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Lin Xu

Publications and source records attributed to Lin Xu.

154 records · Page 9Linked to original sources
PubMed2002

CD44 deficiency in mice protects brain from cerebral ischemia injury.

CD44 is a transmembrane glycoprotein known to be involved in endothelial cell recognition, lymphocyte trafficking, and regulation of cytokine gene expression in inflammatory diseases. In the present study, we demonstrated that the expression of CD44 mRNA was induced in a mouse model of cerebral ischemia. A potential role of CD44 in ischemic brain injury was investigated using CD44-deficient (CD44-/-) mice. Over 50% (p < 0.05, n = 14) and 78% (p < 0.05, n = 10) reduction in ischemic infarct was observed in CD44-/- mice compared with that of wild-type mice following transient (30 min ischemia) and permanent (24 h) occlusion of the middle cerebral artery (MCAO), respectively. Similarly, significant improvement was observed in neurological function in CD44-/- mice as evidenced by spontaneous and forced motor task scores. The marked protection from ischemic brain injury in CD44-/- mice was associated with normal physiological parameters, cytokine gene expression, astrocyte and microglia activation as compared with wild-type mice. However, in CD44-/- mice, significantly lower expression of soluble interleukin-1beta protein was noted after brain ischemia. Our data provide new evidence on the potential role of CD44 in brain tissue in response to ischemia and may suggest that this effect might be associated with selective reduction in inflammatory cytokines such as interleukin-1beta.

Animals↗
PubMed2002

cDNA sequence of porcine thioredoxin.

Several mammalian thioredoxin cDNA sequences, namely that of human, macaca, ovine, bovine, equine and murine have been already registered in the Genbank database; but that of porcine is still not known. In this communication, we report the full-length cDNA sequence of porcine thioredoxin as determined by RT-PCR method. We also compared the protein sequence of thioredoxin from various mammals. Multialignment of the amino acid sequences between porcine and other mammalian species revealed that the sequences are highly conserved. Only one difference exists between the amino acid sequences of porcine and bovine thioredoxin.

Amino Acid Sequence↗
PubMed2002

DNA repair gene XRCC1 and XPD polymorphisms and risk of lung cancer in a Chinese population.

X-ray repair cross-complementing group 1 (XRCC1) and xeroderma pigmentosum group D (XPD) are mainly involved in base excision repair (BER) and nucleotide excision repair (NER) of DNA repair pathways, respectively. Polymorphisms of DNA repair gene XRCC1 and XPD has recently been identified, and there is a growing body of evidence that these polymorphisms may have some phenotypic significance. To investigate the role of XRCC1 polymorphisms (codon 194 and codon 399) and XPD polymorphism (codon 751) in lung cancer, a population-based case-control study of 109 lung cancer patients and 109 healthy control subjects (individually matched on age and gender) in a Chinese population was conducted. XRCC1 and XPD genotypes were identified using PCR-restriction fragments length polymorphism technique. Conditional logistic regression analysis revealed that XRCC1 codon 194Trp/Trp genotype was associated with a borderline increased risk of lung cancer [adjusted odd ratio (OR) = 3.06; confidence interval (CI) 0.94-9.92]. The XPD 751 Lys allele (combined Lys/Lys and Lys/Gln genotypes) was associated with a significantly increased risk of lung cancer (OR = 3.19; CI 1.01-10.07). The risk of lung cancer increased more than additive interaction (adjusted OR = 8.77; CI 1.47-52.31) for the individuals with both putative high-risk genotypes of XRCC1 194 Trp/Trp and XPD 751 Lys allele. Our results suggested that the genotypes of XRCC1 194Trp/Trp and XPD 751 Lys allele might be the risk genotypes for lung cancer in Chinese population.

Case-Control Studies↗
PubMed2002

Pathways regulating Na+/Ca2+ exchanger expression in the heart.

