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Biomedical subjects

B C Yang

Publications and source records attributed to B C Yang.

At least 37 records · Page 2Linked to original sources
PubMed1999

Antioxidant administration inhibits exercise-induced thymocyte apoptosis in rats.

PURPOSE: The purpose of this study was to investigate the effect of antioxidant on exercise-induced apoptosis in rat thymocytes. METHODS: After exercise at 13.8 m x min(-1) for 60-90 min x d(-1) on a motor-driven drum exerciser for 2 consecutive days, rat thymocyte apoptosis was monitored by the feature of DNA fragmentation. To study the effect of antioxidant, rats were administered with butylated hydroxyanisole (BHA) for 7 d before exercise. RESULTS: Exercise could induce thymocyte DNA fragmentation as detected on electrophoretic gel and by cell death detection ELISA kit. Further studies indicated that pretreatment with antioxidant BHA to rats resulted in a blockage of exercise-induced DNA fragmentation. The concentrations of glutathione (GSH) were not significantly changed in rat thymocytes after exercise with or without BHA treatment. CONCLUSION: These results suggest that reactive oxygen species may play a role in thymocyte apoptosis induced by exercise. However, changes in GSH levels were not observed in this exercise model.

Analysis of Variance↗
PubMed1999

Fosinopril: pharmacokinetics and pharmacodynamics in Chinese subjects.

This study examined thepharmacokinetics and pharmacodynamics of fosinopril (IVand oral) in Chinese subjects to determine whether they were different from a group of somewhat heavier and older Western control subjects previously published using the same methods. It was an open-label, randomized, balanced, two-way crossover study comparing oral and IV pharmacokinetics in 12 healthy Chinese subjects in a clinic in Taiwan. Each subject received 10 mg of oral fosinopril or 7.5 mg of IV fosinoprilatin a randomized sequence with sampling for fosinoprilat concentrations over 48 hours. Standard pharmacokinetics, including AUC, Cmax Tmax, T 1/2, Vss, bioavailability, total clearance, and renal and nonrenal clearance, were determined as well as pharmacodynamic effects on angiotensin-converting enzyme (ACE) activity. Following oral administration of 10 mg fosinopril, AUC0-T and AUCinf were 1,556 +/- 586 ng x hr/mL and 1,636 +/- 620 ng x hr/mL, respectively; T 1/2 was 17.4 +/- 11.4 hr; Cmax was 183.4 +/- 59.4 ng/mL; and median Tmax was 4.0 hr, with > 99% protein binding. Following IV administration of 7.5 mg fosinoprilat, AUC0-T and AUCinf were 7,727 +/- 2,638 ng x hr/mL and 7,816 +/- 2,693 ng x hr/mL, respectively; T 1/2 was 13.0 +/- 5.2 hr; and median Tmax was 4.0 hr, with 99.5% +/- 0.22% protein binding and a Vss of 5,850 +/- 2,780 mL. Bioavailability was 22.3% +/- 7.9%. Percent urinary excretion was 7.6% +/- 2.6% after oral dosing and 42.6% +/- 6.1% after IV dosing. After IV, dosing total clearance was 1,088 +/- 439 mL/hr, renal clearance was 472 +/- 213 mL/hr, and nonrenal clearance was 617 +/- 246 mL/hr. ACE inhibition was essentially complete through 12 hours and markedly reduced through 24 hours. Compared to a somewhat heavier and older previously reported control group, pharmacokinetic values were similar except for a slightly lower AUC and total clearance in Chinese and a statistically significantly lower nonrenal clearance. Pharmacodynamic effects on ACE activity were essentially identical. There is no reason to expect significant differences in fosinopril dosing or effect in a Chinese population compared to a Western population.

Administration, Oral↗
PubMed1999

Role of TGF-beta1 in platelet-mediated cardioprotection during ischemia-reperfusion in isolated rat hearts.

