[Peripheral lymphocyte apoptosis induced by lipopolysaccharide].
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Apoptosis↗
Biomedical subjects
H Yi
Publications and source records attributed to H Yi.
Stability of the smectic quantum hall state: a quantitative study.
We present an effective elastic theory which quantitatively describes the stripe phase of the two-dimensional electron gas in high Landau levels ( N>/=2). The dynamical matrix is obtained with remarkably high precision using the time-dependent Hartree-Fock approximation. A renormalization group analysis shows that at T = 0, as the partial filling factor Deltanu identical withnu- left floornu right floor moves away from 1/2, the anisotropic conducting state may undergo quantum phase transitions: stripes may get pinned along their conducting direction by disorder, or may lock into one another to form a crystal. The transitions should be reflected in the temperature dependence of the dissipative conductivity.
Journal Article↗
Telomerase activity of peripheral blood lymphocytes in patients with chronic hepatitis B.
Chronic hepatitis B is the immunocompromising condition. The decrease of lymphocyte telomerase is linked to immunosenescence in hosts. To know whether telomerase activity of lymphocytes is involved in immunopathogenesis in patients with chronic hepatitis B, telomerase activity of peripheral lymphocytes was determined in such patients. The results showed that telomerase activity in resting peripheral lymphocytes of healthy subjects was detectable at low level, and obviously increased (P<0.001) after stimulation in vitro with phytohaemagglutinin (PHA). Telomerase activity of lymphocytes decreased with age in both groups with or without PHA stimulation. Telomerase activity of resting lymphocytes in patients with chronic hepatitis B was also observed at detectable level and markedly upregulated after PHA stimulation. The decreased telomerase activity of resting lymphocytes was found in patients with chronic hepatitis B (n=14, 0.32+/-0.27) compared to that in healthy subjects (n=17, 0. 52+/-0.28; P<0.05). However, there was no difference present between these two groups in telomerase activity of activated lymphocytes with PHA. In addition, no effect of recombinant human interleukin-12 (rhIL-12) on telomerase expression was observed in either the patient group or the healthy group. We concluded that the decreased telomerase activity of lymphocytes in chronic hepatitis B patients is present, which may be partly responsible for immunosuppressive condition in such patients.
Adolescent↗
Localization of M(2) muscarinic acetylcholine receptor protein in cholinergic and non-cholinergic terminals in rat hippocampus.
The muscarinic receptor family (M(1)-M(4)) mediates cholinergic modulation of hippocampal transmission. Pharmacological and physiological studies have indicated that a presynaptic receptor on cholinergic terminals plays a key role in regulating ACh release, although the molecular identity of this subtype is uncertain. In this study, the localization of the M(2) receptor is described in detail for the pyramidal cell layer in the CAl region of the hippocampus. Electron microscopic analysis of M(2) immunoreactivity in this area revealed mainly presynaptic expression of this subtype. Double-labeling experiments using antibodies to M(2) and to the vesicular acetylcholine transporter, a novel, specific marker of cholinergic terminals, were used to investigate the nature of these presynaptic receptors. These studies have revealed that M(2) is located in cholinergic and non-cholinergic terminals. This is the first direct anatomical evidence that suggests that M(2) may indeed function as a cholinergic autoreceptor in the hippocampus. The distribution of the M(2) receptor in non-cholinergic terminals also suggests functional roles for M(2) as a presynaptic heteroreceptor.
Animals↗
Long glutamine tracts cause nuclear localization of a novel form of huntingtin in medium spiny striatal neurons in HdhQ92 and HdhQ111 knock-in mice.
Huntington's disease (HD) is caused by an expanded N-terminal glutamine tract that endows huntingtin with a striatal-selective structural property ultimately toxic to medium spiny neurons. In precise genetic models of juvenile HD, HdhQ92 and HdhQ111 knock-in mice, long polyglutamine segments change huntingtin's physical properties, producing HD-like in vivo correlates in the striatum, including nuclear localization of a version of the full-length protein predominant in medium spiny neurons, and subsequent formation of N-terminal inclusions and insoluble aggregate. These changes show glutamine length dependence and dominant inheritance with recruitment of wild-type protein, critical features of the altered HD property that strongly implicate them in the HD disease process and that suggest alternative pathogenic scenarios: the effect of the glutamine tract may act by altering interaction with a critical cellular constituent or by depleting a form of huntingtin essential to medium spiny striatal neurons.
