Biomedical subjects

G L Yu

Publications and source records attributed to G L Yu.

At least 19 recordsLinked to original sources

PubMed2006

Increased expression of cysteinyl leukotriene receptor-1 in the brain mediates neuronal damage and astrogliosis after focal cerebral ischemia in rats.

Cysteinyl leukotrienes are potent pro-inflammatory mediators. Cysteinyl leukotriene receptor 1 is one of the two cysteinyl leukotriene receptors cloned. We recently reported that cysteinyl leukotriene receptor 1 antagonists protected against cerebral ischemic injury, and an inducible expression of cysteinyl leukotriene receptor 1 was found in neuron- and glial-appearing cells after traumatic injury in human brain. To determine the role of cysteinyl leukotriene receptor 1 in ischemic brain injury, we investigated the temporal and spatial profile of cysteinyl leukotriene receptor 1 expression in rat brain from 3 h to 14 days after 30 min of middle cerebral artery occlusion, and observed the effect of pranlukast, a cysteinyl leukotriene receptor 1 antagonist, on the ischemic injury. We found that cysteinyl leukotriene receptor 1 mRNA expression was up-regulated in the ischemic core both 3-12 h and 7-14 days, and in the boundary zone 7-14 days after reperfusion. In the ischemic core, cysteinyl leukotriene receptor 1 was primarily localized in neurons 24 h, and in macrophage/microglia 14 days after reperfusion; while in the boundary zone it was localized in proliferated astrocytes 14 days after reperfusion. Pranlukast attenuated neurological deficits, reduced infarct volume and ameliorated neuron loss in the ischemic core 24 h after reperfusion; it reduced infarct volume, ameliorated neuron loss and inhibited astrocyte proliferation in the boundary zone 14 days after reperfusion. Thus, we conclude that cysteinyl leukotriene receptor 1 mediates acute neuronal damage and subacute/chronic astrogliosis after focal cerebral ischemia.

Animals↗

PubMed2002

X-ray structures of Torpedo californica acetylcholinesterase complexed with (+)-huperzine A and (-)-huperzine B: structural evidence for an active site rearrangement.

Kinetic and structural data are presented on the interaction with Torpedo californica acetylcholinesterase (TcAChE) of (+)-huperzine A, a synthetic enantiomer of the anti-Alzheimer drug, (-)-huperzine A, and of its natural homologue (-)-huperzine B. (+)-Huperzine A and (-)-huperzine B bind to the enzyme with dissociation constants of 4.30 and 0.33 microM, respectively, compared to 0.18 microM for (-)-huperzine A. The X-ray structures of the complexes of (+)-huperzine A and (-)-huperzine B with TcAChE were determined to 2.1 and 2.35 A resolution, respectively, and compared to the previously determined structure of the (-)-huperzine A complex. All three interact with the "anionic" subsite of the active site, primarily through pi-pi stacking and through van der Waals or C-H.pi interactions with Trp84 and Phe330. Since their alpha-pyridone moieties are responsible for their key interactions with the active site via hydrogen bonding, and possibly via C-H.pi interactions, all three maintain similar positions and orientations with respect to it. The carbonyl oxygens of all three appear to repel the carbonyl oxygen of Gly117, thus causing the peptide bond between Gly117 and Gly118 to undergo a peptide flip. As a consequence, the position of the main chain nitrogen of Gly118 in the "oxyanion" hole in the native enzyme becomes occupied by the carbonyl of Gly117. Furthermore, the flipped conformation is stabilized by hydrogen bonding of Gly117O to Gly119N and Ala201N, the other two functional elements of the three-pronged "oxyanion hole" characteristic of cholinesterases. All three inhibitors thus would be expected to abolish hydrolysis of all ester substrates, whether charged or neutral.

Acetylcholinesterase↗

PubMed2001

Modulation of endothelial cell growth arrest and apoptosis by vascular endothelial growth inhibitor.