Platelets protect myocardium against ischemia-reperfusion injury. This study examined the role of platelet-derived TGF-beta1 in cardioprotection during ischemia-reperfusion. Isolated Sprague Dawley rat hearts were perfused with K-H buffer and subjected to 25 min of global ischemia followed by 30 min of reperfusion. Ischemia-reperfusion resulted in myocardial dysfunction indicated by increase in CPP and LVEDP, and decrease in dLVP. Perfusion of hearts with washed platelets or supernatant of aggregated platelets attenuated (P < 0.01) of myocardial dysfunction following ischemia-reperfusion. Ischemia-reperfusion resulted in a decrease in myocardial TGF-beta1 determined by immunohistochemistry. ELISA showed an increase in latent TGF-beta1, but a decrease in active TGF-beta1. Perfusion of hearts with platelets or aggregated platelet supernatant preserved myocardial TGF-beta1 content upon ischemia-reperfusion. Perfusion of hearts with recombinant TGF-beta1 also resulted in cardioprotection following ischemia-reperfusion qualitatively similar to that observed with platelets or aggregated platelet supernatants. RT-PCR analysis showed an increase in myocardial TGF-beta1 mRNA following ischemia-reperfusion. These observations indicate that platelets protect the myocardium against ischemia-reperfusion-mediated dysfunction at least in part by releasing TGF-beta1. Increase in both TGF-beta1 mRNA and latent TGF-beta1 does not indicate a defect in the translation of mRNA. Reduction in myocardial TGF-beta1 following ischemia-reperfusion suggests a defect in the conversion of latent TGF-beta1 to active TGF-beta1.

Animals↗
PubMed1999

Hypoxia-reoxygenation-induced apoptosis in cultured adult rat myocytes and the protective effect of platelets and transforming growth factor-beta(1).

The outcome of myocardial ischemia-reperfusion has been partially attributed to the degree of apoptosis in cardiomyocytes. Aggregating platelets by release of transforming growth factor-beta(1) (TGF-beta(1)) protect the isolated heart against ischemia-reperfusion injury and preserve myocardial TGF-beta(1) content. To gain more insight into the modulation of hypoxia-reoxygenation-induced injury (apoptosis and necrosis) to myocytes by TGF-beta(1) and aggregating platelets, cultured adult rat myocytes were exposed for 48 or 72 h to hypoxia alone, or to hypoxia followed by 3 h of reoxygenation. Apoptosis in the cells was determined by in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining and DNA fragmentation on gel electrophoresis. Hypoxia alone caused a time-dependent increase in myocyte apoptosis (number of apoptotic cells: 19+/-3% at 48 h and 39+/-5% at 72 h compared with 5+/-1% in control cells, based on a 500-cell count). Three hours of reoxygenation after 48 h of hypoxia further increased the number of apoptotic cells (34+/-8 versus 19+/-3% in hypoxia for 48 h), but reoxygenation after 72 h of hypoxia did not additionally increase the number of apoptotic cells, perhaps because of extensive cell necrosis on prolonged hypoxia. Forty-eight hours of hypoxia followed by 3 h of reoxygenation also resulted in a decrease in Bcl-2 and an increase in Fas protein level. Incubation of myocytes with either recombinant TGF-beta(1) (0.5-5 ng/ml) or aggregated platelet supernatant (from 2-3 x10(7) platelets/ml, containing approximately 0.5 ng/ml of TGF-beta(1)) markedly (P<.01) decreased the number of apoptotic cells after hypoxia-reoxygenation. Incubation with TGF-beta(1) also reduced myocyte necrosis as evident from lactate dehydrogenase release and trypan blue dye exclusion. These data demonstrate that hypoxia-reoxygenation results in apoptosis and necrosis in cultured adult rat myocytes; this can be attenuated by TGF-beta(1). Similarity of data with TGF-beta(1) and aggregated platelet supernatant suggests that platelet-mediated cardioprotection during hypoxia-reoxygenation may relate in part to the release of TGF-beta(1).

Animals↗
PubMed1999

Preliminary study on HA coating percutaneously implanted in bone.

