-fold. Transforming growth factor-beta 1 (TGF-beta 1) is a potent regulator of IgA response. Macrophage culture supernatants contained on average 78 ng/ml of TGF-beta 1. When directly added to cultures, TGF-beta 1 also acted as a suppressive factor on B cell growth (55%) but induced an 7.5-fold increase in IgA secretion. Both macrophage culture supernatant and TGF-beta 1 induced an increase in the expression of surface IgA. Further study indicated that the augmenting effect of the macrophage culture supernatant on IgA secretion could be inhibited (50%) by an anti-TGF beta 1 antibody, and that the suppressive effect of the macrophage culture supernatant on the B-cell growth could be overcome by the same antibody, suggesting that TGF-beta 1 was one of the cytokines in the macrophage culture supernatant that regulated B-cell function.

Animals↗
PubMed1993

Receptor-mediated activation of multiple serine/threonine kinases in human leukocytes.

Activation of the microbicidal response of phagocytes requires cytosolic ATP and is associated with extensive protein phosphorylation, suggesting the involvement of protein kinases in the signal transduction cascade. An in vitro renaturation assay was used to identify the protein kinase(s) activated by chemoattractants in human blood neutrophils. Four distinct kinases were activated by the chemotactic peptide formyl-methionyl-leucyl-phenyl-alanine with molecular masses of 72, 65, 49, and 41 kDa (designated PK72, PK65, PK49, and PK41, respectively). PK72 and PK65 were activated very rapidly (5-15 s), yet transiently. By comparison, PK49 and PK41 responded in a slower, more sustained manner. Treatment of extracts of activated cells with alkaline phosphatase reverted the stimulation of the kinases, suggesting that phosphorylation is the post-translational modification that underlies activation of the kinases. Stimulation of PK72 and PK65 by chemoattractant was independent of calcium and protein kinase C. In contrast, elevation of cytosolic free calcium levels was sufficient and appeared to be necessary for full activation of PK49 and PK41. While phorbol esters can mimic the effects of formyl-methionyl-leucyl-phenylalanine on PK49 and PK41, inhibition of protein kinase C by staurosporine did not prevent the receptor-mediated activation of these kinases. PK41 most likely corresponds to the Erk-1 isoform of mitogen-activated protein (MAP) kinase. Accordingly, PK41 effectively phosphorylated myelin basic protein, known to be a good substrate for Erk-1. The electrophoretic mobility of PK49 is similar to that of MAP kinase-kinase (MAP/Erk kinase). However, immunoprecipitation experiments indicated that PK49 is not MAP/Erk kinase. The identity of this and other kinases remains to be defined, but possible candidates are discussed. In addition to autophosphorylating, PK72, PK65, and PK41 were shown to effectively phosphorylate exogenous substrates. These kinases may therefore play a role in signal transduction during stimulation by chemoattractants.

Base Sequence↗
PubMed1993

Immunity and responses of circulating leukocytes and lymphocytes in monkeys to aerosolized staphylococcal enterotoxin B.

Rhesus monkeys immunized intramuscularly or orally with staphylococcal enterotoxin B (SEB) toxoid or SEB toxoid incorporated in microspheres made of poly(DL-lactide-co-glycolide) were challenged with a lethal dose of aerosolized SEB to study their immunity and cellular responses in the circulation. It was found that circulating antibodies play a critical role in preventing SEB from triggering toxicosis. Monkeys with high levels of antibodies survived, while those with low levels underwent 2 to 3 days of toxicosis and died. Intramuscular immunization induced high levels and oral immunization induced low levels of antibodies. The circulating antibodies in surviving monkeys decreased dramatically within 20 min and started to rebound at 90 min after SEB challenge. At 90 min, the dying monkeys showed in the circulation a dramatic increase of polymorphonuclear leukocytes and decreases of NK cells and monocytes (CD16 and CD56 markers) as well as of lymphocytes with HLA-DR, CD2, CD8, and IL2R alpha (CD25) markers. The number of polymorphonuclear leukocytes showed an inverse correlation with the numbers of monocytes and various lymphocyte subpopulations which, except for IL-2R, CD16, and CD56(+) cells, showed a direct correlation with one another. The changes in the populations of leukocytes, monocytes, NK cells, and lymphocytes seem to be an indication of initial toxicosis; however, the roles of these cells in toxicosis and death remain to be defined.

Aerosols↗
PubMed1993

The ontogeny of inter- and intrasexual vocal muscle dimorphisms in a sound-producing fish.

