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L Mei

Publications and source records attributed to L Mei.

At least 55 records · Page 3Linked to original sources
PubMed1998

Study on the metastatic mechanisms of human giant-cell lung carcinoma comparison between the strains C and D.

The biologic characteristics of the two human giant-cell lung carcinoma strains with high (strain D) and low metastatic potential (strain C) were studied, including karyotype of chromosome, intracellular free calcium ([Ca2+]i), morphologic changes of cell surface and the expression of nm23-H1, p53, ras, c-myc, c-erbB2, bcl-2 genes and PCNA. The correlation between different biologic features and the metastatic potential of the two strains was analyzed. We found: 1) Both strains had the karyotypic abnormality of -13, -14, -15, +20, +21 with seven same marker chromosomes. Only strain D had the karyotypic abnormality of +7, -17, -18, +X, 7p+; 2) [Ca2+]i of the strain C (984.7 +/- 573.8) and D (517.6 +/- 216.6) was significantly different (p < 0.05). The amplitude of intracellular calcium oscillations of strain C was lower than the one of strain D; 3) strain C had more villous-like protrusions on the cell surface, whereas strain D had more bubble-like protrusions; 4) The expression of nm23-H1 and p53 protein of strain C was all higher than that of strain D. The expression of PCNA of strain C was lower than strain D; 5) nm23-H1 mRNA levels of strain C was lower than that of strain D. We consider that the karyotype of chromosomes, intracellular free calcium, the structure of cell membrane and the expression of nm23-H1 gene, p53 gene, PCNA could be closely related to the metastatic potential of human giant-cell lung carcinoma. They could be used as the sign for judging whether the tumor will metastasize in clinical practice as well as in judging the prognoses of patients.

Calcium↗
PubMed1998

[Long-term results of combined splenorenal shunt and porta-azygos devascularization in patients with portal hypertension].

OBJECTIVE: To investigate the long-term effects of combined splenorenal shunt and porta-azygos devascularization in patients with portal hypertension. METHOD: We analysed retrospectively the follow-up results of 140 portal hypertensive patients undergoing the combined therapy in our hospital from April 1978 to April 1997. Changes of portal hemodynamics were studied by Doppler Flowmeter and DSA pre- and-postoperatively and direct FPP measurement intraoperatively. RESULT: The operative mortality was 3.6%. No rebleeding was noted in a short period and rebleeding rate was 8.3% in a long term follow-up. The rate of postoperative hepatic encephalopathy was 5.0%. The long-term survival rate of 5-, 10- and 15-years was 83.6%, 64.5% and 54.5%, respectively. After operation FPP and PVP decreased significantly (P < 0.01) and FPP maintained at the level of 3.2 +/- 0.4 kPa. CONCLUSION: The combined procedure is a rational and practical procedure for the treatment of patients with portal hypertension.

Adolescent↗
PubMed1998

Hemangioma of the ovary. A case report.

BACKGROUND: Ovarian hemangioma is extremely rare. CASE: We report a case of a 32-year-old woman who complained of pelvic pain due to a large right adnexal mass. On color Doppler sonography the mass showed very rich and complex vascularity, with prominent blood flow. A 10 x 8-cm hemangioma of the right ovary was resected. CONCLUSION: Hemangiomas should be considered when a richly vascularized tumor with prominent blood flow is detected on color Doppler sonography or magnetic resonance imaging.

Adult↗
PubMed1997

Identification of an element required for acetylcholine receptor-inducing activity (ARIA)-induced expression of the acetylcholine receptor epsilon subunit gene.