Vascular endothelial growth inhibitor (VEGI), a new member of the tumor necrosis factor family, is an endothelial cell-specific gene and a potent inhibitor of endothelial cell proliferation, angiogenesis, and tumor growth. We report here that VEGI mediates the following two activities in endothelial cells: early G(1) arrest in G(0)/G(1) cells responding to growth stimuli, and programmed death in proliferating cells. G(0)/G(1)-synchronized bovine aortic endothelial cells were treated with VEGI before and after the onset of the growth cycle. When the cells were stimulated with growth conditions but treated simultaneously with VEGI, a reversible, early-G(1) growth arrest occurred, evidenced by the lack of late G(1) markers such as hyperphosphorylation of the retinoblastoma gene product and upregulation of the c-myc gene. Additionally, VEGI treatment led to inhibition of the activities of cyclin-dependent kinases CDK2, CDK4, and CDK6. In contrast, VEGI treatment of cells that had entered the growth cycle resulted in apoptotic cell death, as evidenced by terminal deoxytransferase labeling of fragmented DNA, caspase 3 activation, and annexin V staining, all of which were lacking in nonproliferating cells treated with VEGI. Additionally, stress-signaling proteins p38 and JNK were not as fully activated by VEGI in quiescent as compared with proliferating populations. These findings suggest a dual role for VEGI, the maintenance of growth arrest and induction of apoptosis, in the modulation of the endothelial cell cycle.

Animals↗

PubMed2001

[Contrast of losartan, fosinopril and amlodipine on cardiomyocyte apoptosis and left ventricular remolding in hypertensive rats].

OBJECTIVE: To investigate effects of losartan, fosinopril and amlodipine on cardiomyocyte apoptosis, cardiac remolding in the spontaneously hypertensive rats (SHR). METHODS: SHRs were treated with lorsartan (SHR-L), fosinopril (SHR-F), amlodipine (SHR-A), and untreated (SHR-C) respectively for 8 and 16 weeks. Cardiomyocyte apoptotic index (APOI), left ventricular mass, left ventricular mass index (LVM, LVMI), and plasma and myocardium angiotensin II(PAng II, MAng II) concentrations were examined. RESULTS: 1. The systolic blood pressure was decreased similarly in all treatment groups in 8 and 16 weeks. LVMIs were reduced significantly in all treatment groups. LVMI was significantly lower in SHR-F group than that in other two treatment groups in 16 weeks. 2. APOIs were decreased significantly in SHR-F group in 8 weeks and in all treatment groups, especially in SHR-F group in 16 weeks. 3. Compared with SHR-C group in both periods, PAng II and MAng II were significantly increased in SHR-L group, but MAng II concentration was only decreased significantly in SHR-F group in 8 weeks, and in SHR-F and SHR-A groups in 16 weeks. CONCLUSION: Losartan, amlodipine, and especially fosinopril can inhibit cardiomyocyte apoptosis, prevent myocardial fibrosis, and reverse heart hypertrophy. Inhibition of myocardium rennin--angiotension--aldsteron system may be the mechanism of the three drugs' cardioprotective effects.

Amlodipine↗

PubMed2001

[Effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin II and cardiac remolding in hypertensive rats].

OBJECTIVE: To investigate effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin II and cardiac remolding in the spontaneously hypertensive rats (SHR). METHODS: 16-week-old SHRs were divided randomly into 3 groups: SHR-L (treated with lorsartan), SHR-F (treated with fosinopril) and SHR-C (untreated), each group consisting of 10 rats. After 8 weeks' and 16 weeks' therapeutic period, collagen volume fraction (CVF), perivascular circumferential area (PVCA), plasma and myocardium angiotensin II concentrations were examined by pathological examination with computed processing and radioimmunoassay respectively. RESULTS: (1) Compared with SHR-C after 8 weeks' and 16 weeks' therapeutic period, the systolic blood pressure (SBP) was decreased similarly in both treatment groups. Heart and left ventricular weights, heart weight and eft ventricular mass indexes were lower significantly in both treatment groups than in SHR-C. Left ventricular mass index was reduced to a lower extent in SHR-F group than in SHR-L group after 16 weeks. (2) Compared with SHR-C, CVF, PVCA after 8 weeks and 16 weeks were reduced significantly in SHR-F and SHR-L. Meanwhile, CVF after 16 weeks in SHR-F than in SHR-L. (3) Compared with SHR-C after both therapeutic periods, plasma and myocardium angiotensin II concentrations were increased Significantly in SHR-L, but plasma angiotensin II concentrations were not altered significantly in SHR-F. However, myocardium angiotensin II concentrations were reduced significantly in SHR-F after 8 weeks and 16 weeks in SHR-F. CONCLUSION: Lorsartan, fosinopril inhibit myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these above effects than Lorsartan. The mechanism of the both drug's cardioprotective effects was related to inhibition of myocardium rennin-angiotension-aldsteron system.

Angiotensin II↗

PubMed1999

VEGI, a new member of the TNF family activates nuclear factor-kappa B and c-Jun N-terminal kinase and modulates cell growth.