A comparative investigation on the possibility of hydroxyapatite (HA) coating and pure Ti column to form biological sealing with skin tissue was completed in this study. HA coating and pure Ti column were percutaneously implanted in the tibia of rabbits. Compared with titanium (Ti) implant, HA coating forms epithelial sealing with skin tissue at 6 weeks postoperatively, while the Ti implant may loosen from the implanted site and be lost. The Ti column loosing rate at this time was 50%. However, once the Ti implant becomes fixed with the bone tissue, it can form epithelial sealing with skin tissue just like the HA coating, at 8 weeks postoperatively. At 8 weeks postoperatively, the epithelial sealing is not destroyed in spite of the fact that the HA coating is biodegraded. Our results show that the HA coating can become fixed with the bone faster than the Ti, which is beneficial for epithelial sealing formation. The main role of HA coating for epithelial sealing is beneficial for sealing at the initial period after it is implanted.

Animals↗
PubMed1998

Critical role of AT1 receptor expression after ischemia/reperfusion in isolated rat hearts: beneficial effect of antisense oligodeoxynucleotides directed at AT1 receptor mRNA.

To examine the relevance of angiotensin II type 1 receptor (AT1R) expression in the determination of myocardial function after ischemia/reperfusion, Sprague-Dawley rats were treated intravenously with antisense oligodeoxynucleotides (AS-ODNs) directed at AT1R mRNA (100 microg/rat, n=9) or scrambled antisense oligodeoxynucleotides (Scr-ODNs, 100 microg/rat, n=6). Both AS-ODNs and Scr-ODNs were given along with 300 microg/rat of liposome DOTAP/DOPE, a positive electron carrier (wt:wt= 1:1). The hearts from AS-ODN- or Scr-ODN-treated rats were excised 24 hours later, perfused in vitro, and subjected to 25 minutes of global ischemia followed by 30 minutes of reperfusion. Parallel groups of rats were given the specific AT1R antagonist losartan (10 mg/kg IV, n=6) or saline (n=7) 4 to 6 hours before excising the hearts. Ischemia/reperfusion resulted in a significant increase in myocardial AT1R expression (autoradiography and binding assay) and myocardial dysfunction, indicated by increases in coronary perfusion pressure and left ventricular end-diastolic pressure and a decrease in developed left ventricular pressure (all P<0.01 versus baseline) in the saline-treated group. AT1R protein and mRNA levels also increased in ischemic/ reperfused myocardial tissues. Administration of AS-ODNs or losartan, but not Scr-ODNs, preserved myocardial function and blocked the increased AT1R binding after ischemia/reperfusion (both P<0.01). Myocardial AT1R mRNA levels were not affected by either AS-ODNs or losartan, and the AT1R protein levels were significantly reduced by AS-ODN, but not losartan, treatment. Plasma angiotensin II levels increased after administration of losartan but not after administration of AS-ODNs. These observations imply a critical role of AT1R upregulation in determining myocardial function immediately after ischemia/reperfusion. AS-ODNs to AT1R mRNA may be more beneficial than losartan, because losartan does not affect the plasma angiotensin II level. The sustained increase in AT1R mRNA, but diminished protein expression, in rat hearts treated with AS-ODNs suggests that AS-ODNs block AT1R at the translational level.

Analysis of Variance↗
PubMed1998

Bacteria in semen used for IVF affect embryo viability but can be removed by stripping cumulus cells by vortexing.

Bacterial contamination of in vitro vs in vivo produced embryos presents a particular danger because of the alteration of the zona pellucida and the use of various biological products during culture. Our objective was to investigate the effects of semen contaminated with bacteria on IVF of bovine oocytes and to determine if removal of cumulus cells by vortexing as opposed to pipetting would reduce contamination and improve subsequent embryonic development. Semen from 5 bulls of the Native Korean breed (Bulls A, B, C, D, E) was used for IVF of matured oocytes. Preliminary studies had shown that the semen from Bulls A, B, D and E but not Bull C was contaminated with various species of common bacteria. After IVF, the cumulus cells surrounding the oocytes were removed either by pipetting or vortexing. Viability and cleavage rates of the resulting zygotes was assessed after 44 h in culture. When cumulus cells were removed by pipetting, only zygotes derived from oocytes that were fertilized with uncontaminated semen from Bull C developed to morula and blastocyst stages; zygotes derived from oocytes that were fertilized with contaminated semen from Bulls A, B, D and E started to degenerate, and the culture media became noticeably turbid. When cumulus cells were removed by vortexing, zygotes derived from oocytes fertilized with either contaminated or uncontaminated semen showed good rates of development (16 to 32%) to morula or blastocyst stages. From these results it can be concluded that the bacteria introduced with the semen contaminated the in vitro system and severely reduced the viability of the embryos. In contrast, complete removal of the cumulus cells with vortexing, as opposed to pipetting, reduced the contamination of the culture medium, allowing embryonic development to take place.