Animals↗
Phylogenetic and phenotypic diversity of 4-chlorobenzoate-degrading bacteria isolated from soils.
Twenty numerically dominant 4-chlorobenzoate (4-CBA)-degrading bacteria were isolated from agricultural soils. The isolates were able to utilize 4-CBA as a sole source of carbon and energy. A total of 65% of the isolates was identified to the species level by fatty acid methyl ester (FAME) analysis, and the isolates were strains of Micrococcus, Pseudomonas, Oerskovia, Cellulomonas, and Arthrobacter species. The chromosomal DNA patterns of the isolates obtained by polymerase chain reaction (PCR) amplification of repetitive extragenic palindromic (REP) sequences were distinct from each other. Most of the isolates grew rapidly in 4-CBA medium, but their substrate utilization capabilities were generally restricted. Plasmid DNAs were detected from 55% of the isolates, and one strain, HR7, was shown to have self-transmissible, 4-CBA degradative plasmids. 4-CBA degradative enzymes were inducible by the presence of 4-CBA and most of the isolates appeared to mineralize it through 4-hydroxybenzoate rather than 4-chlorocatechol.
Journal Article↗
Glycine receptor (gephyrin) immunoreactivity is present on cholinergic neurons in the dorsal vagal complex.
We previously demonstrated that microinjection of exogenous glycine into the nucleus tractus solitarii of anesthetized rats elicits responses that are qualitatively like those elicited by microinjection of acetylcholine at the same site. The responses to glycine, like those to acetylcholine, are blocked by administration of a muscarinic receptor antagonist and prolonged by administration of an acetylcholinesterase inhibitor. Furthermore, glycine leads to release of acetylcholine from the nucleus tractus solitarii and surrounding dorsal vagal complex. An anatomical framework for interactions between glycinergic and cholinergic neurons was established by studies that identified glycine terminals and receptors in the dorsal vagal complex. The current study investigated the relationship between glycine receptors and neuronal elements that were immunoreactive for choline acetyltransferase in the dorsal vagal complex. Neurons that were immunoreactive for choline acetyltransferase were located in the dorsal motor nucleus of the vagus, hypoglossal nucleus and nucleus ambiguus, and stained cells were also present in medial, intermediate, and ventrolateral subnuclei of the nucleus tractus solitarii. We found that glycine receptors, immunolabeled with an antibody to gephyrin, were present on cholinergic dendrites in the nucleus tractus solitarii. Gephyrin immunoreactivity was also present on dendrites that did not stain for choline acetyltransferase. These data further support the contribution of cholinergic neurons in mediating cardiovascular responses to glycine in the nucleus tractus solitarii.
Acetylcholine↗
Effect of nitric oxide modulation on TGF-beta1 and matrix proteins in chronic cyclosporine nephrotoxicity.
BACKGROUND: Chronic cyclosporine (CsA) nephrotoxicity is characterized by interstitial fibrosis and afferent arteriolar hyalinosis. L-arginine (L-Arg), the substrate for nitric oxide (NO) synthase and N-nitro-L-arginine-methyl ester (L-NAME), the NO synthase inhibitor, were shown to modulate acute CsA nephrotoxicity. However, the mechanism of fibrosis in chronic CsA nephrotoxicity remains unclear. Thus, we examined the effect of NO modulation on fibrosis and the expression of transforming growth factor-beta1 (TGF-beta1) and matrix proteins in chronic CsA nephrotoxicity. METHODS: Rats were administered CsA (7.5 mg/kg), CsA + L-Arg (1.7 g/kg), CsA + L-NAME (3.5 mg/kg), vehicle (VH), VH + L-Arg, and VH + L-NAME, and were sacrificed at 7 or 28 days. NO production, physiologic parameters, and histology were studied in addition to the mRNA expression of TGF-beta1, plasminogen activator inhibitor-1 (PAI-1) and the matrix proteins biglycan and collagens type I and IV by Northern and the protein expression of PAI-1 and fibronectin by enzyme-linked immunosorbent assay. RESULTS: While L-NAME strikingly reduced NO biosynthesis and worsened the glomerular filtration rate and CsA-induced fibrosis, L-Arg had the opposite beneficial effect. In addition, the CsA-induced up-regulated expression of TGF-beta1, PAI-1, and the matrix proteins biglycan, fibronectin, and collagen I was significantly increased with L-NAME and strikingly improved with L-Arg. Collagen IV expression was not affected. Also, NO modulation did not affect VH-treated rats. CONCLUSIONS: Chronic CsA nephrotoxicity can be aggravated by NO blockade and ameliorated by NO enhancement, suggesting that NO maintains a protective function. NO modulation was associated with a change in TGF-beta1 expression, which, in turn, was associated with alterations in matrix deposition and matrix degradation through its effect on PAI-1.
