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Biomedical subjects

C G Liu

Publications and source records attributed to C G Liu.

At least 19 recordsLinked to original sources
PubMed2006

MicroRNA deregulation in human thyroid papillary carcinomas.

MicroRNAs (miRNAs) are a class of small non-coding RNAs involved in a wide range of basic processes such as cell proliferation, development, apoptosis and stress response. It has recently been found that they are also abnormally expressed in many types of human cancer. We analyzed the genome-wide miRNA expression profile in human thyroid papillary carcinomas (PTCs) using a microarray (miRNACHIP microarray) containing hundreds of human precursor and mature miRNA oligonucleotide probes. Using this approach, we found an aberrant miRNA expression profile that clearly differentiates PTCs from normal thyroid tissues. In particular, a significant increase in miRNA (miR)-221, -222 and -181b was detected in PTCs in comparison with normal thyroid tissue. These results were further confirmed by northern blot and quantitative RT-PCR analyses. Moreover, RT-PCR revealed miR-221, -222 and -181b overexpression in fine needle aspiration biopsies corresponding to thyroid nodules, which were eventually diagnosed as papillary carcinomas after surgery. Finally, miR-221, -222 and -181b overexpression was also demonstrated in transformed rat thyroid cell lines and in mouse models of thyroid carcinogenesis. Functional studies, performed by blocking miR-221 function and by overexpressing miR-221 in human PTC-derived cell lines, suggest a critical role of miR-221 overexpression in thyroid carcinogenesis. In conclusion, these data, taken together, indicate an miRNA signature associated with PTCs, and suggest miRNA deregulation as an important event in thyroid cell transformation.

Animals↗
PubMed2001

[Studies of biochemical markers of four isonucleus-alloplasmic lines of common wheat].

The peroxidase isozyme and the soluble peoteins of four isonucleus-alloplasmic lines of common wheat--D2-CA8057 (fertile, BC14), CMS line msD2-CA8057(BC11), CMS line msA-CA8057(BC12), CA8057 (nucleus donor) in different developmental stages were studies by polyacrylamide gel electrophoresis (PAGE) and gradient SDS-PAGE respectively. The peroxidase isozyme of bionucleus-stage anther, milk-stage endosperm and the soluble proteins of bionucleus-stage anther, leaf (the beginning and ending overwinter), dry-seed endosperm among fertile line, msD2-CA8057 and msA-CA8057 were evidently different (but few differences between CA8057 and D2-CA8057). These differences resulted from the pecially-regulated expression of (male-sterile) cytoplasmic genes to nuclear genes and could be used to identify the four isonucleus-alloplasmic lines. These results showed that msD2-CA8057 and msA-CA8057 were two different kinds of new CMS pattern.

Biomarkers↗
PubMed2001

[Blind patch clamp whole-cell recording technique for neurons in hippocampal slices].

The blind patch clamp whole-cell recording technique for CA1 pyramidal neurons in hippocampal slices was carefully introduced, the key procedures and the points for attention were emphasized. Using the "blind" method, we analyzed the properties of synaptic activity, the current features of Ca2+ channels and glutamate, GABA receptors. Our results provide a scientific basis for study of dynamic properties of ion channels on hippocampal neurons and the effects of drugs on synaptic activity by using the blind whole-cell recording technique.

Animals↗
PubMed2000

[Studies of salt tolerance of alloplasmic wheat].

Using Aegilops crassa cytoplasm wheat as test material, salt tolerance of alloplasmic wheat was identified by tissue culture, nutrient solution culture and artificial saline pond, from calli, seeding stage, recovering stage and mature period. The results showed Ae. crassa cytoplasm lines indicated the difference of salt tolerance in varying degree; the difference of cytoplasm effect among different nucleoplasm combinations showed certain nucleoplasm interaction relation. The salt tolerance of (Ae. crassa)-jian 26 was stronger than that other tested alloplasmic lines. The result demonstrated that at recovering date and at mature period indicated salt tolerance of alloplasmic lines was not only stronger than its nuclear parent but also over control variety. As compared with common wheat, lines having strong salt tolerance were more proportions in tested alloplasmic lines. The study of alloplasmic wheat should be significant for breeding salt tolerance wheat.