This study documents the development of inter- and intrasexual dimorphisms in the vocal ('sonic') muscles of the swimbladder in the plainfin midshipman fish, Porichthys notatus. Midshipman have two male reproductive morphs, Types I and II. Only Type I males build nests and generate mate calls to attract females; Type II males sneak or satellite spawn. Vocal muscles in the mate-calling Type I males were 25-fold larger in absolute size (sixfold larger when scaled to body size) compared with females or non-calling Type II males. Dimorphisms in muscle mass were correlated with dimorphisms in fiber number and diameter. Only nascent Type I males experienced a pre-maturational, fourfold increase of fiber number followed by a rapid, fivefold increase in fiber cross-sectional area at sexual maturity. Also specific to Type I males was a striking change in cell structure: the ratio of sarcoplasm to myofibril area increased fivefold. By contrast, Type II males and females matured without showing any of these changes in sonic muscle--the trajectories which described juvenile growth continued to hold through maturity and adulthood. The results indicate distinct, non-sequential, ontogenetic trajectories for Type I and Type II males. The origin of the Type II male morphotype is described as paedomorphosis by progenesis: size distributions of free-living animals suggest that Type II males can mature precocially as one-year-old fish, whereas Type I males defer reproduction until they are at least two years of age.

Air Sacs↗
PubMed1993

Inhibitory effect of lipopolysaccharide-stimulated P388D1 macrophage-like cells on plasmacytoma cells.

Culture supernatants of lipopolysaccharide-stimulated P388D1 macrophage-like tumor cells showed a growth inhibitory effect on plasmacytoma MOPC-315, MPC-11 and myeloma FO cells, but had no effect on J558 plasmacytoma cells. Based on the results of trypan blue staining and a 51Cr release assay, the supernatant had both cytotoxic and cytostatic activity for MOPC-315 plasmacytoma cells. The inhibitory activity was trypsin-sensitive, heat-stable at 100 degrees C for 20 min., but sensitive to 2-mercaptoethanol and cystein HCl. At least 6 hrs of exposure period were required for the P388D1 culture supernatant to show an inhibitory effect on plasmacytoma cells. Since the inhibitory activity could not be blocked by protease inhibitor or neutralized by antibodies to mouse IL-1 beta, IL-6 and TNF-alpha, the inhibitory factor(s) was distinct from the defined cytotoxic factors. After partial purification with DEAE-Sephacel and Sephacryl S-300 chromatography, four major active peaks with the molecular mass of 874-KDa (near the void volume), 112-KDa, 45-KDa and 18-KDa were obtained.

Animals↗
PubMed1992

Activation of vacuolar-type proton pumps by protein kinase C. Role in neutrophil pH regulation.

Activated neutrophils undergo a large burst of metabolic acid generation, yet maintain their cytosolic pH (pHi) within physiological limits. To analyze the underlying regulatory mechanisms, pHi was measured fluorimetrically in suspensions of human neutrophils. In acid loaded but otherwise unstimulated cells, pHi recovered rapidly via Na+/H+ exchange. Upon Na+ removal, recovery from an imposed acid load was negligible. Phorbol ester activation of acidified cells induced a rapid recovery of pHi partly due to a Zn(2+)-sensitive H(+)-conductive pathway. A third component of the regulatory response was apparent in Na(+)-free media containing Zn2+. Acid extrusion through this alternate pathway was voltage sensitive and capable of translocating H+ equivalents against their electrochemical gradient. This active H+ transport was inhibited by N-ethylmaleimide, by N,N'-dicyclohexylcarbodiimide and by nanomolar doses of bafilomycins A1 or B1, suggesting the involvement of vacuolar (V)-type H+ pumps. Cytosolic alkalinization was accompanied by extracellular acidification, indicative of translocation of H+ equivalents across the surface membrane and consistent with the sensitivity of the alkalinization to changes in plasma membrane potential. The activity of the V-type H+ pumps was virtually undetectable in resting cells, becoming apparent only after treatment with phorbol esters or other, chemically unrelated agonists of protein kinase C. These H+ pumps are likely to play a role in pHi homeostasis during the metabolic burst that accompanies neutrophil activation during infection and inflammation.

Adult↗
PubMed1992

Effects of staphylococcal enterotoxin B on rodent mast cells.

Staphylococcal enterotoxin B (SEB) was tested in rodent mast cell cultures for the release of serotonin. Both rat RBL-2H3 mast cells and murine peritoneal cells released serotonin after SEB stimulation in culture. Release of serotonin in RBL-2H3 cells depended on the concentration of SEB; an appreciable release was seen at 50 micrograms/ml. The release of serotonin was not due to cell death. Serotonin release could be enhanced by bradykinin but not by vasoactive intestinal peptide, substance P, lipopolysaccharide from Salmonella typhimurium, the calcium ionophore A23187, acetylcholine, adenosine, 5-hydroxyeicosatetraenoic acid, indomethacin, or phorbol myristate acetate. SEB bound directly to the membrane of RBL-2H3 mast cells, and the SEB-binding site, the presumptive receptor, appeared to be a protein. The SEB receptor could not be capped under membrane-capping conditions, and serotonin release could not be enhanced by attempts to cross-link the receptor. These results suggest that mast cells may be an important cell type involved in SEB toxicosis and that release of serotonin may be enhanced by activation of the kinin-kallikrein system.