Animals↗
PubMed1998

Disassociation of sigma subunit from RNA polymerase of Xanthomonas oryzae pv. oryzae by phage Xp10 infection.

The sigma subunit of Xanthomonas oryzae pv. oryzae is disassociated from host RNA polymerase after phage Xp10 infection. To clarify the possible mechanism for this observation, sigma subunit was purified and an antiserum against sigma subunit was prepared. Immunoprecipitation of RNA polymerase by the anti-core RNA polymerase antiserum, followed by immunoblotting with anti-sigma subunit antibody, revealed that sigma subunit was lost from RNA polymerase within 10 minutes after Xp10 infection. Loss of sigma subunit was not observed under other stress conditions including heat and cold stress, starvation and growth to stationary phase. Two-dimensional immunoblotting analysis did not reveal any covalent modification of either sigma subunit or RNA polymerase after Xp10 infection. These results suggest that separation of th subunit from RNA polymerase may be due to competition with other binding factors.

Antibodies, Bacterial↗
PubMed1998

The expression of soluble intercellular adhesion molecule-1 in endometriosis.

OBJECTIVE: To investigate the association between concentrations of soluble intercellular adhesion molecule-1 (ICAM-1) and interferon-gamma (IFN-gamma) with regard to the severity of endometriosis. DESIGN: Cross-sectional study. SETTING: Infertility unit in a university hospital. PATIENT(S): Seventy-one infertile patients who underwent laparoscopic evaluation were divided into two groups: 36 patients with endometriosis served as cases, and 35 patients without endometriosis served as control subjects. INTERVENTION(S): Peripheral blood and peritoneal fluid (PF) were collected from these patients during laparoscopic examination. MAIN OUTCOME MEASURE(S): Quantitative determination of levels of human ICAM-1 and IFN-gamma was performed with the use of an ELISA. The data were evaluated by Student's t-test, analysis of variance, and regression analysis. RESULT(S): Significantly elevated levels of soluble ICAM-1 were found in the sera of patients with endometriosis, especially those with advanced stages of the disease. Decreased IFN-gamma levels, which were negatively correlated with serum levels of soluble ICAM-1, also were noted in the PF of patients with endometriosis. CONCLUSION(S): The increased serum levels of ICAM-1 found in patients with endometriosis may indicate the presence of an active disease process. Further, the increased levels of soluble ICAM-1 in peripheral blood were inversely correlated with the concentrations of IFN-gamma in PF. The increased levels of soluble ICAM-1 in plasma may be associated with an immunologic feedback response that blocks further infiltration of immune cells. These findings may be of value in the diagnosis and evaluation of endometriosis.

Adult↗
PubMed1998

Increased superoxide anion generation and altered vasoreactivity in rabbits on low-potassium diet.

