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Biomedical subjects

G Li

Publications and source records attributed to G Li.

At least 847 records · Page 47Linked to original sources
PubMed1995

[t(14:18) chromosomal translocation and over expression of bcl-2 protein in follicular type non-Hodgkin's lymphoma].

Polymerase chain reaction (PCR) and immunohistochemical staining methods were used to detect the bcl-2/IgH fusion gene [t(14:18)] and the overexpression of bcl-2 protein in 28 cases of follicular lymphomas and 18 cases of reactive follicular hyperplasia. The results showed that the bcl-2/IgH fusion gene was present in 57% of follicular lymphomas and that this translocation was also present in 33% of the reactive follicular hyperplasia cases. The over expression of bcl-2 protein was found in 78% of follicular lymphomas, but none in follicular hyperplasia, therefore bcl-2 protein staining may be a useful immunohistochemical method to differentiate follicular lymphoma and follicular hyperplasia.

Chromosomes, Human, Pair 14↗
PubMed1995

Hairy root culture of Artemisia annua L. by Ri plasmid transformation and biosynthesis of artemisinin.

The hairy root culture system of the medical plant Artemisia annua L. was established by infection with Agrobacterium rhizogenes R1601. The transgenic state of transformed roots was confirmed by Southern blot hybridization with TL-DNA of pFw302. The expression of NPTII gene was confirmed by enzymic assay. The important secondary metabolites-artemisinin was obtained in the hairy root culture. The effects of various physical and chemical factors on the growth of the hairy roots and production of artemisinin were studied. Artemisinin could be detected in hairy roots cultures in the light. The optimum pH value of the medium was 5.4. Fast growth of the hairy roots and maximal production of artemisinin was observed in the presence of 3% sucrose. Low concentration of naphthylacetic acid (0.025 mg/L) enhanced the growth of the roots but inhibited the production of artemisinin. The growth and artemisinin production in hairy root cultures were greatly promoted by the addition of gibberellin (GA3) to the medium. Its optimum concentration was 4.8 mg/L.

Antimalarials↗
PubMed1995

[Vitrectomy for treatment of vitreous hemorrhage associated with age-related macular degeneration].

Age-related macular degeneration (AMD) is an aging disorder which has been a leading cause for blindness among old people. The wet type AMD is the main cause which deteriorates visual function rapidly because of the complications including detachment of retinal pigment epithelium, formation of subretinal neovascular membrane and scar, subretinal and vitreous hemorrhage. This assay reports the results of vitrectomy for treatment of 10 cases with vitreous hemorrhage associated with AMD. The follow-up periods ranged from 1/2 to 28 months. The visual acuities in 9 cases were increased and in 1 case decreased. The factors affecting the postoperative visual acuity, operative complications and therapeutic prospects of the surgery were discussed.

Age Factors↗
PubMed1995

Crash and violation experience of pilots involved in prior commuter and air taxi crashes: a historical cohort study.

BACKGROUND: Commuter flights and air taxis represent a major category of aviation losses in terms of both human life and economic resources. Previous studies have examined human factors involved in these crashes. A retrospective study revealed that pilots' prior crash and violation records are associated with an increased risk of being involved in a commuter aircraft or an air taxi crash. HYPOTHESIS: Pilots who are involved in crashes are at increased risk of involvement in future crashes and violations. METHODS: Pilots who had been involved in and survived commuter aircraft or air taxi crashes during 1983-88 (crash group, n = 580) and a random sample of pilots who were flying for these commercial operations (control group, n = 1555) were followed up for 3 yr. The crash/incident and violation experience during the 3 yr of follow-up was compared between the two groups at univariate level and at multivariate level. RESULTS: During the 3 yr of follow-up, the incidence rate of crashes/incidents was significantly higher for the crash group than for the control group (12.4% vs. 7.2%, p < 0.01). The crash group also was more likely to have a violation record than the control group during the 3 yr of follow-up (8.6% vs. 3.7%, p < 0.01). These differences were not changed by adjusting for pilot age, total flight time and medical class. CONCLUSIONS: Pilots who were involved in commuter aircraft or air taxi crashes have significantly higher subsequent crash and violation rates than their counterparts. In order to develop effective prevention strategies, environmental and psychosocial factors that predispose pilots to increased risk of involvement in aviation crashes and violations should be examined.