Acetylcholine Receptor (AChR)-inducing activity (ARIA) is believed to be the trophic factor utilized by motoneurons to stimulate AChR synthesis in the subsynaptic area. Among the four AChR subunit genes, the epsilon subunit gene is strictly expressed in nuclei localized to the synaptic region of the muscle. To understand mechanisms of the regulation of synapse-specific transcription, we studied the promoter activity of the 5'-flanking region of the AChR epsilon subunit gene in response to ARIA. Transgenes containing the wild type or mutant 5'-flanking regions upstream of a luciferase gene were transfected in C2C12 muscle cells. The promoter activity of these transgenes was determined by assaying activity of expressed luciferase. Analyzing a combination of 5' deletion and site-directed mutants, we identified a 10-nucleotide element (position -55/-46), which was crucial for ARIA-induced expression from the epsilon subunit promoter. This element was named ARE for ARIA-responsive element. Mutation of ARE greatly diminished ARIA-induced transgene expression and deletion of ARE abolished completely the ARIA response. Electrophoretic mobility shift analyses revealed a DNA binding activity in muscle nuclear extract that interacted with ARE. Such interaction was enhanced by ARIA stimulation of muscle cells and appeared to be dependent on nuclear protein phosphorylation.

Animals↗
PubMed1997

Regulation of sesquiterpene cyclase gene expression. Characterization of an elicitor- and pathogen-inducible promoter.

The promoter for a tobacco (Nicotiana tabacum) sesquiterpene cyclase gene, a key regulatory step in sesquiterpene phytoalexin biosynthesis, has been analyzed. The EAS4 promoter was fused to the beta-glucuronidase (GUS) reporter gene, and the temporal and spatial expression patterns of GUS activity were examined in stably transformed plants and in transient expression assays using electroporated protoplasts of tobacco. No GUS activity was observed in any tissues under normal growth conditions. A low level of GUS activity was detected in wounded leaf, root, and stem tissues, whereas a much higher level was observed when these tissues were challenged with elicitors or microbial pathogens. The GUS expression pattern directed by the EAS4 promoter was identical to the induction patterns observed for the endogenous sesquiterpene cyclase genes. Neither exogenous salicylic acid nor methyl jasmonate induced GUS expression; and H2O2 induced GUS expression to only a limited extent. Although the EAS4 promoter contains cis-sequences resembling previously identified transcriptional control motifs, other cis-sequences important for quantitative and qualitative gene expression were identified by deletion and gain-of-function analyses. The EAS4 promoter differs from previously described pathogen-/elicitor-inducible promoters because it only supports inducible gene expression and directs unique spatial expression patterns.

Acetates↗
PubMed1996

Induction of acetylcholine receptor gene expression by ARIA requires activation of mitogen-activated protein kinase.

Transcription of genes encoding nicotinic acetylcholine receptor (AChR) subunits (alpha, beta, gamma or epsilon, and delta) is highest in nuclei localized to the synaptic region of the muscle, which contributes to maintain a high density of AChRs at the postjunctional membrane. ARIA (AChR inducing activity) is believed to be the trophic factor utilized by motor neurons to stimulate AChR synthesis in the subsynaptic area. To elucidate the signaling mechanism initiated by ARIA, we established stable C2C12 cell lines carrying the nuclear lacZ gene under the control of the mouse epsilon subunit promoter or chicken alpha subunit promoter. ARIA stimulated tyrosine phosphorylation of erbB proteins in these C2C12 cells within 15 s with a peak at 5 min. Immediately following tyrosine phosphorylation of erbB proteins, mitogen-activated protein (MAP) kinase was activated which occurred within 30 s and peaked at 8 min after ARIA stimulation. Concomitantly, expression of AChR genes was induced by ARIA. ARIA-induced AChR subunit transgene expression was observed only in differentiated myotubes and not in myoblasts, suggesting that downstream signaling component(s) are regulated in a manner dependent on the myogenic program. Inhibition of the MAP kinase activity by using a specific MAP kinase kinase inhibitor or by overexpressing dominant negative mutants of Raf or MAP kinase kinase attenuated or abolished the ARIA-induced activation of AChR alpha and epsilon subunit gene expression. These results indicate that regulation of AChR gene expression by ARIA in C2C12 cells requires activation of the MAP kinase signaling pathway.

Androstadienes↗
PubMed1996

Differential expression of PTP1D, a protein tyrosine phosphatase with two SH2 domains, in a slow and fast skeletal muscle fibers.