Recently a new member of the human tumor necrosis factor (TNF) family named as VEGI was reported. However, very little is known about the biological activities displayed by this cytokine. In this report, we show that in myeloid cells VEGI activated the transcription factor kappa B (NF-kappa B) as determined by the electrophoretic mobility shift assay, induced degradation of I kappa B alpha, and nuclear translocation of p65 subunit of NF-kappa B. VEGI also activated NF-kappa B-dependent reporter gene expression. In addition, VEGI activated c-Jun N-terminal kinase. When examined for growth modulatory effects, VEGI inhibited the proliferation of breast carcinoma (MCF-7), epithelial (HeLa), and myeloid (U-937 and ML-1a) tumor cells; and activated caspase-3 leading to PARP cleavage. VEGI-induced cytotoxicity was potentiated by inhibitors of protein synthesis. VEGI also induced proliferation of normal human foreskin fibroblast cells. The activity of VEGI could neither be neutralized by antibodies against TNF, nor could it compete with TNF binding, indicating that the activity of VEGI is not due to TNF and it binds to a distinct receptor. These results suggest that VEGI, a new member of the TNF family, has a signaling pathway similar to TNF and is most likely a multifunctional cytokine.

Base Sequence↗

PubMed1999

Vicinal-thiol-containing molecules enhance but mono-thiol-containing molecules reduce nickel-induced DNA strand breaks.

Several thiol-containing molecules (TCM) are currently used as antidotes for nickel, and vicinal TCM seem to be more effective in mobilizing tissue nickel than are mono TCM. Using single cell alkaline electrophoresis, we have shown that the vicinal TCM, meso-2, 3-dimercaptosuccinic acid (DMSA), 2,3-dimercaptopropane-1-sulfonate, and 2,3-dimercaptopropanol markedly enhanced, whereas the mono TCM, D-penicillamide, glutathione, beta-mercaptoethanol, and diethyl dithiocarbomate, reduced nickel chloride (Ni)-induced DNA breaks in a human leukemia cell line, NB4 cells. Ni or TCM alone did not induce plasmid DNA breaks in test tubes and neither did Ni plus mono TCM; however, Ni plus vicinal TCM did. Vicinal TCM did, but mono TCM did not generate H(2)O(2) in solution. H(2)O(2) alone did not, but H(2)O(2) plus Ni induced plasmid DNA breaks. Although Ni plus glutathione did not break DNA, Ni plus glutathione plus H(2)O(2) did. The Ni-DMSA-induced DNA breaks in NB4 cells, as well as in plasmids, were completely prevented by d-mannitol or partially prevented by several antioxidants. Therefore, the DNA breaks induced by Ni plus vicinal TCM seem to be due to the complex of Ni with TCM in concert with the H(2)O(2) produced by the vicinal TCM. The results that DMSA at a concentration as low as 5 microM enhanced the Ni-induced DNA breaks suggest a further evaluation of the TCM as nickel chelators is needed.

Cell Line↗

PubMed1999

Inhibition of angiogenesis and breast cancer xenograft tumor growth by VEGI, a novel cytokine of the TNF superfamily.

Recently, we reported a novel protein of the tumor necrosis factor (TNF) superfamily, named vascular endothelial cell growth inhibitor (VEGI), which is expressed predominantly in endothelial cells. When a secreted form of this new protein was overexpressed in mouse colon cancer cells, the growth of tumors formed by these cells in black mice was inhibited. We now report that recombinant VEGI inhibits the proliferation of endothelial cells but not that of other types of cells examined. The protein also inhibits formation of capillary-like structures by endothelial cells in collagen gels, and the growth of capillaries into collagen gels placed on the chick chorioallantoic membrane. The anticancer potential of VEGI was examined in a breast cancer xenograft tumor model in which the cancer cells were co-injected with Chinese hamster ovary cells overexpressing a secreted form of the protein. The co-injection resulted in potent inhibition of xenograft tumor growth. Our findings are consistent with the view that VEGI is an endothelial cell-specific negative regulator of angiogenesis.

Animals↗

PubMed1999

Identification and characterization of a novel cytokine, THANK, a TNF homologue that activates apoptosis, nuclear factor-kappaB, and c-Jun NH2-terminal kinase.