Accident Proneness↗
PubMed1995

[Study of primary organotypic culture of the chicken auditory sensory epithelia].

Organotypic explants of auditory sensory epithelia-basilar papilla (BP) were prepared from 8-16 days postnatal chicken and cultured in vitro for up to 7 days using primary culture technique. The survival status and histological features of the BP were studied. The results showed that morphologic integrity of hair cells and supporting cells was well maintained in the duration of culture and was comparable to those in vivo. The paradigm anchorage-bottom with bFGF/collagen as a substrate provided the best result, whereas the free-floating method was optimal for a short period of culture within 48 hours. This could be a valuable experimental means for further research of the auditory hair cells in vitro.

Animals↗
PubMed1994

Dual effect of sodium nitroprusside on potentials recorded from mouse hippocampal slices.

The purpose of this research was to estimate the usefulness of sodium nitroprusside (SNP) as a donor of nitric oxide (NO) in the study of synaptic plasticity. The influence of SNP, K3Fe(CN)6 and K4Fe(CN)6 on the evoked potential recorded from mouse hippocampal slices was evaluated. When slices were exposed to 1 mM SNP for no longer than 15 min, a facilitation of the population spike was observed following perfusion. Longer, 60 min exposure of the slices to 1 mM SNP prevented this perfusion-induced amplification of the potential and blocked the induction of LTP by subsequently applied high frequency stimulation (HFS). SNP at lower concentrations (0.2 mM) had no effect. SNP (1 mM) suppressed the NMDA component of the population spike. Light inactivated, 1.0 mM SNP, when applied for 15 min, reduced the potential and subsequently induced LTP. However, longer exposure of the slices to the light inactivated 1 mM SNP made the potential unstable and blocked induction of LTP. K3Fe(CN)6 and K4Fe(CN)6, molecules structurally related to SNP but unable to generate NO, transiently amplified the population spike and its NMDA component. We suggest that SNP, which is often used as nitric oxide donor, exerts a dual inhibitory and facilitatory action on hippocampal evoked potentials. The possible mechanisms of these actions are discussed.

Animals↗
PubMed1994

Enhanced thrombolysis, reduced coronary reocclusion and limitation of infarct size with liposomal prostaglandin E1 in a canine thrombolysis model.

OBJECTIVES: The purpose of this study was to test the hypothesis that liposomal prostaglandin E1 (TLC C-53) would result in more rapid thrombolysis, less reocclusion and smaller infarct size when administered with heparin and streptokinase in a canine thrombolysis model. BACKGROUND: In experimental animals, prostaglandin E1 has been shown to augment thrombolysis, improve coronary flow and reduce infarct size when infused directly into the left atrium. TLC C-53 is a stable preparation of prostaglandin E1 bound by phospholipid microspheres that produces fewer adverse hemodynamic effects during intravenous use. METHODS: To investigate the effects of TLC C-53 on coronary patency and infarct salvage, we studied 30 conditioned open chest dogs. After coil-induced left anterior descending coronary artery occlusion and 1 h of clot maturation, the dogs were randomly assigned to receive a 10-min intravenous infusion of either TLC C-53 (2 micrograms/kg body weight) or placebo. Both groups then received intravenous heparin and streptokinase. Hemodynamic variables and Doppler coronary flow were monitored, and myocardial blood flow was determined using radioactive microspheres. Infarct size was assessed with triphenyltetrazolium chloride staining. RESULTS: Thrombolysis time was accelerated from 79 +/- 38 to 47 +/- 9 min (mean +/- SD), and coronary patency was greater (100% vs. 50%) with TLC C-53 than with placebo (p < 0.05). Moreover, for arteries that recanalized, coronary Doppler flow and myocardial perfusion were more severely impaired with placebo. Infarct size as a percent of the area at risk was higher (p < 0.05) with placebo (51 +/- 15%) than with TLC C-53 (33 +/- 14%). Neutrophil infiltration into ischemic myocardium determined by myeloperoxidase assay was also significantly greater in the placebo group. CONCLUSIONS: TLC C-53 administered intravenously before thrombolytic therapy resulted in a significant acceleration of thrombolysis time, improvement in coronary patency and blood flow during reperfusion and a reduction in infarct size.