Animals↗
Morphogenetic proteins SpoVID and SafA form a complex during assembly of the Bacillus subtilis spore coat.
During endospore formation in Bacillus subtilis, over two dozen polypeptides are assembled into a multilayered structure known as the spore coat, which protects the cortex peptidoglycan (PG) and permits efficient germination. In the initial stages of coat assembly a protein known as CotE forms a ring around the forespore. A second morphogenetic protein, SpoVID, is required for maintenance of the CotE ring during the later stages, when most of proteins are assembled into the coat. Here, we report on a protein that appears to associate with SpoVID during the early stage of coat assembly. This protein, which we call SafA for SpoVID-associated factor A, is encoded by a locus previously known as yrbA. We confirmed the results of a previous study that showed safA mutant spores have defective coats which are missing several proteins. We have extended these studies with the finding that SafA and SpoVID were coimmunoprecipitated by anti-SafA or anti-SpoVID antiserum from whole-cell extracts 3 and 4 h after the onset of sporulation. Therefore, SafA may associate with SpoVID during the early stage of coat assembly. We used immunogold electron microscopy to localize SafA and found it in the cortex, near the interface with the coat in mature spores. SafA appears to have a modular design. The C-terminal region of SafA is similar to those of several inner spore coat proteins. The N-terminal region contains a sequence that is conserved among proteins that associate with the cell wall. This motif in the N-terminal region may target SafA to the PG-containing regions of the developing spore.
Amino Acid Motifs↗
[Telomerase activity of peripheral blood mononuclear cells in patients with acquired immune dysfunction].
OBJECTIVE: To investigate telomerase activity of peripheral blood mononuclear cells (PBMC) in patients with acquired immune dysfunction. METHODS: Telomerase activity of peripheral PBMC isolated from 4 groups including healthy subjects (17), chronic hepatitis B patients (14), diabetic patients (8) and chronic renal failure patients (8) was assayed with PCR-ELISA. RESULTS: (1) Telomerase activity was detectable at low levels in resting PBMC of all the 4 groups. It increased obviously after in vitro phytohemagglutinin (PHA) stimulation; (2) Telomerase activity of the resting PBMC in chronic hepatitis B patients was significantly lower than that in normal subjects, and was upregulated to the same level in the both groups after PHA stimulation; (3) No effect of recombinant human interleukin-12 on telomerase activity of activated T lymphocytes was found. CONCLUSIONS: PBMC may express telomerase activity and the decreased telomerase activity of PBMC in patients with chronic hepatitis B may partially be responsible for immune dysfunction in these patients.
Adolescent↗
Phytochrome signalling is mediated through nucleoside diphosphate kinase 2.
Because plants are sessile, they have developed intricate strategies to adapt to changing environmental variables, including light. Their growth and development, from germination to flowering, is critically influenced by light, particularly at red (660 nm) and far-red (730 nm) wavelengths. Higher plants perceive red and far-red light by means of specific light sensors called phytochromes(A-E). However, very little is known about how light signals are transduced to elicit responses in plants. Here we report that nucleoside diphosphate kinase 2 (NDPK2) is an upstream component in the phytochrome signalling pathway in the plant Arabidopsis thaliana. In animal and human cells, NDPK acts as a tumour suppressor. We show that recombinant NDPK2 in Arabidopsis preferentially binds to the red-light-activated form of phytochrome in vitro and that this interaction increases the activity of recombinant NDPK2. Furthermore, a mutant lacking NDPK2 showed a partial defect in responses to both red and farred light, including cotyledon opening and greening. These results indicate that NDPK2 is a positive signalling component of the phytochrome-mediated light-signal-transduction pathway in Arabidopsis.
