Chlorinated organic contaminants in surface sediments from the Yangtze Estuary and nearby coastal areas, China.
Explore the source record for details and available documents.
China↗
Biomedical subjects
L Hou
Publications and source records attributed to L Hou.
PKC and PKA, but not PKG mediate LPS-induced CGRP release and [Ca(2+)](i) elevation in DRG neurons of neonatal rats.
Calcitonin gene-related peptide (CGRP), is produced in dorsal root ganglia (DRG) neurons and released from primary afferent neurons to mediate hemodynamic effects and neurogenic inflammation. In this work, we determined whether lipopolysaccharide (LPS), an inflammatory stimulator, could trigger CGRP release from cultured DRG neurons and if so, which cellular signaling pathway was involved in this response. Cytoplasmic concentration of calcium ([Ca(2+)](i)) plays a key role in neurotransmitter release, therefore [Ca(2+)](i) was also determined in cultured DRG cells using fluo-3/AM. The results showed that LPS (0.1-10 microg/ml) evoked CGRP release in a time- and concentration-dependent manner from DRG neurons. LPS also increased [Ca(2+)](i) in a concentration-dependent manner. The protein kinase C (PKC) inhibitors, calphostin C 0.5 microM or RO-31-8220 0.1 microM, and the cAMP-dependent protein kinase (PKA) specific inhibitor RP-CAMPS 30 microM or nonspecific inhibitor H8 1 microM inhibited 1 microg/ml LPS-evoked CGRP release and [Ca(2+)](i) increase from DRG neurons. The cGMP-dependent protein kinase (PKG) inhibitor Rp-8-pCPT-cGMPS 30 microM did not block the LPS response. These data suggest that LPS may stimulate CGRP release and [Ca(2+)](i) elevation through PKC and PKA, but not PKG signaling pathway in DRG neurons of neonatal rats.
Animals↗
Analysis of SOX10 function in neural crest-derived melanocyte development: SOX10-dependent transcriptional control of dopachrome tautomerase.
SOX10 is a high-mobility-group transcription factor that plays a critical role in the development of neural crest-derived melanocytes. At E11.5, mouse embryos homozygous for the Sox10(Dom) mutation entirely lack neural crest-derived cells expressing the lineage marker KIT, MITF, or DCT. Moreover, neural crest cell cultures derived from homozygous embryos do not give rise to pigmented cells. In contrast, in Sox10(Dom) heterozygous embryos, melanoblasts expressing KIT and MITF do occur, albeit in reduced numbers, and pigmented cells eventually develop in nearly normal numbers both in culture and in vivo. Intriguingly, however, Sox10(Dom)/+ melanoblasts transiently lack Dct expression both in culture and in vivo, suggesting that during a critical developmental period SOX10 may serve as a transcriptional activator of Dct. Indeed, we found that SOX10 and DCT colocalized in early melanoblasts and that SOX10 is capable of transactivating the Dct promoter in vitro. Our data suggest that during early melanoblast development SOX10 acts as a critical transactivator of Dct, that MITF, on its own, is insufficient to stimulate Dct expression, and that delayed onset of Dct expression is not deleterious to the melanocyte lineage.
Animals↗
Identification of a new form of death-associated protein kinase that promotes cell survival.
In this study, two alternatively spliced forms of the mouse death-associated protein kinase (DAPK) have been identified and their roles in apoptosis examined. The mouse DAPK-alpha sequence is 95% identical to the previously described human DAPK, and it has a kinase domain and calmodulin-binding region closely related to the 130-150 kDa myosin light chain kinases. A 12-residue extension of the carboxyl terminus of DAPK-beta distinguishes it from the human and mouse DAPK-alpha. DAPK phosphorylates at least one substrate in vitro and in vivo, the myosin II regulatory light chain. This phosphorylation occurs preferentially at Ser-19 and is stimulated by calcium and calmodulin. The mRNA encoding DAPK is widely distributed and detected in mouse embryos and most adult tissues, although the expression of the encoded 160-kDa DAPK protein is more restricted. Overexpression of DAPK-alpha, the mouse homolog of human DAPK has a negligible effect on tumor necrosis factor (TNF)-induced apoptosis. Overexpression of DAPK-beta has a strong cytoprotective effect on TNF-treated cells. Biochemical analysis of TNF-treated cell lines expressing mouse DAPK-beta suggests that the cytoprotective effect of DAPK is mediated through both intrinsic and extrinsic apoptotic signaling pathways and results in the inhibition of cytochrome c release from the mitochondria as well as inhibition of caspase-3 and caspase-9 activity. These results suggest that the mouse DAPK-beta is a negative regulator of TNF-induced apoptosis.