By using the amino acid sequence motif of tumor necrosis factor (TNF), we searched the expressed sequence tag data base and identified a novel full-length cDNA encoding 285 amino acid residues and named it THANK. THANK is a type II transmembrane protein with 15-20% overall amino acid sequence homology to TNF, LT-alpha, FasL, and LIGHT, all members of the TNF family. The mRNA for THANK was expressed at high levels by peripheral blood leukocytes, lymph node, spleen, and thymus and at low levels by small intestine, pancreas, placenta, and lungs. THANK was also prominently expressed in hematopoietic cell lines. The recombinant purified protein expressed in the baculovirus system had an approximate molecular size 20 kDa with amino-terminal sequence of AVQGP. Treatment of human myeloid U937 cells with purified THANK activated nuclear transcription factor-kappaB (NF-kappaB) consisting of p50 and p65. Activation was time- and dose-dependent, beginning with as little as a 1 pM amount of the cytokines and as early as 15 min. Under the same conditions, THANK also activated c-jun NH2-terminal kinase (JNK) in U937 cells. THANK also strongly suppressed the growth of tumor cell lines and activated caspase-3. Although THANK had all the activities and potency of TNF, it did not bind to the TNF receptors. Thus our results indicate that THANK is a novel cytokine that belongs to the TNF family and activates apoptosis, NF-kappaB, and JNK through a distinct receptor.

Amino Acid Sequence↗

PubMed1999

Evaluation of nitrate tolerance in patients with coronary heart disease by vascular ultrasonography and treadmill exercise.

The aim of this study was to evaluate nitrate tolerance in patients with coronary heart diseases by vascular ultrasonography and treadmill exercise. According to the dosage interval of isosorbide dinitrate, 66 patients with coronary heart disease were divided into group A and group B in a random, control and double-blind method. Isosorbide dinitrate was given every 6 hours in group A and every 12 hours in group B for one week. Before and after the therapeutic period, the diameters of brachial arteries were measured by vascular ultrasonography at baseline and 5 min after sublingual administration of 10 mg isosorbide dinitrate, and the treadmill exercise test was performed in all subjects. The results showed that diameters of brachial arteries were increased significantly after sublingual isosorbide dinitrate in both groups before the therapeutic period. After the therapeutic period, dilation of brachial arteries induced by sublingual isosorbide dinitrate was more marked in group B than in group A. Compared with those before the therapeutic period, sigmaST segment depression decreased and treadmill walking time increased significantly in group B but not in group A after the therapeutic period. These findings suggest that less frequent doses of isosorbide dinitrate may prevent development of nitrate tolerance, which is confirmed by vascular ultrasonography combined with treadmill exercise in patients with coronary heart disease.

Adult↗

PubMed1999

Identification of a novel activation-inducible protein of the tumor necrosis factor receptor superfamily and its ligand.

Among members of the tumor necrosis factor receptor (TNFR) superfamily, 4-1BB, CD27, and glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) share a striking homology in the cytoplasmic domain. Here we report the identification of a new member, activation-inducible TNFR family member (AITR), which belongs to this subfamily, and its ligand. The receptor is expressed in lymph node and peripheral blood leukocytes, and its expression is up-regulated in human peripheral mononuclear cells mainly after stimulation with anti-CD3/CD28 monoclonal antibodies or phorbol 12-myristate 13-acetate/ionomycin. AITR associates with TRAF1 (TNF receptor-associated factor 1), TRAF2, and TRAF3, and induces nuclear factor (NF)-kappaB activation via TRAF2. The ligand for AITR (AITRL) was found to be an undescribed member of the TNF family, which is expressed in endothelial cells. Thus, AITR and AITRL seem to be important for interactions between activated T lymphocytes and endothelial cells.

Amino Acid Sequence↗

PubMed1999

TL1, a novel tumor necrosis factor-like cytokine, induces apoptosis in endothelial cells. Involvement of activation of stress protein kinases (stress-activated protein kinase and p38 mitogen-activated protein kinase) and caspase-3-like protease.