Cytoplasm↗
PubMed2000

Blocking effect of tricyclopinate on nicotinic receptors in cultured sympathetic neurons.

AIM: To investigate the mechanism of tricyclopinate, an antagonist of nicotinic receptor, on neuronal nicotinic acetylcholine receptors (nAChR). METHODS: A tight seal whole-cell recording patch-clamp technique was performed to record nicotine-evoked currents in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG). RESULTS: Tricyclopinate inhibited the nicotine-induced currents competitively and the inhibition was voltage-independent. The decay of the nicotine-induced current was accelerated significantly in the presence of tricyclopinate. CONCLUSION: Tricyclopinate inhibits neuronal nAChR by interacting with the allosteric sites rather than the open ionic channels or acetylcholine recognition site of the receptor.

Animals↗
PubMed2000

[Analysis of P/N leak subtraction of pClamp acquisition software].

Using blind whole cell recording technique on rat hippocampal slices, the function and mechanisms of P/N leak subtraction of Clampex program in pClamp acquisition software were studied. The ways of picking up sub-pulse current and properly selecting parameters, including time course, polarization, sub-holding potential, numbers and location of P/N sub-pulse were analyzed in detail. Our results indicate that voltage-gated ion channel currents recorded by Clampex will be more accurate and reproducible by properly using P/N leak subtraction.

Animals↗
PubMed1998

Structural organization and sequence of CLN2, the defective gene in classical late infantile neuronal ceroid lipofuscinosis.

Mutations in the CLN2 gene result in classical late infantile neuronal ceroid lipofuscinosis (LINCL), a fatal childhood neurodegenerative disease. In this report, we present the complete sequence of the human CLN2 gene and define its physical relationship with two other genes that have been previously mapped to chromosome 11p15. The CLN2 gene consists of 13 exons and 12 introns and spans 6.65 kb. By S1 mapping and primer extension, the 5'-terminus of the CLN2 mRNA was mapped to 32 nucleotides upstream of the proposed initiation codon. A number of other elements were found to be located in close proximity to CLN2, including the gene encoding transcription factor TAFII30, the gene encoding intregrin-linked kinase, and an approximately 914-bp fragment that is 82% identical to antithrombin III. In addition, an EST cDNA clone that is transcribed on the strand opposite to CLN2 and that overlaps a portion of the CLN2 gene was identified. Finally, a set of primer pairs are presented for the amplification of the coding sequences, putative promoter, and splice junctions of the CLN2 gene. Taken together, this information will facilitate the molecular analysis of and genetic testing for classical LINCL.

Amino Acid Sequence↗
PubMed1998

Effects of nicotine on 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine-induced depression of striatal dopamine content and spontaneous locomotor activity in C57 black mice.

The present study examined the effects of nicotine on the levels of dopamine and its metabolite 3,4-dihydroxy-phenylacetic acid (DOPAC) in the striatum and on spontaneous locomotor activity of C57 black mice that had been treated with the neurotoxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). The levels of dopamine and DOPAC in the striatum were significantly reduced 10 days after two injections of MPTP (40 mg kg-1, i.p., 24 h apart) in mice. Chronic treatment of nicotine (2.0 mg kg-1, s.c., four injections per day) did not influence the striatal content of dopamine and DOPAC, but it significantly antagonised MPTP-induced depression of dopamine. However, the chronic nicotine treatment did not significantly affect MPTP-induced depression of DOPAC. It was demonstrated that the lethal effect of MPTP was also partly protected by the chronic nicotine treatment. The chronic nicotine treatment also significantly protected MPTP-depressed spontaneous locomotor activity in mice. The results suggest that both MPTP-depressed behaviour and MPTP-induced striatal dopamine depletion in C57 black mice are partly protected by chronic nicotine treatment.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1998

Neostigmine competitively inhibited nicotinic acetylcholine receptors in sympathetic neurons.