Acetylcholine↗
PubMed1992

Suppression of tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6 and granulocyte-monocyte colony stimulating factor secretion from human monocytes by an extract of Poria cocos.

Fu-Ling, the sclederma of Poria cocos (Schw.) Wolf, has long been used as a sedative and diuretic. However, data in this report suggest that Fu-Ling is a potential suppressor of cytokine secretion from human peripheral blood monocytes under in vitro condition. Monocyte culture medium containing 10% of Fu-Ling extract significantly inhibited secretion of TNF-alpha, IL-beta, IL-6 and GM-CSF from the monocyte monolayer. However, as Fu-Ling extract content was gradually reduced, cytokine secretion was augmented in comparison with the cytokine secretion in drug-free controls. This augmentative effect resulted from the trace amount (1.24 ng/ml in 0.62% of Fu-Ling extract) of lipopolysaccharide (LPS) which contaminated the Fu-Ling extract during the preparation process, since TNF-alpha, IL-1 beta and IL-6 secretion induced by 0.62% Fu-Ling extract could be significantly inhibited by polymyxin B, an LPS inhibitor. Furthermore, the amounts of TNF-alpha IL-1 beta and IL-6 induced by 1 ng/ml of LPS without the presence of drug were more than that induced by 0.62% of Fu-Ling extract. Thus, cytokine secretion induced by LPS contamination (1.24 ng/ml) in the Fu-Ling extract was partially suppressed by 0.62% of the Fu-Ling extract itself. GM-CSF secretion in the medium containing 0.62% of Fu-Ling extract was not induced by LPS since: a) GM-CSF induced by 0.62% Fu-Ling extract could not be inhibited by polymyxin B; b) LPS at 1 ng/ml showed no activity indicating induction of GM-CSF secretion.

Cytokines↗
PubMed1989

The effect of human C-reactive protein on the cell-attachment activity of fibronectin and laminin.

We have previously reported that purified human C-reactive protein (CRP) specifically binds to the cell-binding region of plasma fibronectin (Fn) in a Ca2+-dependent reaction that is saturable at a molar ratio of CRP/Fn of approximately 9. In this study, the binding of CRP to Fn was found to interfere with the cell-attachment promoting activity of Fn. The inhibition of cell attachment was dependent on the concentration of the CRP and involved the phosphorylcholine (PC) binding site of CRP since inhibition was prevented by allowing the CRP to react with either PC (or closely related monophosphate compounds) or a mAb specific for the PC-binding site of CRP. Binding of CRP to laminin was also Ca2+-dependent; however, this binding did not alter the cell-attachment promoting activity of laminin. CRP by itself does not mediate cell attachment. Since CRP is selectively deposited at sites of tissue damage along with plasma Fn and has the ability to bind to Fn and alter its cell-binding activity, CRP may modulate early events in tissue repair.

Animals↗
PubMed1989

Clinical pharmacology of alpha2-agonist and beta-adrenergic blocker.

The pharmacological properties of centrally acting alpha2-receptor agonists such as clonidine suggest a potentially important role as ideal adjuvants for anesthesia since they produce sedation, analgesia anxiolysis, xerostomia and cardiovascular stability without respiratory depression, development of tolerance or addiction liability. Further clinical experience with this exciting development will undoubtedly establish the ultimate role and optimal use of alpha2 -receptor agonists in anesthetic practice. Beta-blockage can result in significant bradycardia, atrial ventricular conduction problems, bronchospasm and left ventricular contractile dysfunction. Thus, the use of long-acting beta-blockers is of limited value in the perioperative period. Esmolol, because of its ultrashort action, cardioselective properties and titratability, has been shown to be safe and effective for the treatment of tachycardia and hypertension. Doses from 50 to 300 micrograms/kg/min for up to 7 hours in the perioperative period have been shown to cause no apparent cumulative effect. It has been used in the treatment of asthmatic patients with tachycardia and hypertension without significant increases in airway resistance. Studies using esmolol during general anesthesia have demonstrated no significant interaction with several anesthetic regimens.

Adrenergic alpha-Agonists↗
PubMed1988

Binding of human C-reactive protein (CRP) to plasma fibronectin occurs via the phosphorylcholine-binding site.