Alprostadil↗
PubMed1994

CCAAT box binding protein NF-Y facilitates in vivo recruitment of upstream DNA binding transcription factors.

NF-Y binds a CCAAT motif found in many eukaryotic polymerase II-dependent promoters. In the HLA-DRA promoter it has been demonstrated that stereo-specific alignment between this motif and the upstream elements X1 and X2 is required for activation. To study the underlying mechanism for this requirement, a panel of transfected cell lines that maintained integrated, wild-type and mutant promoters were analyzed by in vivo genomic footprinting. Cell lines harboring a mutated CCAAT element exhibited a loss of interactions at the CCAAT site, as expected, and no transcriptional activity. Most importantly, mutation of the CCAAT sequence nearly abolished in vivo binding at the X1 and X2 sites, while mutations of X1 and X2 had little effect on CCAAT box binding. However, X1 and X2 binding was interdependent. In vitro, X1 binding activities are known to be stabilized by NF-Y binding. Interaction between NF-Y and X box binding proteins was demonstrated by reciprocal co-immunoprecipitation in the absence of DNA and co-affinity purification in the presence of DNA. Collectively, these studies indicate that occupancy of the CCAAT element represents an early event affecting other protein-DNA interactions and suggest that NF-Y stabilizes and interacts with X box factors to mediate this function. These findings may represent a common theme among promoters containing a CCAAT element.

Antiporters↗
PubMed1994

Blockage of NF-kappa B signaling by selective ablation of an mRNA target by 2-5A antisense chimeras.

Activation of 2-5A-dependent ribonuclease by 5'-phosphorylated, 2',5'-linked oligoadenylates, known as 2-5A, is one pathway of interferon action. Unaided uptake into HeLa cells of 2-5A linked to an antisense oligonucleotide resulted in the selective ablation of messenger RNA for the double-stranded RNA (dsRNA)-dependent protein kinase PKR. Similarly, purified, recombinant human 2-5A-dependent ribonuclease was induced to selectively cleave PKR messenger RNA. Cells depleted of PKR activity were unresponsive to activation of nuclear factor-kappa B (NF-kappa B) by the dsRNA poly(I):poly(C), which provides direct evidence that PKR is a transducer for the dsRNA signaling of NF-kappa B.

Adenine Nucleotides↗
PubMed1994

Rab5, an early acting endosomal GTPase, supports in vitro endosome fusion without GTP hydrolysis.

Endocytosis is regulated by several GTPases including Rab5 and one or more heterotrimeric G proteins. We show here that Rab5, in the GTP gamma S (guanosine 5'-O-(thiotriphosphate))-bound form, fully supports in vitro endosome fusion, indicating that GTP hydrolysis is not required, whereas Rab5:S34N and Rab5:N133I, mutants unable to bind GTP, are potent inhibitors of endosome fusion. Double mutants (Rab5:S34N/delta C4 and Rab5:N133I/delta C4) lacking the C-terminal prenylation site were inactive, indicating that prenylation is required. Endosomes became resistant to the inhibitory effects of Rab5:S34N by preincubating the vesicles with cytosol prior to the addition of the inhibitor. The acquisition of resistance to Rab5:S34N was more rapid than to N-ethylmaleimide, indicating that Rab5 mutants are early acting. G beta gamma subunits of heterotrimeric G proteins block endosome fusion. However the effect of G beta gamma was abrogated by Rab5-GTP gamma S, indicating that a heterotrimeric G protein may operate upstream of Rab5.

Endocytosis↗
PubMed1994

Dynamics of Ca2+ and guanosine 5'-[gamma-thio]triphosphate action on insulin secretion from alpha-toxin-permeabilized HIT-T15 cells.