The present experiment investigates the effect of neostigmine on nicotinic acetylcholine receptors (nAChRs) in the cultured neurons from neonatal rat superior cervical ganglia (SCG). Using whole-cell patch clamp techniques, we found that the amplitudes of the currents induced by 50 microM dimethylphenylpiperazinium (DMPP) were 21.5+/-10.7%, 52.9+/-9.2% and 86.9+/-4.9% depressed at the increased concentrations of neostigmine 100, 200 and 400 microM, respectively. The inhibition of neostigmine decreased gradually with the increased concentration of nicotine from 10 to 160 microM. Lineweaver-Burk's double-reversible plot illustrated that neostigmine blocked neuronal nAChRs in a competitive manner. Hyperpolarization of membrane potential from -40 mV to -100 mV did not significantly influence the blockade of neostigmine. Neostigmine could not accelerate the decay of the DMPP-induced currents, neither evoke any detectable currents in SCG neurons. The results indicate that neostigmine depress neuronal nAChRs in a competitive, concentration-dependent and voltage-independent manner, and can not facilitate desensitization of the receptors. The present data suggest that neostigmine blocks neuronal nAChRs by interacting with the ACh binding sites of the receptors.

Animals↗
PubMed1998

Anti-nicotinic properties of anticholinergic antiparkinson drugs.

The nature of the antagonism by anticholinergic compounds of nicotine-induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to brain tissue in-vitro, these compounds are thought to be non-competitive antagonists in the brain, pharmacological evidence is lacking. This study describes the anti-nicotinic properties of the clinically used anticholinergic antiparkinson drugs, benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl. Nicotine-induced convulsion and arecoline-induced tremor in mice were effectively prevented by these drugs. The concentrations of benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl affording 50% prevention of nicotine-induced convulsion (ED50 values) were 7.4, 4.6, 7.8, 4.9, 3.1 and 3.3 mg kg(-1), respectively. The classical muscarinic receptor antagonist atropine had potent anti-muscarinic effects but very weak anti-nicotinic activity. The classical nicotinic receptor antagonist mecamylamine had potent anti-nicotinic activity but no anti-muscarinic effects. The pattern of shift of the dose-response curve for nicotine-induced convulsion in mice was determined in the presence of increasing concentrations of the anticholinergic antiparkinson drugs. These drugs were found to increase the ED50 (0.49 mg kg(-1)) of nicotine-induced convulsion in a dose-related manner. The maximum effect of nicotine and the slope of nicotine dose-response curve were not significantly influenced by either low or high doses of benztropine, procyclidine or trihexylphenidyl, which suggests competitive action. Biperiden, caramiphen and ethopropazine, at low doses which significantly increased the ED50 of nicotine, did not affect the maximum effect of nicotine or the slope of the nicotine dose-response curve; at higher doses, however, they reduced the maximum effect and the slope, which suggests that these drugs have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice. The experiments demonstrate that the anticholinergic antiparkinson drugs and mecamylamine effectively antagonize nicotine-induced convulsion, but atropine does not; some of these drugs have competitive properties whereas others seem to have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice.

Animals↗
PubMed1997

Association of mutations in a lysosomal protein with classical late-infantile neuronal ceroid lipofuscinosis.

Classical late-infantile neuronal ceroid lipofuscinosis (LINCL) is a fatal neurodegenerative disease whose defective gene has remained elusive. A molecular basis for LINCL was determined with an approach applicable to other lysosomal storage diseases. When the mannose 6-phosphate modification of newly synthesized lysosomal enzymes was used as an affinity marker, a single protein was identified that is absent in LINCL. Sequence comparisons suggest that this protein is a pepstatin-insensitive lysosomal peptidase, and a corresponding enzymatic activity was deficient in LINCL autopsy specimens. Mutations in the gene encoding this protein were identified in LINCL patients but not in normal controls.

Amino Acid Sequence↗
PubMed1997

Modulation of apomorphine-induced rotations in unilaterally 6-hydroxydopamine lesioned rats by cholinergic agonists and antagonists.