We show that PTP1D, a protein tyrosine phosphatase that contains two SH2 domains, is preferentially expressed in slow skeletal muscle fibers. Immunohistochemical staining using polyclonal antibodies against PTP1D demonstrated that PTP1D was expressed in a subpopulation of rodent muscle fibers. These fibers were identified as slow Type I fibers based on histochemical ATPase assays and slow myosin heavy chain expression. Northern and Western analyses showed that PTP1D levels were higher in predominantly slow muscles than in predominantly fast muscles. This differential expression of PTP1D in slow muscle fibers appeared by birth. In cultures of mouse myogenic cells, PTP1D was expressed after MyoD and myogenin and appeared in myotubes derived from embryonic, fetal, and postnatal myoblasts. Remarkably, PTP1D was organized into sarcomeres in a pattern coincident with myosin heavy chain, suggesting that PTP1D associates with a component of the thick filament. These results show that PTP1D is preferentially expressed in slow muscle fibers. We speculate that PTP1D may play a role in slow muscle fiber function and differentiation.

Animals↗
PubMed1996

Surgical denervation increases protein tyrosine phosphatase activity in skeletal muscle.

Protein tyrosine phosphorylation, which plays an important role in synapse formation at the neuromuscular junction, appears to be regulated by presynaptic neurons. Innervation increases whereas denervation decreases the phosphotyrosine content at the neuromuscular junction. The innervation-dependent tyrosine phosphorylation may result from elevated activity of protein tyrosine kinases; alternatively innervation may down-regulate the protein tyrosine phosphatase activity in the skeletal muscle. To investigate the possible neuronal control of protein tyrosine phosphatase activity at the neuromuscular junction, we have characterized protein tyrosine phosphatase activity in rat skeletal muscle and studied the effects of surgical denervation on the phosphatase activity. Protein tyrosine phosphatase activity in the skeletal muscle, assayed using src [32P]-phosphorylated myelin basic protein as a substrate, was both time- and protein concentration-dependent and was inhibited by micromolar concentrations of vanadate and zinc ion, both of which are known to inhibit tyrosine phosphatases specifically. It was not affected, however, by chemicals known to inhibit acid and alkaline phosphatases or serine/threonine phosphatases. Surgical denervation caused an increase in protein tyrosine phosphatase activity in rat hindlimb muscles. The increase in phosphatase activity reached a maximum (2-fold above the normal) 4 days post-denervation and maintained a plateau for up to 24 days. The biochemical properties of the phosphatase activity in denervated muscle were similar to those of the phosphatase activity in the innervated muscles. These results demonstrate that protein tyrosine phosphatase activity in skeletal muscle is regulated by motoneurons.

Animals↗
PubMed1996

[Building up of an animal model of conditioned immunosuppression and analysis of its possible mechanism].

In the present study, camphor odor and intraperitoneal (ip) injection of cyclophosphamide (CY) were used as conditional and unconditional stimulus, respectively, in mice. Mice were exposed to camphor odor for 1 h in their cage in a closed area followed by an ip injection of CY (75 mg.kg-1). This association trial session was repeated once on the next day. Delayed type hypersensitivity response (DTH) was induced as follows: six days after the second association trial session the mice were sensitized by smearing dinitrochlorobenezene (DNCB) on their abdominal skin. The mice were challenged by smearing DNCB on the left ear 5 days after the antigen sensitization. The left and right ears were removed 24 h after the challenge and weighed, the weight ratio of left/right ears was calculated for identification of the response. The ratio was 1.30 +/- 0.113 (+/- s, P < 0.001), indicating that the challenged ear was heavier than the other and DTH was induced. In the unconditioned response (UCR) group, CY (75 mg.kg-1) was given 24 h prior to the challenge and the ratio was 1.09 +/- 0.024 (P < 0.001) indicating that DTH was suppressed by unconditional stimulus (CY). In the conditioned response (CR) group mice were reexposed to camphor odor 24 h prior to the challenge and normal saline was injected instead of CY. The ratio was 1.13 +/- 0.074 (P < 0.001), indicating that DTH was also suppressed by conditional stimulus (camphor odor). These results show that a conditioned immunosuppressive response was induced. In the experiment, many other groups, including unconditioned response group, CYE group and camphor control group, were described in more details in the text. In order to further analyse the mechanisms of the conditioned response, the blood from the mice in CR group was obtained 6 h after reexposure to camphor odor and the serum was injected to normal mice 6 h prior to the challenge. DTH was found to be suppressed significantly when compared with the mice injected with normal serum. The conditioned serum was dialyzed against a membrane with a 10,000 molecular weight cut off. The suppressive activity of the conditioned serum disappeared, suggesting that the molecular weight of the suppressive element in the serum was probably less than 10,000 kDa.