The time course of Ca2+ and GTP-analogue effects on insulin secretion was investigated in HIT-T15 cells permeabilized with Staphylococcus alpha-toxin. These cells responded to Ca2+ in the range 0.1-10 microM and could be used in a dynamic perifusion system because of the minimal run-down of the secretory response. High Ca2+ (10 microM) elicited a monophasic ATP-dependent stimulation of insulin secretion that reached a peak within 5 min (approximately 20-fold increase) and rapidly decreased during the subsequent 15 min to a plateau remaining above basal rates (0.1 microM Ca2+). The decrease in Ca(2+)-induced insulin secretion with time could not be attributed to decreased capacity to respond to Ca2+ after prolonged perfusion at low Ca2+ (run-down), nor to depletion of a particular secretory-granule pool. It was rather due to desensitization of the secretory machinery to Ca2+ that was not reversed by selective inhibition of the Ca2+/calmodulin-dependent kinase II with KN-62. However, an intermediate Ca2+ concentration (2 microM) increased insulin secretion to stable level without causing any desensitization. Imposed oscillations of Ca2+ (0.1-10 microM) produced phasic oscillations of insulin secretion, but did not prevent desensitization to Ca2+. Poorly hydrolysable GTP analogues increased insulin secretion at low Ca2+, whereas they strongly inhibited Ca(2+)-induced insulin secretion. By contrast, GTP did not affect basal secretion, and slightly increased Ca(2+)-evoked secretion. These results indicate the following. (1) Oscillations of insulin secretion are tightly coupled to cytosolic Ca2+ oscillations. (2) Oscillations of Ca2+ do not prevent high-Ca(2+)-induced desensitization to Ca2+; this result does not support the idea of a greater efficiency of oscillations compared with sustained Ca2+ rises in triggering exocytosis. (3) Activation of G-proteins modulates exocytosis in a bimodal manner.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Mitotic regulation of microtubule cross-linking activity of CENP-E kinetochore protein.

CENP-E is a kinesin-like protein that is transiently bound to kinetochores during early mitosis, becomes redistributed to the spindle midzone at anaphase, and is degraded after cytokinesis. At anaphase, CENP-E may cross-link the interdigitating microtubules in the spindle midzone through a motor-like binding site at the amino terminus and a 99-amino acid carboxyl-terminal domain that bound microtubules in a distinct manner. Phosphorylation of the carboxyl terminus by the mitotic kinase maturation promoting factor (MPF) inhibited microtubule-binding activity before anaphase. Thus, MPF suppresses the microtubule cross-linking activity of CENP-E until anaphase, when its activity is lost.

Anaphase↗
PubMed1994

Structural features of the GTP-binding defective Rab5 mutants required for their inhibitory activity on endocytosis.

Rab5 is a Ras-like small GTPase that regulates early events of endocytosis. Previous work indicates that two GTP-binding defective Rab5 mutants (Rab5:S34N and Rab5:N133I) are dominant inhibitors of endocytosis. In this report, we have initiated experiments to address the structural features necessary for the inhibitory activity of these two Rab5 mutants. Second-site mutations were introduced into Rab5:S34N and Rab5:N133I, respectively, and the resulting double mutants were expressed in cultured BHK-21 cells via a Sindbis virus expression vector. Endocytic activity of the cells was monitored by following the uptake of a fluid-phase endocytic marker (horseradish peroxidase). The effects of the Rab5 mutants on endosome fusion in vitro were also examined. Truncation of the C-terminal isoprenylation motif CCSN abolished the inhibitory activity of both Rab5:S34N and Rab5:N133I. The same held true when the secondary mutation was a substitution mutation (F57S) in the effector domain. Another substitution mutation in this region (I53A) had no effect on the inhibitory activity of either Rab5:S34N or Rab5:N133I. The final mutation (R81A) was created immediately downstream of the second GTP binding motif (WDTAGQER), i.e. in the loop 4 region based on the structural model of Ras. This mutation greatly decreased the isoprenylation of Rab5:N133I and its inhibitory activity on endocytosis. It is believed that Rab5 function requires protein-protein interactions with Rab5-specific regulators and effectors. Some of these interactions are disrupted by Rab5:S34N and Rab5:N133I. By analogy to Ras, both Rab5:S34N and Rab5:N133I are likely to sequester a Rab5-specific guanine nucleotide exchange factor. This interaction requires the effector domain Phe57 residue and C-terminal isoprenylation of Rab5.

Amino Acid Sequence↗