Alternative Splicing↗
Association of a 27-bp repeat polymorphism in ecNOS gene with ischemic stroke in Chinese patients.
OBJECTIVE: To investigate the association between a 27-bp repeat polymorphism of the ecNOS gene in 364 patients with ischemic stroke and 516 control subjects. BACKGROUND: The incidence of stroke in China is higher than that of coronary artery disease. Furthermore, ischemic stroke is more prevalent than hemorrhagic stroke. A 27-bp repeat polymorphism in intron 4 of the endothelial constitutive nitric oxide synthase (ecNOS) gene has been reported to associate with coronary artery disease in an Australian population, but no association was found between this polymorphism and ischemic stroke in a Japanese population. METHODS: All patients and unrelated control subjects were screened by CT. All participants lived in central China. Multivariate logistic regression analysis was used to determine the independent roles of this ecNOS gene polymorphism and covariates in ischemic stroke. RESULTS: These results indicated an association between the ecNOS a allele and ischemic stroke in the Chinese patients studied (7.8 versus 17.0%; OR = 2.44; 95% CI = 1.60 to 3.71, p < 0.0001). CONCLUSION: The ecNOS a allele in intron 4 may be an independent risk factor for ischemic stroke in the Chinese population studied, especially in those lacking other conventional risk factors.
Aged↗
Studies on flavans. 1. Facile synthesis of (+/-)-7-hydroxy-3',4'-methylenedioxyflavan and (+/-)-4'-hydroxy-7-methoxyflavan by a BF3.Et2O-mediated pyran cyclization.
A facile approach for the synthesis of flavans was developed by employing a BF3.Et2O-catalyzed pyran cyclization in an aprotic polar solvent as a key step, by which concise total syntheses of (+/-)-7-hydroxy-3',4'-methylenedioxyflavan (1) and (+/-)-4'-hydroxy-7-methoxyflavan (2), two naturally occurring flavans, were achieved.
Cyclization↗
Monoclonal antibodies against human telomerase reverse transcriptase (hTERT): preparation, characterization, and application.
The catalytic subunit of human telomerase reverse transcriptase (hTERT), is the necessary and rate-limiting component to telomerase activation in cancer cells. To develop monoclonal antibodies (MAbs) against hTERT, a peptide-hTERT(9)-derived from specific motif T of hTERT was synthesized. Through fusion of splenocytes of BALB/c mice immunized with hTERT(9) with mouse myeloma cells, hybridomas were generated and clones secreting anti-hTERT(9) antibody were screened. After three rounds of limited dilution of candidate clones, three of which present stable and constant antibody production. The MAbs were hTERT(9)-specific and reactive with native hTERT of human cancer cells or tissues in Western blot and immunohistochemistry. The heavy chain variable regions from three hybridomas were cloned and sequenced confirming their mouse Ig derivation. The described investigation suggested that the generated MAbs to hTERT(9) could recognize native hTERT and be useful to cancer research.
Amino Acid Sequence↗
Coronary artery disease risk in Chinese type 2 diabetics: is there a role for paraxonase 1 gene (Q192R) polymorphism?
OBJECTIVE: Heredity plays an important role in the predisposition to atherosclerotic coronary artery disease (CAD), and its thrombotic complications. Paraoxonase, a high-density lipoprotein-associated enzyme capable of hydrolyzing lipid peroxides, is presumed to contribute to atherosclerosis and CAD. This study investigates the role of human paraoxonase 1 (PON 1) gene (Q192R) polymorphism in CAD risk among Chinese type 2 diabetic cases. DESIGN: A population-based case-control study of paraoxonase 1 gene (Q192R) polymorphism and the risk of CAD in Chinese type 2 diabetics. METHODS: Subjects included 201 angiographically documented CAD patients with type 2 diabetes and 231 control subjects with type 2 diabetes alone living in central China. Single strand conformational polymorphism (SSCP) analysis was used to screen for PON 1 gene (Q192R) polymorphism. RESULTS: Frequency of the R allele was 21.5% in the CAD patients and 12.0% in the control subjects. The presence of the R allele was significantly associated with risk of CAD (odds ratio (OR)=1.97; 95% confidence interval (CI)=1.36--2.86). CONCLUSION: Frequency of the 192R allele of the human paraoxonase 1 gene may be an independent risk factor for CAD in the Chinese type 2 diabetics studied.