Animals↗
PubMed1995

Tyrosine phosphorylation and synapse formation at the neuromuscular junction.

Protein tyrosine phosphorylation is prevalent throughout the nervous system. It has been implicated to play an important role in the development and maintenance of neuronal functions. In the past few years significant advances have been made in our understanding of the molecular mechanisms of synapse formation and synaptic plasticity. Protein tyrosine phosphorylation appears to be important in the neuron-induced synthesis of the nicotinic acetylcholine receptor and aggregation of synaptic proteins at the neuromuscular junction during development. In addition, protein tyrosine phosphorylation may regulate the ion channel activity of the nicotinic acetylcholine receptor.

Animals↗
PubMed1995

[Intracerebroventricular injection of interleukin 1 receptor antagonist antagonises on the generation of immuno-suppressive factor in restraint mice].

Our previous work showed that a lymphocyte proliferation suppressing factor could be found in the serum of restraint mice. In the present work, it was found that intracerebroventricular (icv) injection of IL-1 receptor antagonist (IL-1Ra) was found capable of suppressing the production of such a serum protein under restraint stress. Nearly complete suppression could be achieved by 5.0 micrograms IL-1Ra. Intracerebroventricular injection of IL-1 beta (1 pg), however, increased the generation of the supressive protein. Neither intraperitoneal (ip) injection of IL-1Ra or IL-1 beta had any effect on the generation of the protein. The fact that icv. injection of a very small dose of IL-1 beta (0.06 fmol) was effective on the generation of the supressive protein led us to suggest that IL-1 in brain might act as an important mediator between CNS and the immune system.

Animals↗
PubMed1994

Characterization of substrate specificity of the protein tyrosine phosphatase purified from the electric organ of Torpedo californica.

The nicotinic receptor is highly phosphorylated on tyrosine residues both in vivo and in vitro. Tyrosine phosphorylation has been shown to regulate the functional properties of the receptor. We have purified a protein tyrosine phosphatase from the electric organ of Torpedo californica that dephosphorylates the nicotinic receptor. The unique biochemical properties of the purified enzyme suggest that it may be a novel phosphotyrosine protein phosphatase. In this report, substrate specificity of the protein purified from T. californica was characterized using four different tyrosine-phosphorylated substrate proteins. In addition to the nicotinic receptor, the Torpedo phosphatase dephosphorylated insulin receptor and Reduced Carboxamidomethylated and Meleylated lysozyme (RCM lysozyme), however, at a rate much slower than for the nicotinic receptor. In contrast, it appeared to have no effect on the phosphotyrosine level of pp15, a fatty acid binding protein (O-phospho-tyr19-422/aP2) phosphorylated by insulin receptor kinase in 3T3-L1 adipocytes. Interestingly, a protein tyrosine phosphatase (HA1) purified from adipocyte dephosphorylated both nicotinic receptor and pp15 at a similar rate. These results suggest that the Torpedo protein tyrosine phosphatase is relatively specific for the nicotinic receptor.

Animals↗
PubMed1994

RNA splicing regulates the activity of a SH2 domain-containing protein tyrosine phosphatase.