TL1 is a recently discovered novel member of the tumor necrosis factor (TNF) cytokine family. TL1 is abundantly expressed in endothelial cells, but its function is not known. The present study was undertaken to explore whether TL1 induces apoptosis in endothelial cells and, if so, to explore its mechanism of action. Cultured bovine pulmonary artery endothelial cells (BPAEC) exposed to TL1 showed morphological (including ultrastructural) and biochemical features characteristic of apoptosis. TL1-induced apoptosis in BPAEC was a time- and concentration-dependent process (EC50 = 72 ng/ml). The effect of TL1 was not inhibited by soluble TNF receptors 1 or 2. TL1 up-regulated Fas expression in BPAEC at 8 and 24 h after treatment, and significantly activated stress-activated protein kinase (SAPK) and p38 mitogen-activated protein kinase (p38 MAPK). The peak activities of SAPK and p38 MAPK in TL1-treated BPAEC were increased by 9- and 4-fold, respectively. TL1-induced apoptosis in the BPAEC was reduced by expression of a dominant-interfering mutant of c-Jun (62.8%, p < 0.05) or by a specific p38 inhibitor, SB203580 (1-10 microM) dose-dependently. TL1 also activated caspases in BPAEC, and TL1-induced apoptosis in BPAEC was significantly attenuated by the caspase inhibitor, ZVAD-fluromethyl-ketone. The major component activated by TL1 in BPAEC was caspase-3, which was based on substrate specificity and immunocytochemical analysis. These findings suggest that TL1 may act as an autocrine factor to induce apoptosis in endothelial cells via activation of multiple signaling pathways, including stress protein kinases as well as certain caspases.

Animals↗

PubMed1999

VEGI, a novel cytokine of the tumor necrosis factor family, is an angiogenesis inhibitor that suppresses the growth of colon carcinomas in vivo.

A novel member of the tumor necrosis factor (TNF) family has been identified from the human umbilical vein endothelial cell cDNA library, named vascular endothelial growth inhibitor (VEGI). The VEGI gene was mapped to human chromosome 9q32. The cDNA for VEGI encodes a protein of 174 amino acid residues with the characteristics of a type II transmembrane protein. Its amino acid sequence is 20-30% identical to other members of the TNF family. Unlike other members of the TNF family, VEGI is expressed predominantly in endothelial cells. Local production of a secreted form of VEGI via gene transfer caused complete suppression of the growth of MC-38 murine colon cancers in syngeneic C57BL/6 mice. Histological examination showed marked reduction of vascularization in MC-38 tumors that expressed soluble but not membrane-bound VEGI or were transfected with control vector. The conditioned media from soluble VEGI-expressing cells showed marked inhibitory effect on in vitro proliferation of adult bovine aortic endothelial cells. Our data suggest that VEGI is a novel angiogenesis inhibitor of the TNF family and functions in part by directly inhibiting endothelial cell proliferation. The results further suggest that VEGI maybe highly valuable toward angiogenesis-based cancer therapy.

Amino Acid Sequence↗

PubMed1998

LIGHT, a novel ligand for lymphotoxin beta receptor and TR2/HVEM induces apoptosis and suppresses in vivo tumor formation via gene transfer.

LIGHT is a new member of tumor necrosis factor (TNF) cytokine family derived from an activated T cell cDNA library. LIGHT mRNA is highly expressed in splenocytes, activated PBL, CD8(+) tumor infiltrating lymphocytes, granulocytes, and monocytes but not in the thymus and the tumor cells examined. Introduction of LIGHT cDNA into MDA-MB-231 human breast carcinoma caused complete tumor suppression in vivo. Histological examination showed marked neutrophil infiltration and necrosis in LIGHT expressing but not in the parental or the Neo-transfected MDA-MB-231 tumors. Interferon gamma (IFNgamma) dramatically enhances LIGHT-mediated apoptosis. LIGHT protein triggers apoptosis of various tumor cells expressing both lymphotoxin beta receptor (LTbetaR) and TR2/HVEM receptors, and its cytotoxicity can be blocked specifically by addition of a LTbetaR-Fc or a TR2/HVEM-Fc fusion protein. However, LIGHT was not cytolytic to the tumor cells that express only the LTbetaR or the TR2/HVEM or hematopoietic cells examined that express only the TR2/HVEM, such as PBL, Jurkat cells, or CD8(+) TIL cells. In contrast, treatment of the activated PBL with LIGHT resulted in release of IFNgamma. Our data suggest that LIGHT triggers distinct biological responses based on the expression patterns of its receptors on the target cells. Thus, LIGHT may play a role in the immune modulation and have a potential value in cancer therapy.

Apoptosis↗

PubMed1998

TRANK, a novel cytokine that activates NF-kappa B and c-Jun N-terminal kinase.

We searched the expressed sequence tag database using sequence homology and identified a novel cytokine, which we have named TRANK (thioredoxin peroxidase-related activator of NF-kappa B and c-Jun N-terminal kinase). The predicted amino acid sequence of TRANK was highly homologous to that of the thiol-specific antioxidant proteins. Unlike these proteins, however, TRANK had a putative secretory signal polypeptide and was found to be secreted by cells. TRANK was expressed in most tissues and cell lines, and the gene that encodes it was mapped to chromosome Xp21-22.1. TRANK activated NF-kappa B and induced the degradation of the inhibitory subunit of NF-kappa B. In addition, TRANK up-regulated the expression of NF-kappa B-dependent gene products, ICAM-1, and inducible nitric oxide synthase. TRANK also activated c-Jun N-terminal kinase and induced the proliferation of normal human foreskin fibroblasts. Its homology with antioxidant proteins, wide distribution in tissues, and ability to activate NF-kappa B and c-Jun N-terminal kinase suggest that TRANK plays an important role in inflammation.