Aged↗
Association of a novel point mutation (C159G) of the CTLA4 gene with type 1 diabetes in West Africans but not in Chinese.
Here, we report on the detection of a novel point mutation of the CTLA4 gene at nucleotide position 159 (C-->G) leading to amino acid substitution at position 53 (I-->M), as well as its association with type 1 diabetes in two ethnically distinct populations. Subjects included 182 unrelated type 1 diabetes children and 201 control subjects from Ghana, West Africa. The Chinese study population consisted of 350 type 1 diabetic children and 420 healthy control subjects from central China. Polymerase chain reaction-single-strand conformation polymorphism and sequence analysis were used to screen for polymorphisms in the CTLA4 gene. CTLA4 49 (A-->G) mutation conferred a risk of type 1 diabetes in the Chinese children (odds ratio 1.78, 95% CI 1.58-2.0), but not in the West African children (1.17, 0.84-1.64). On the other hand, the novel CTLA4 159 (C-->G) mutation conferred a risk of type 1 diabetes in the West African children (2.1, 1.54-2.86), but not in the Chinese type 1 diabetic children. The novel CTLA4 gene polymorphism at nucleotide position 159 significantly associated with type 1 diabetes in West Africans, but not in Chinese. On the other hand, the CTLA4 gene polymorphism at nucleotide position 49 significantly associated with type 1 diabetes in Chinese, but not in West Africans.
Abatacept↗
Molecular mechanism about lymphogenous metastasis of hepatocarcinoma cells in mice.
AIM: To investigate the correlation between lymphogenous metastasis and matrix metalloproteinases (MMPs) activity and the expression of Fas ligand of tumor cells in lymph nodes. METHODS: Fifty-six inbred 615-mice were equally divided into 2 groups and inoculated with Hca-F and Hca-P cells. Their lymph node metastatic rates were examined. Growth fraction of lymphocytes in host lymph nodes was detected by flow cytometry. The Hca-F and Hca-P cells were cultured with extract of lymph node, liver or spleen. The quantity of MMPs in these supernatants was examined by zymographic analysis. The expression of Fas ligand, PCNA, Bcl-2 protein of Hca-F and Hca-P cells in the mice were examined by immunohistochemistry. The apoptosis signals of macro-phages in lymph nodes were observed with in situ DNA fragmentation. RESULTS: On the 28th day post-inoculation, the lymph node metastatic rate of HcaF was 80%(16/20), whereas that of Hca-P was 25%(5/20). The growth fraction of lymphocytes was as follows: in the Hca-F cells, the proliferating peak of lymphocytes appeared on the 14th day post inoculation and then decreased rapidly, while in HcaP cells, the peak appeared on the 7th day post inoculation and then kept at a high level. With the extract of lymph node, the quantity of the MMP-9 activity increased (P<0.01) and active MMP-9 and MMP-2 were produced by both Hca-F and Hca-P tumor cells, which did not produce MMPs without the extract of lymph node or with the extracts of the liver and spleen. The expression of Fas Ligand of Hca-F cells was stronger than that of Hca-P cells (P <0.01). The expressions of PCNA and Bcl-2 protein of Hca-F cells in the tumors of inoculated area were the same as that of Hca-P cells. In situ DNA fragmentation showed that the positive signals of macrophages were around Hca-F cells. CONCLUSION: Secretion of MMPs which was associated with metastatic ability of Hca-F and Hca-P tumor cells depends on the environment of lymph nodes. The increased expression of Fas ligand protein of Hca-F tumor cells with high lymphogenous metastatic potential in lymph nodes may help tumor cells escape from being killed by host lymphocytes.
Animals↗
[An AFLP marker related to fibrogenesis in upland cotton (Gossypium hirsuturm L.)].