Potassium reduces blood pressure in populations at high risk of developing hypertension, which suggests that potassium depletion may increase vascular resistance. This study was designed to examine the effect of potassium depletion on the L-arginine-nitric oxide pathway in arterial tissues. New Zealand White rabbits were fed either a control diet, containing a normal amount of potassium, or a low-potassium diet for 1-3 wk. As expected, the low-potassium diet resulted in reduced serum and urinary potassium levels. Carotid arteries were excised, and their contractile and relaxant responses were determined in vitro. Carotid arterial ring contractile response to norepinephrine was enhanced, and relaxation in response to the endothelium-dependent vasodilators acetylcholine and calcium ionophore A-23187 was attenuated, in rabbits fed low-potassium diet (all P < 0.01 compared with responses in rabbits fed control diet). The vasomotor responses were similarly altered in rabbits fed low-potassium diet for 1 or 3 wk. Both the enhanced contraction and attenuated relaxation were abolished by treatment of arterial rings with superoxide dismutase but not by treatment with L-arginine or indomethacin. Carotid artery rings from rabbits fed the low-potassium diet showed approximately 100% greater superoxide anion formation than those from rabbits fed control diet (P < 0.01), whereas plasma and urinary nitrite levels were similar in both groups of rabbits. These observations indicate that low-potassium diet enhances the sensitivity of the carotid artery to vasoconstrictor stimuli and reduces the sensitivity to endothelium-dependent stimuli. Attenuation of endothelium-dependent relaxation appears to be secondary to increased free radical generation, which may degrade nitric oxide. Altered vasoreactivity may underlie the genesis of hypertension in populations consuming diets low in potassium.

Acetylcholine↗
PubMed1998

Increased angiotensin II type 1 receptor expression in hypercholesterolemic atherosclerosis in rabbits.

Angiotensin II (Ang II) promotes vascular smooth muscle growth and may be involved in the initiation and progression of atherosclerosis. To examine whether Ang II receptor expression in vascular tissues is altered in atherosclerosis, male New Zealand White rabbits were fed a high-cholesterol diet (1% cholesterol + 4% coconut oil mixed with regular chow; hypercholesterolemic group, n=12) or regular chow (control group, n=8) for 10 weeks. At the end of this period, the serum cholesterol level in the rabbits fed the high-cholesterol diet was higher than that in the control group (3616 +/- 144 versus 30 +/- 1 mg/dL, P<0.001). There was no atherosclerosis in the aortas of the control group, whereas 51 +/- 6% of the aorta was covered with atherosclerosis in the hypercholesterolemic group. Total Ang II receptor expression in the atherosclerotic aortic tissues was increased 5-fold in the hypercholesterolemic rabbits (292 +/- 28 versus 51 +/- 32 fmol/mg tissue, mean +/- SE, P<0.001), and the increased Ang II receptor expression was entirely due to enhanced Ang II type 1 (AT1) receptor expression (289 +/- 38 versus 38 +/- 18 fmol/mg, P<0.001), as Ang II type 2 receptor expression was unaltered (7 +/- 5 versus 3 +/- 2 fmol/mg, P=NS). AT1 receptors were localized primarily in the media and to some extent in the intima of the atherosclerotic aorta, as determined by immunohistochemistry with specific monoclonal and polyclonal AT1 receptor antibodies. Increased synthesis of AT1 receptor mRNA in atherosclerotic tissues was confirmed by reverse transcription-polymerase chain reaction. To evaluate the functional significance of increased AT1 receptor expression, the constrictor response of aortic rings to Ang II was examined and found to be markedly enhanced in atherosclerotic aortic rings (P<0.01 versus control aortic rings). The endothelium-dependent relaxation of aortic rings from hypercholesterolemic rabbits was markedly attenuated (P<0.001). This study shows that hypercholesterolemia in rabbits results in atherosclerosis, loss of endothelium-dependent relaxation, and increased Ang II receptor (entirely AT1 receptor) expression in aortic tissues, which may result in altered vasoreactivity.

Acetylcholine↗
PubMed1998

Serum soluble interleukin-6 receptor and biochemical markers of bone metabolism show significant variations during the menstrual cycle.