Arabidopsis↗
Mitogen-activated protein kinase pathway mediates peroxynitrite-induced apoptosis in human dopaminergic neuroblastoma SH-SY5Y cells.
Peroxynitrite, a product of nitric oxide and superoxide, is one of the most potent oxidants and it has been suggested to be involved in many neurodegenerative disorders. The mechanism of the cytotoxicity by peroxynitrite was examined using 3-morpholinosydonimine (SIN-1) as a peroxynitrite donor and SH-SY5Y cells as a model of dopamine neurons. SIN-1 was found to induce apoptotic cell death with typical nucleosomal DNA fragmentation with activation of caspase 3-like proteases. The signal transduction of apoptosis was studied in concern to mitogen-activated protein kinases (MAPKs). After SIN-1 treatment, phosphorylation of p38 was detected, followed by that of Erk. SB202190, an inhibitor of p38, suppressed Erk phosphorylation to the basal level and partially reduced the activation of caspase 3-like proteases and also the cell death. These results suggest that peroxynitrite may activate p38 MAPK pathway to induce apoptosis in dopamine cells via activation of caspase 3-like proteases.
Antioxidants↗
Nuclear and neuropil aggregates in Huntington's disease: relationship to neuropathology.
The data we report in this study concern the types, location, numbers, forms, and composition of microscopic huntingtin aggregates in brain tissues from humans with different grades of Huntington's disease (HD). We have developed a fusion protein antibody against the first 256 amino acids that preferentially recognizes aggregated huntingtin and labels many more aggregates in neuronal nuclei, perikarya, and processes in human brain than have been described previously. Using this antibody and human brain tissue ranging from presymptomatic to grade 4, we have compared the numbers and locations of nuclear and neuropil aggregates with the known patterns of neuronal death in HD. We show that neuropil aggregates are much more common than nuclear aggregates and can be present in large numbers before the onset of clinical symptoms. There are also many more aggregates in cortex than in striatum, where they are actually uncommon. Although the striatum is the most affected region in HD, only 1-4% of striatal neurons in all grades of HD have nuclear aggregates. Neuropil aggregates, which we have identified by electron microscopy to occur in dendrites and dendritic spines, could play a role in the known dendritic pathology that occurs in HD. Aggregates increase in size in advanced grades, suggesting that they may persist in neurons that are more likely to survive. Ubiquitination is apparent in only a subset of aggregates, suggesting that ubiquitin-mediated proteolysis of aggregates may be late or variable.
Amino Acid Sequence↗
Cymbidium hybrida dihydroflavonol 4-reductase does not efficiently reduce dihydrokaempferol to produce orange pelargonidin-type anthocyanins.
Some angiosperms are limited to a range of possible flower colors. This limitation can be due to the lack of an anthocyanin biosynthetic gene or to the substrate specificity of a key anthocyanin biosynthetic enzyme, dihydroflavonol 4-reductase (DFR). Cymbidium hybrida orchid flowers primarily produce cyanidin-type (pink to red) anthocyanins and lack the pelargonidin-type (orange to brick-red) anthocyanins. To investigate the underlying molecular mechanism of this flower color range, we cloned a Cymbidium DFR gene and transformed it into a DFR- petunia line. We found that the Cymbidium DFR did not efficiently reduce dihydrokaempferol (DHK), which is an essential step for pelargonidin production. Phylogenetic analysis of a number of DFR sequences indicate that the inability to catalyze DHK reduction has occurred at least twice during angiosperm evolution. Our results indicate that developing a pelargonidin-type orange flower color in Cymbidium may require the transformation of a DFR gene that can efficiently catalyze DHK reduction.
Alcohol Oxidoreductases↗
Expression of apoptosis regulatory genes in chronic cyclosporine nephrotoxicity favors apoptosis.