In the present study, we examined the effects of the agonists and antagonists of cholinergic receptors on central dopaminergic function using the 6-hydroxydopamine model of dopamine receptor supersensitivity. Unilateral lesioning of the substantia nigra with 6-hydroxydopamine was carried out in Wistar rats. Two weeks after surgery, the rats were tested for the presence of dopaminergic supersensitivity by their response to the dopamine receptor agonist, apomorphine. Apomorphine-induced rotations were significantly reinforced by the muscarinic receptor antagonist, atropine. In contrast to atropine, the muscarinic receptor agonist oxotremorine attenuated apomorphine's effects. Acute treatment of nicotine significantly reduced apomorphine-induced rotations. However, when increasing doses of nicotine were given for nine days, the rotations of the nicotine-dependent rats were significantly enhanced. So the fact that both muscarinic and nicotinic cholinergic activity could modulate apomorphine-induced rotations was readily apparent in these experiments.

Animals↗
PubMed1997

Anticholinergic activity in mice and receptor-binding properties in rats of a series of synthetic tropane derivatives.

A tropane ester, three tropane ethers, atropine and mecamylamine were compared in mice for their anti-muscarinic and anti-nicotinic activity against arecoline-induced tremor and nicotine-induced convulsions, respectively. Their receptor-binding characteristics were studied in neuronal membranes prepared from rat cerebral cortex. The results showed that the tropane ester, 2 alpha R-tropanyl benzylate, was more potent than atropine in its anti-muscarinic activity, but the anti-muscarinic activity of the tropane ethers, 2 alpha-(2',2'-diphenyl-2'-hydroxy-ethoxy)tropane (alpha-DPT) and its two isomers (1R,2 alpha R- and 1S,2 alpha S-) were less potent than that of atropine. In contrast with their anti-muscarinic potency, 2 alpha R-tropanyl benzylate and the three tropane ethers were equipotent in their anti-nicotinic activities. The order of potencies of these compounds to displace the binding of [3H]quinuclidinyl benzylate to brain membranes was similar to that of their anti-muscarinic potencies. The binding of [3H]nicotine to nicotinic receptors from brain was not inhibited by these compounds. Analyses of structure-activity relationships of these compounds suggested that it is the ester groups that determine the anti-muscarinic potencies of 2 alpha R-tropanyl benzylate; their anti-nicotinic activities were independent of the structural changes and of the anti-muscarinic activities of these compounds.

Animals↗
PubMed1997

Kinetic properties of nicotinic receptors in cultured rat sympathetic neurons from superior cervical ganglia.

AIM: To analyze the kinetic properties of the effect of nicotine on nicotinic acetylcholine receptors (nAChR) in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG). METHODS: The whole-cell recording method of patch-clamp technique was used to record the currents induced by different concentrations of nicotine. The concentration-response of nicotine was fitted with Clark equation. RESULTS: Hill coefficient (1.097) was determined by fitting the nicotine responses of neuronal nAChR with Clark equation. The theoretical values of nicotine effect, calculated with Clark equation with H = 1, were basically identical with the practically recorded currents. CONCLUSIONS: Interaction of nicotine and nAChR in rat SCG fits a single binding site model.

Animals↗
PubMed1997

Physostigmine blocked nicotinic acetylcholine receptors in rat sympathetic ganglion neurons.

AIM: To study the blocking mechanism of physostigmine (Phy) on nicotinic acetylcholine receptors (NAChR) in sympathetic neurons. METHODS: The whole-cell patch-clamp technique was used to observe the effects of Phy on NAChR in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG). RESULTS: Phy 5 -20 mumol.L-1 inhibited neuronal NAChR in a concentration-dependent manner and accelerated the desensitization of NAChR. Changing the membrane potential from -50 to -90 mV did not affect the blocking effect of Phy. Phy 200 mumol.L-1 did not induce any noticeable response in SCG neurons. CONCLUSION: Phy blocked NAChR in the sympathetic ganglion neurons by interacting with the allosteric sites out of the binding sites and the open ionic channels of the receptors. Phy did not possess excitative effect on NAChR in SCG neurons.

Animals↗