We examined sequential changes of bone-resorbing cytokines and bone metabolic markers and the effect of ovarian hormones on bone metabolism during the menstrual cycle in 10 healthy Japanese women, aged 22-43 yr, with normal ovarian function. Serum soluble interleukin-6 receptor (sIL-6R) showed a significant variation; a rise during the early and late follicular periods followed by a fall during the early luteal period (P = 0.0423, P = 0.0334) and an increase during the mid and late luteal periods. There were significant changes in the levels of markers of bone formation: a rise in serum bone-specific alkaline phosphatase (ALP) during the mid and late follicular (P = 0.0265) periods and a fall in serum carboxyl-terminal propeptide of type I procollagen (PICP) during the midluteal period (P = 0.0161). As for the levels of bone resorption markers, urinary type I collagen C-telopeptide breakdown products (CTx) and free deoxypyridinoline (D-Pyr) decreased significantly during the early and midfollicular periods, urinary free D-Pyr and serum pyridinoline cross-linked carboxyl-terminal telopeptide of type I collagen (ICTP) (P = 0.0440) increased significantly during the early luteal period, and urinary CTx, free D-Pyr, and serum ICTP decreased significantly during the late luteal period (P = 0.0170-0.0008). The serum PTH level was significantly higher during the follicular than the luteal period (P = 0.0132). Serum sIL-6R significantly correlated with urinary CTx (r = 0.190, P < 0.05) and serum ALP (r = 0.209, P < 0.05) and serum estradiol with intact osteocalcin (r = 0.309, P < 0.0005) and serum ALP (r = 0.181, P < 0.05). These observations strongly suggest that cyclic variations in the levels of bone formation and resorption markers and of a bone-resorbing cytokine may be modulated by cyclic changes in serum steroid hormones during the menstrual period. In addition, the specific days of biochemical events in the menstrual cycle are crucial for evaluating osteoclastic and osteoblastic activities in pre- and perimenopausal women or in women starting GnRH agonist therapy.

Adult↗
PubMed1998

Differential expression of cytokine genes and apoptosis in glioma cell lines upon exposure to bacteria and lipopolysaccharides.

The influences of Escherichia coli, Streptococcus pyogenes and lipopolysaccharides (LPSs) on the expression of cytokines and apoptosis were investigated in two glioma cell lines. IL-1beta and TNF-alpha genes were modulated by bacteria in a time dependent fashion and their expression levels varied from sources of bacteria and cell lines used. E. coli and LPSs induced apoptosis in a very limited cell population as judged by cell counts, membrane alternation and DNA break in situ. The expression of fas and IL-6 genes was not affected by bacterial components. In conclusion, aberrant expression of cytokines but not apoptosis may be the major responses of the cells of glial origin upon exposure to bacteria and their components.

Apoptosis↗
PubMed1998

Effects of insulin on protein phosphorylation and protein kinase C activity in human malignant gliomas.

Modulation of protein phosphorylation activities by insulin was investigated in glioma and normal glial cells. Insulin suppressed the in vitro protein phosphorylation of glioma cells in a dose-dependent manner while it stimulated that of meningiomas, neurilemmomas and glial cells. Although gliomas and glial cells contained different species of tyrosyl phosphoproteins before treatment, they expressed similar kinds of tyrosyl phosphoproteins in response to insulin. Insulin increased the activities of casein kinase II and total protein kinase C (PKC) in glioma and normal glial cells. The membrane-bound PKC activity in U373-MG cells was elevated by insulin. The PKC isozymes, including subtypes alpha, beta, delta, epsilon and gamma, were detected in gliomas, but few were found in glial cells. Insulin down regulated the cytosolic PKC-gamma and the membrane-bound PKC-epsilon proteins in gliomas. These results indicate that an altered insulin signaling pathway exists in human gliomas, which might involve differential regulation of PKC isozymes.

Casein Kinase II↗
PubMed1997

Increase in angiotensin II type 1 receptor expression immediately after ischemia-reperfusion in isolated rat hearts.