UNLABELLED: Expression of apoptosis regulatory genes in chronic cyclosporine nephrotoxicity favors apoptosis. BACKGROUND: Chronic cyclosporine (CsA) nephrotoxicity is characterized by interstitial fibrosis, tubular dropout, and loss of cellularity in areas of fibrosis. Apoptosis was found to play a role in CsA-induced fibrosis. We evaluated the role of the death genes p53, Bax, and Fas-L (ligand), survival gene Bcl-2, interleukin-converting enzyme (ICE), and caspase-3. METHODS: Salt-depleted rats were administered CsA 15 mg/kg/day or vehicle (VH) and were sacrificed at 7 or 28 days. Apoptosis was detected by TdT-mediated dUTP-biotin nick end labeling assay. p53 and Bax expressions were evaluated by Northern and Western blot analysis. Fas-L and Bcl-2 expressions were evaluated by immunofluorescence. In addition to ICE mRNA, caspase-3 enzymatic activity was assayed. RESULTS: Although no differences were seen at one week, apoptosis-positive cells increased with CsA at four weeks (P < 0.05) and correlated with tubular atrophy and interstitial fibrosis (r = 0.8, P < 0.05). CsA induced the expression of p53 (P < 0.05) and Bax (P < 0.01) and decreased that of Bcl-2 (P < 0.05). CsA up-regulated Fas-L expression (P < 0.001). ICE mRNA and caspase-3 activity were also increased (P < 0.01). The changes occurred as early as one week and remained statistically significant at four weeks. CONCLUSIONS: Specific apoptotic genes are increased in chronic CsA nephrotoxicity. The balance favors the induction of apoptosis. Increased apoptosis could explain the tubular dropout and loss of cellularity with fibrosis. This then may impair the ability of the tubulointerstitium to remodel. Apoptosis could also contribute to some of CsA immunosuppressive effects on activated lymphocytes.
Animals↗
[A study on hemostatic and immunological actions of fresh and dry Dihuang].
OBJECTIVE: To investigate the difference between fresh and dry Dihuang (Radix Rehmanniae) in hemostatic and immunological actions. METHODS: The hemostatic action was assessed in aspirin-treated mice; immunological action was assessed by phagocytosis of macrophages in dexamethasone-treated mice; and Con A-induced mitogenesis and LPS-induced alkaline phosphatase activity of splenocytes were determined in thyroxin-treated mice. RESULT: The blood clotting in mice induced by aspirin was inhibited by oral administrations of juice decoction of fresh Dihuang or decoction of dry Dihuang alike. The action of fresh Dihuang juice was stronger than that of dry Dihuang decoction. Oral administrarion of fresh Dihuang juice or decoction for 10 days enhanced LPS-induced alkaline phosphatase activity of splenocytes in thyroxin-treated mice. The juice also enhanced Con A-induced splenocyte mitogenesis. The action of dry Dihuang decoction was weaker than that of fresh juice in increasing LPS-induced alkaline phosphatase activity. CONCLUSION: It is recommended to follow the tradition of using fresh Dihuang juice or decoction to treat some diseases such as hemorrhagenic troubles.
Animals↗
[Determination of C1-C5 composition of liquefied petroleum gas by capillary gas chromatography].
In this paper, thirteen C1-C5 hydrocarbons in liquefied petroleum gas were separated and determined by using capillary gas chromatography. The cloumn used was 50 m x 0.53 mm i.d. HP PLOT-Al2O3. A standard mixture of known composition was used for the determination of correction factots and the corrected area mormalization was used for quantification. The relative standard deviations (n = 5) were 0.39%-5.4%. Ethane, ethylene and butene were separated to baseline.
English Abstract↗
Ataxin-1 nuclear localization and aggregation: role in polyglutamine-induced disease in SCA1 transgenic mice.
Transgenic mice carrying the spinocerebellar ataxia type 1 (SCA1) gene, a polyglutamine neurodegenerative disorder, develop ataxia with ataxin-1 localized to aggregates within cerebellar Purkinje cells nuclei. To examine the importance of nuclear localization and aggregation in pathogenesis, mice expressing ataxin-1[82] with a mutated NLS were established. These mice did not develop disease, demonstrating that nuclear localization is critical for pathogenesis. In a second series of transgenic mice, ataxin-1[77] containing a deletion within the self-association region was expressed within Purkinje cells nuclei. These mice developed ataxia and Purkinje cell pathology similar to the original SCA1 mice. However, no evidence of nuclear ataxin-1 aggregates was found. Thus, although nuclear localization of ataxin-1 is necessary, nuclear aggregation of ataxin-1 is not required to initiate pathogenesis in transgenic mice.
Animals↗