By using AFLP technique polymorphism analysis was performed between a fuzzlesslintless mutant line and its isogenic wild-type line, Xuzhou 142. Out of 6,360 bands produced by 64 pairs primers, a fragment, named as CF1, appearing stably in wild-type line, Xuzhou 142. This polymorphism was further verified using several normal fiber varieties and F2, F3 populations from the cross of fuzzless-lintless mutant line with a high-lint-percentage variety Yumian No. 1. The cosegregation of CF1 and fibrogenesis was proved, which suggested that CF1 can be used as a molecular marker for cotton fibrogenesis. The CF1 segment was cloned into PUCm-T Vector and then sequenced. The putative amino acid sequences, is an analogue to phenol hydroxylase alpha subunit, outer surface protein C, NADH dehydrogenase subunit 1, NADH-ubiquinone oxidoreductase, 2-oxoacid ferredoxin oxidoreduct and hypothetical 14.5kD protein.
Base Sequence↗
[The expression of HCV RNA polymerase in E.coli and the study of its solubility and antigenicity].
OBJECTIVE: To express HCV RNA polymerase and study its soluble condition and antigenicity. METHODS: We constructed expression vectors pQE-5B-Fl and pQE-5B-C21 and expressed them in E.coli (M15). We analyzed their solubility in different conditions and purified soluble pQE-5B-C21 protein by Ni-NTA column, then detected its antigenicity by ELISA and western blot. RESULTS: We obtained the purified soluble pQE-5B-C21 protein in the induction conditions of 18 degrees C and the protein was proved to be of good antigenicity by ELISA and western blot. CONCLUSIONS: The RNA polymerase of HCV expressed in E.coli has good solubility and antigenicity.
Blotting, Western↗
[Studies on mimotopes of hepatitis C virus E1 protein].
OBJECTIVE: To study the B-cell epitope of E1 protein of hepatitis C virus. METHODS: By induction of IPTG, the E.coli M15 strains harboring the pQE30-HCVe118 expressed truncated C-terminal HCV E1 protein (Pte1). The proteins were purified with preparative electrophoreses system, which captured anti-E1 IgG in HCV (+) sera. By applying the antibodies as selective molecular 12 mers random peptide libraries were panned, and positive clones were obtained by ELISA. Amino acid sequences of display peptide were compared with that of HCV E1 protein. RESULTS: The purified HCV E1 proteins could react specifically with partly anti-HCV sera by ELISA. Among 10 phage display peptides, 6, 6, 2 were the most homologous to HCV E1 protein at position 320-336aa, 251-263aa, 225-248, respectively. CONCLUSIONS: There exist multiple B-cell epitopes in HCV E1 protein. At least one preponderant epitope is mapped at residues 320-336 of HCV E1 protein.
Amino Acid Motifs↗
Mechanisms of multiple organ damages in acute necrotizing pancreatitis.
OBJECTIVE: To determine the role of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), and evaluate the progress from SIRS to MODS and the therapeutic strategies for acute necrotizing pancreatitis (ANP). METHODS: Rat ANP models were made by retrograde injection of 3.5% sodium taurocholate 2.5 ml/kg into the pancreatic duct. Serum interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF alpha), amylase, endotoxin, and albumin were examined. The morphology and pathology of the pancreas, liver, lung, kidney and heart after ANP were observed. Finally, TNF alpha mRNA in the liver, lung, kidney and heart after ANP were observed by reverse transcriptase-polymerase chain reactions, and the efficiency of somatostatin and growth hormone were also observed in this experiment. RESULTS: ANP led to remarkable elevation of the inflammatory mediators which were positively correlated with the development of ANP and MODS. Somatostatin and growth hormone inhibited inflammatory mediators and TNF alpha mRNA overexpressions, reduced the risk of MODS, corrected hypoalbuminemia, reversed negative nitrogen balance, and controlled the reduction of cell groups with functions and reasonably intervened SIRS caused by ANP. CONCLUSION: TNF alpha mRNA plays an important role in ANP progression. The amelioration of ANP by combination treatment with somatostatin and growth hormone leads to the reduction of complications and marked increase in survival.
Animals↗
[Study on vibration mode of different phonatory source and compensation after partial laryngectomy].