BACKGROUND: Myocardial ischemia is known to upregulate the systemic renin-angiotensin system, which influences myocardial ischemic events by affecting hemodynamics and hemostatic activity. This study was designed to examine whether angiotensin II (Ang II) receptor expression in the myocardium is altered immediately after ischemia-reperfusion. METHODS AND RESULTS: Isolated buffer-perfused Sprague-Dawley rat hearts were subjected to continuous perfusion (control, n=5) or to 25 minutes of global ischemia followed by 30 minutes of reperfusion (n=10). Autoradiographic analysis for Ang II receptors of multiple myocardial sections was performed. Whereas continuous perfusion of hearts resulted in minor changes in coronary perfusion pressure (CPP), left ventricular end-diastolic pressure (LVEDP), and developed left ventricular pressure (dLVP=LVSP-LVEDP), ischemia-reperfusion caused a marked increase in CPP and LVEDP and a decrease in dLVP, indicating severe cardiac dysfunction. Concurrently, total myocardial Ang II receptor expression was greater (P<.05) in hearts subjected to ischemia-reperfusion than in the continuously perfused control hearts. Most of the increase in Ang II receptor expression was due to an increase in type 1 receptor (AT1) expression (34.6+/-6.5 versus 18.2+/-4.4 fmol/g, P<.05), because Ang II type 2 receptor expression was unaffected. To examine the importance of AT1 receptor expression, another group of isolated rat hearts (n=5) was perfused with buffer containing losartan (10(-5) mol/L) and subjected to ischemia followed by reperfusion. Perfusion of hearts with losartan attenuated the ischemia-reperfusion-induced cardiac dysfunction. Perfusion of hearts with losartan also blocked the ischemia-reperfusion-induced increase in myocardial AT1 binding. CONCLUSIONS: These observations indicate that myocardial AT1 expression increases immediately after ischemia-reperfusion and contributes to cardiac dysfunction.

Animals↗
PubMed1997

TNF receptor-2-triggered apoptosis is associated with the down-regulation of Bcl-xL on activated T cells and can be prevented by CD28 costimulation.

Stimulation of recently activated T cells results in apoptosis of the responding cells, a process referred to as activation-induced cell death. This process is believed to play an important role in the regulation of immune homeostasis and is suggested to be mediated mainly by interactions between Fas and Fas ligand. Recent evidence indicates that TNF-alpha and TNFR2 interaction plays an important role in down-regulating activated T cells. The role of TNFR2 signaling in activation-induced cell death, however, has not been directly examined. We demonstrate here that 48-h activated T cells are most sensitive to TNFR2-induced apoptosis. Cross-linking of TNFR2 on activated T cells results in down-regulated protein and mRNA expression of Bcl-xL. Furthermore, CD28 costimulation can prevent anti-TNFR2-induced apoptosis and restore Bcl-xL expression. These results have potential implications for understanding the role of TNFR2 signaling in the regulation of T cell responses.

Animals↗
PubMed1997

Enhanced interleukin-4 expression in patients with endometriosis.

OBJECTIVE: To investigate the expression of cytokines by T-helper cells type 1 (interleukin [IL]-2 and interferon-gamma [IFN-gamma]) and type 2 (IL-4 and IL-10) in peripheral blood monocytes and peritoneal fluid (PF) cells from patients with endometriosis. DESIGN: Peripheral blood (PB) monocytes and PF cells from patients with endometriosis were isolated and the expression of cytokines investigated. SETTING: Institute for the treatment of endometriosis and research institute in university-based medical center. PATIENT(S): The study included 7 women with normal pelvic structure, 36 patients with endometriosis, and 7 women with pelvic adhesion but without apparent endometriotic lesion. The existence and severity of endometriosis was determined by laparoscopic examination. INTERVENTION(S): All patients received laparoscopic operation to identify the existence and stages of endometriosis. Danazol (200 mg, twice daily) was prescribed for those with endometriosis. MAIN OUTCOME MEASURE(S): Transcription of cytokines were directly analyzed using the reverse transcriptase-polymerase chain reaction method. The concentrations of cytokines in peritoneal fluids and sera were analyzed by the ELISA. RESULT(S): Levels of IL-4 messenger RNA (mRNA) and protein in the PB and peritoneal cells of patients with endometriosis were higher than those of normal patients, whereas levels of IFN-gamma mRNA and protein were suppressed. There were no significant changes in the mRNA or protein levels of IL-2 or IL-10 in both peritoneal fluids and sera. The level of IL-4 was reduced to normal after combined treatment with laparoscopic surgery and danazol. The secretion of IFN-gamma was elevated after treatment. CONCLUSION(S): Cytokine secretion by T-helper cells type 1 and type 2 is altered in women with endometriosis, suggesting that these T-helper subsets play a role in the immunologic responses to endometriosis.

Ascitic Fluid↗