Amino Acid Sequence↗

PubMed1998

Clinical significance of QT dispersion after exercise in patients with previous myocardial infarction.

To evaluate the clinical significance of QT dispersion after exercise in patients with previous myocardial infarction, QT dispersion (QTd) and corrected QTd (QTcd) were assessed with standard 12 leads electrocardiogram in 90 patients with previous myocardial infarction and 30 healthy persons before and 3 min after a treadmill exercise test. In addition, 24 h ambulatory electrocardiogram and echo-cardiography were examined in all the subjects studied. Patients were followed up for 37.25 +/- 10.71 months. The results showed that there were no significant differences in the QTd and QTcd between the patients and the controls before exercise (36.11 +/- 13.42 ms versus 34.81 +/- 12.32 ms, P>0.05, 41.22 +/- 13.49 as versus 39.91 +/- 13.56 ms, P>0.05). Compared with those before exercise, QTd and QTcd were significantly increased in the patients 3 min after the exercise test (36.11 +/- 13.42 ms versus 47.20 +/- 14.41 ms, P<0.01, 41.22 +/- 13.49 ms versus 59.57 +/- 18.90 ms, P<0.01), but not in the controls (34.81 +/- 12.32 ms versus 38.76 +/- 12.09 ms, P>0.05, 39.91 +/- 13.56 ms versus 43.27 +/- 17.77 ms, P>0.05). The incidences of abnormal contraction of the left ventricular wall, aneurysms, NYHA III class, >III class of Lown's ventricular arrhythmia classification and cardiac sudden death were significantly higher in group A with QTcd >50 ms than that of group B with QTcd <50 ms (P<0.01). These findings indicate that the increased QT dispersion after exercise in 12 standard leads electrocardiogram might be associated with high incidences of sudden cardiac death and ventricular arrhythmia in the patients with previous myocardial infarction.

Adult↗

PubMed1998

LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator.

Herpes simplex virus (HSV) 1 and 2 infect activated T lymphocytes by attachment of the HSV envelope glycoprotein D (gD) to the cellular herpesvirus entry mediator (HVEM), an orphan member of the tumor necrosis factor receptor superfamily. Here, we demonstrate that HVEM binds two cellular ligands, secreted lymphotoxin alpha (LTalpha) and LIGHT, a new member of the TNF superfamily. LIGHT is a 29 kDa type II transmembrane protein produced by activated T cells that also engages the receptor for the LTalphabeta heterotrimer but does not form complexes with either LTalpha or LTbeta. HSV1 gD inhibits the interaction of HVEM with LIGHT, and LIGHT and gD interfere with HVEM-dependent cell entry by HSV1. This characterizes herpesvirus gD as a membrane-bound viokine and establishes LIGHT-HVEM as integral components of the lymphotoxin cytokine-receptor system.

Amino Acid Sequence↗

PubMed1998

An improved electrogastrographic system in measuring myoelectrical parameters.

This study assessed the reliability of an improved electrogastrographic (EGG) system in recording stomach myoelectrical parameters and tried to establish the normal ranges of myoelectricity using this system. The analytical software of the current system mainly included an autoregressive modelling program to compute myoelectrical frequency and power. Forty healthy subjects were enrolled to receive myoelectrical measurement in two consecutively fasting and one postprandial 30 min sessions. The myoelectrical frequencies in both fasting and postprandial sessions were almost three cycles per min (c.p.m.) and showed little variation. The percentage of dominant frequencies (2.5-3.5 c.p.m.) in three sessions was approximately 80% while the computed myoelectrical powers in the first and second fasting sessions exhibited a significant correlation (r=0.84, P<0.001). Meal ingestion increased the myoelectrical powers by 6.8dB compared with the second fasting recording (P< 0.001). The mean variation in myoelectrical amplitude for the ratio of second: first fasting session was 110.3+/-88.8% (16-478%, median 88%). This new EGG system is, indeed, reliable for measuring myoelectrical frequency and power, whereas the interassay of recorded amplitudes appears markedly variable.

Adult↗