A cDNA which encodes a protein tyrosine phosphatase with two src homology 2 (SH2) domains was isolated from a rat brain cDNA library. This phosphatase appears to be a rat homologue of PTP1D based on its amino acid sequence. The gene is expressed in a variety of tissues, and its mRNA is enriched in the brain, skeletal muscle, and lung. An RNA splice variant (PTP1Di) was also isolated which has four additional amino acid residues (Ala-Leu-Leu-Gln) in the catalytic domain. The catalytic domains of PTP1D and PTP1Di were expressed in Escherichia coli as glutathione S-transferase fusion proteins and purified to near homogeneity. Whereas both PTP1D and PTP1Di had catalytic activity, the Vmax of PTP1Di relative to that of PTP1D was 8-fold lower for para-nitrophenylphosphate, 20-fold lower for nicotinic acetylcholine receptor, and 14-fold lower for myelin basic protein. The Km values of PTP1Di were lower than those of PTP1D for both nicotinic acetylcholine receptor and myelin basic protein, suggesting a higher affinity of PTP1Di for a protein substrate. These two forms also differed in optimum pH for para-nitrophenylphosphate and sensitivity to the inhibitory effects of vanadate, molybdate, and spermidine. In order to see if this insert would affect the catalytic activity of other related phosphatases, the 4-amino acids were inserted in the corresponding region of the catalytic domain of PTP1C. Whereas both the wild type and PTP1Ci which contained the 4-amino acid insert dephosphorylated para-nitrophenylphosphate, nicotinic receptor, and myelin basic protein, the enzyme activity of PTP1Ci was only 11-24% of that of PTP1C wild type. These results demonstrate that the 4-amino acid insert in the catalytic domains of PTP1D down-regulates its phosphatase activity and suggests that RNA splicing may serve as a regulatory mechanism of protein tyrosine phosphatase activity.

Amino Acid Sequence↗
PubMed1994

Effect of electroacupuncture tolerance by different frequencies on the opioid inhibition to cardiovascular activity in the spinal cord of rats.

Continuous 2-15 Hz or 2 Hz electroacupuncture (EA) of 6 h applied to rats resulted in electroacupuncture tolerance (ET). The effect of 2-15 Hz ET on the recovery of mean arterial blood pressure (MAP) and heart rate (HR) of rats after hemorrhagic shock, and the effect of intrathecal (i.t.) injection of [D-ala2, D-leu5]enkephalin (DADLE) on MAP and HR of 2 Hz ET rats were observed. The results were as follows: 1) there was no dramatic difference between the 2-15 Hz ET group and the control group in the recovery of MAP and HR from hemorrhagic shock; 2) DADLE (25 micrograms) caused almost the same depressor effect in the 2 Hz ET group as that in the control group. These data suggest that the spinal lateral horn cells (supposed to be involved in regulating blood pressure) are insensitive to EA and cannot be made tolerant to continuous EA, which is different from the dorsal horn cell (supposed to be involved in analgesia).

Animals↗
PubMed1993

The antagonistic effect of cholecystokinin octapeptide (CCK-8) on opioid effects in cardiovascular activities was mediated by CCK-B receptor.

Previous studies have shown that CCK-8 has distinct antiopioid effect in the central sites related with pain control and blood pressure control. The aim of this study was to explore the receptor mechanism by which CCK-8 antagonized the depressor effect of u- and k-opioid agonists, and to observe whether CCK-8 could antagonize the depressor effect induced by muscimol, a nonopioid substance. The results showed that (i) The antagonistic effect of CCK-8 on opioid-induced hypotension could be blocked by intrathecal (i. t.) administration of CCK-B antagonist L-365, 260 at nanogram doses, or by CCK-A antagonist devazepide at doses 20-40 times higher than L-365, 260, indicating that it was the CCK-B receptor which mediates the antiopioid effect. (ii) The depressor effect induced by intrathecal muscimol, a GABA agonist, was blocked neither by naloxone nor by CCK-8, supporting the notion that CCK-8 is an endogenous opioid antagonist rather than a universal anti-hypotension agent.

Animals↗