Human C-reactive protein (CRP) is an acute phase reactant that is selectively deposited at sites of tissue damage. CRP binds with high affinity to purified plasma fibronectin (Fn) when the Fn is immobilized on a surface or matrix via either specific IgG antibody or by gelatin. The CRP to Fn binding is saturable at a molar ratio of CRP/Fn of approximately 9 with a Kd = 1.47 x 10(-7) M and requires Ca2+. The binding site on Fn for CRP was localized to the C-terminal portion by using monoclonal antibodies (mAbs) to Fn as competitive inhibitors of CRP. The binding involves the phosphorylcholine (PC)-binding site of CRP since the addition of PC inhibits binding to Fn and those mAbs to CRP that bind at or near the PC-binding site selectively inhibit the CRP to Fn binding. In addition the mouse IgA myeloma protein TEPC-15, which is specific for PC, also competes with CRP for binding sites on Fn. A mAb to the mouse PC-binding idiotype T-15, which also reacts with the PC-binding site of CRP, inhibits the binding of CRP to Fn. The findings suggest that CRP may play a role in the formation of the extracellular matrix needed for tissue repair. The CRP-Fn interaction may be one of the explanations for the observation of selective deposition of CRP at sites of tissue injury.

Animals↗
PubMed1987

Generation of competent virus in the REV helper cell line C3.

We have studied the generation of replication-competent virus in cultures of the helper cell line C3, which harbors a packaging-defective provirus derived from reticuloendotheliosis virus. We transfected the C3 line with a defective provirus encoding the chicken growth hormone gene and carrying the HSV-1 tk gene. The appearance of competent virus was assayed by infection of Spafas C/E CEF, monitoring reverse transcriptase activity, and rescue of the TKTU assayed on BRLtk- cells. Our results indicate that cultures of C3 producing TKTU can release viruses which have variable growth characteristics and which can remain latent in culture for extended periods of time.

Animals↗
PubMed1986

Binding specificity of mouse serum amyloid P-component for fibronectin.

Binding between purified mouse serum amyloid P-component (SAP) and plasma fibronectin (Fn) occurred when either one of the proteins was immobilized by specific antibody and the second protein was offered in a soluble form. Binding of Fn to immobilized SAP was cooperative and saturable at a molar ratio of SAP/Fn = 7.1. The molar ratio at saturation was 3.7 for SAP/Fn when SAP was allowed to bind to immobilized Fn. The binding required 2 to 3mM amounts of Ca++. The binding of SAP to Fn was selectively inhibited by a monoclonal antibody specific for the mid-molecule region of Fn, by soluble gelatin, and by heparin in the presence of 3mM Ca++. We conclude that the SAP binding site was localized at the mid-molecule region of Fn that includes the adjacent gelatin-binding domain and the heparin-I binding domain.

Animals↗
PubMed1984

Repopulation of the gut lamina propria with IgA-containing cells by lymphoid cells isolated from the gut lamina propria.

Migration and lodging properties of IgA cells and their precursors of the gut lamina propria (GLP) were studied by transfer of highly purified GLP lymphoid cells between immunoglobulin allotype-congenic mice (CB-20 to BALB/c). The donor IgA-containing ( cIgA ) cells appeared in the GLP of the recipients at day 1, peaked at days 12-15 (late repopulation peak) and persisted up to day 20 after cell transfer. An additional peak at day 3 (early repopulation peak) was seen only when large numbers of GLP B cells were transferred. Few cIgA cells appearing in spleen and mesenteric lymph nodes were seen mainly at days 12-15. The early repopulation peak was probably formed by the differentiation and accumulation of IgA blasts, recirculating IgA-bearing cells and some IgA precursors. The former 2 cell types homed directly back, while the later homed indirectly via spleen to the GLP. The late repopulation peak was possibly formed by the homing and differentiation of Peyer's patch IgA precursors arriving in the GLP with membrane immunoglobulins unchanged. These GLP IgA precursors migrated first to the spleen and later back to the GLP, where they differentiated into IgA plasma cells.

Animals↗
PubMed1984

A population of resting IgM-IgD double-bearing lymphocytes in Peyer's patches: the major precursor cells for IgA plasma cells in the gut lamina propria.

The precursor cells in Peyer's patches and mesenteric lymph nodes responsible for repopulating IgA plasma cells in the gut lamina propria were identified by using cell separation and by using cell transfer in Ig allotype congeneic mice (CB-20 and BALB/cJ mice). It was found that the IgA precursor cells are mainly resting lymphoid cells bearing IgM and IgD on their surface. The IgA-bearing cells are also precursors; their repopulation efficiency, however, is remarkably low. The majority of the IgA precursor cells also bear complement receptors on their surface; this suggests that they are relatively mature B cells.

Animals↗