OBJECTIVE: To investigate the nature of pathological voice production and compensatory mechanism after partial laryngectomy. METHODS: Vocal function of 93 cases following partial laryngectomy (28 cases of horizontal partial laryngectomy, 35 vertical partial laryngectomy, 30 horizontal-vertical partial laryngectomy) were examined by acoustic analysis, aerodynamic analysis and videostroboscopic examination. RESULTS: Horizontal supraglottic laryngectomy(HL) resulted in slight dysphonia after operation. The cover of vocal fold was hypertrophic and edematous. Mucosa wave was increased. Acoustic analysis showed significant difference between normal and horizontal laryngectomy groups(P < 0.05). Vertical laryngectomy(VL) resulted in moderate-severe dysphonia. Acoustic analysis was significantly worse in VL than in normal group(P < 0.01). The nonglottic phonatory source was the contralateral ventricular fold or contralateral vestibular mucosa (arytenoid mucosa, root mucosa of glottis) to approximate the reconstructed flap. It was noted that contralateral vocal fold did not participate in vibration. Horizontal-vertical partial laryngectomy (HVL) resulted in moderate-severe dysphonia. Acoustic analysis of HVL was significantly worse than that of normal phonation(P < 0.01). The site of compensatory mucosa vibration upon phonation was the contralateral vocal fold or contralateral hypertrophic arytenoid mucosa. The thinner the flap, the better the vocal quality was. Vocal quality of VL was worse than that of HVL in regard to shimmer, jitter, normalized noise energy, maximal phonation time and harmonic-noise ratio, but there was no significant difference between them. CONCLUSIONS: Partial laryngectomy has different vibrating compensatory modes: Voice function of horizontal partial laryngectomy was the best as it preserved the normal vibration mode; vertical partial laryngectomy was the worst with the nonglottic vibrating source of reconstructed flap-ventricular fold. The reconstructed flap, ventricular fold, mucosa of epiglottis and arytenoid take predominantly part in neoglottal vibration. The situation, volume and pliability characteristic of reconstructed flap was also important to vocal quality.
Aged↗
The membrane glycoprotein gp150 is encoded by the lagC gene and mediates cell-cell adhesion by heterophilic binding during Dictyostelium development.
gp150 is a membrane glycoprotein which has been implicated in cell-cell adhesion in the postaggregation stages of Dictyostelium development. An analysis of its tryptic peptides by mass spectrometry has identified gp150 as the product of the lagC gene, which was previously shown to play a role in morphogenesis and cell-type specification. Antibodies raised against the GST-LagC fusion protein specifically recognized gp150 in wild-type cells and showed that it is missing in lagC-null cells. Immunolocalization studies have confirmed its enrichment in cell-cell contact regions. In mutant cells that lack the aggregation stage-specific cell adhesion molecule gp80, gp150 is expressed precociously. Moreover, these cells acquire EDTA-resistant cell-cell binding during aggregation, suggesting a role for gp150 in this process. Cells in which the genes encoding gp80 and gp150 are both inactivated do not acquire EDTA-resistant cell adhesion during aggregation. Strains transformed with an actin 15::lagC construct express gp150 precociously, but do not show EDTA-resistant adhesion during early development. However, vegetative cells expressing gp150 can be recruited into aggregates of 16-h lagC-null cells. These results, together with those obtained with the cell-to-substratum binding assay, indicate that gp150 mediates cell-cell adhesion via heterophilic interactions with another component that accumulates during the aggregation stage.
Animals↗
Sonic hedgehog promotes proliferation and tyrosine hydroxylase induction of postnatal sympathetic cells in vitro.
The role of Sonic hedgehog (shh) in neural crest development was initially suggested by its involvement in patterning of the neural tube. While largely implicated in cell fate determination during development, its recently discovered role in the development of neurons postnatally prompted the possibility that neural crest derivatives of the sympathoadrenal lineage may respond to Shh postnatally. In the present study, we show that Shh promotes proliferation of postnatal sympathetic cells in culture. While it has been previously found to induce tyrosine hydroxylase (TH) production in the developing midbrain, we also demonstrated that Shh is capable of promoting TH induction of mature sympathetic neurons in vitro. This duality in Shh can be inhibited by activation of protein kinase A. These findings suggest that cell response to Shh is conserved in sympathetic ganglia derived from the neural crest, and further supports the notion that Shh can function postnatally in a dose-dependent manner to mediate neuronal cell fate.
Animals↗
IL-10, but not IL-4, suppresses infection-stimulated bone resorption in vivo.
Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1alpha in the murine model. The production and activity of IL-1alpha is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10(-/-) mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4(-/-) exhibited no increased resorption. IL-10(-/-) had markedly elevated IL-1alpha production within periapical inflammatory tissues (>10-fold) compared with wild type (p < 0.01), whereas IL-4(-/-) exhibited decreased IL-1alpha production (p < 0.05). IL-10 also suppressed IL-1alpha production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1alpha expression.
Animals↗