The Na(+)/Ca(2+) exchanger (NCX1) is regulated at the transcriptional level in cardiac hypertrophy, ischemia, and failure. Following pressure overload, activation of MAPKs coincides with the kinetics of NCX1 gene upregulation in adult cardiocytes. Using adenoviral gene delivery, we begin to identify the molecular pathways responsible for upregulation of the exchanger gene. Inhibition of ERK with the MEK inhibitor UO126, the ERK protein phosphatase MKP-3, inhibited ERK activation, but only inhibited alpha-adrenergic-induced NCX1 upregulation by 30%. Overexpression of DN-JNK lowered basal NCX1 expression. Overexpression of activated MKK-3 was sufficient for alpha-adrenergic-stimulated upregulation of the reporter gene. Together, this data indicates that (1) JNK mediates basal cardiac expression of the NCX1 gene, (2) ERK and p38 play a role in alpha-adrenergic-stimulated NCX1 upregulation, and (3) p38 activation alone is sufficient for NCX1 upregulation.

5' Untranslated Regions↗
PubMed2002

Dual actions of lanthanides on ACTH-inhibited leak K(+) channels.

Bovine adrenal zona fasciculata cells express background K(+) channels (I(AC) channels) whose activity is potently inhibited by ACTH. In whole cell patch clamp recordings, it was discovered that the trivalent lanthanides (Ln(3+)s) lanthanum and ytterbium interact with two binding sites to modulate K(+) flow through these channels. Despite large differences in ionic radii, these Ln(3+)s inhibited I(AC) channels half-maximally with IC(50) values near 50 microM. In addition, these Ln(3+)s blocked and reversed ACTH-mediated inhibition of I(AC) K(+) channels at similar concentrations. The Ln(3+)s did not alter inhibition of I(AC) by angiotensin II or cAMP. Ln(3+)-induced uncoupling of ACTH receptor activation from I(AC) inhibition was prevented by raising the external Ca(2+) concentration from 2 to 10 mM. The divalent cation Ni(2+) (500 microM) also blocked ACTH-dependent inhibition of I(AC) through a Ca(2+)-sensitive mechanism. The results are consistent with a model in which Ln(3+)s produce opposing actions on I(AC) K(+) currents through two separate binding sites. In addition to directly inhibiting I(AC), Ln(3+)s (and Ni(2+)) bind with high affinity to a Ca(2+)-selective site associated with the ACTH receptor. By displacing Ca(2+) from this site, Ln(3+)s prevent ACTH from binding and accelerate its dissociation. These results identify Ln(3+)s as a relatively potent group of noncompetitive ACTH receptor antagonists. Allosteric actions of trivalent and divalent metal cations on hormone binding, mediated through Ca(2+)-specific sites, may be common to a variety of peptide hormone receptors.

Adenosine Triphosphate↗
PubMed2002

[Changes of thioredoxin mRNA level in neurons insulted by sodium azide].

Oxidative stress has been considered to be associated with many neurodegenerative diseases, while mitochondrial damage is one of the important reasons that aggravate oxidative stress. Sodium azide (NaN3) is a specific inhibitor of mitochondrial cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. In this experiment, the neurotoxic effects of NaN3 on cultured primary neurons were detected by means of cell viability measurement (MTT assay) and morphological observation, and an in vitro model of neuronal injury induced by NaN3 were established. Further the changes of thioredoxin mRNA level in cultured neurons insulted by NaN3 were analyzed by semiquantitative RT-PCR in order to explore the role of Trx, an important redox regulatory protein, in the process of neuronal injury. It was found that cultured neurons could be damaged by NaN3 in a dose- and time-dependent manner and the expression of Trx decreased during certain dose (0-32mmol/L) and time (0-4hr) of NaN3 treatment. The above data suggest that decreased the expression of Trx may be associated with oxidative stress induced by neuronal respiratory chain injury, which could impair neuronal protective mechanism.

Animals↗
PubMed2001

Effect of simvastatin on the proliferation of rat cardiac fibroblasts.

OBJECTIVE: To investigate the effects of simvastatin on the proliferation of rat cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP). METHODS: CFs of neonatal Sprague-Dawley (SD) rats were isolated by trypsin digestion method and growth-arrested CFs were stimulated with 1x10-7 mol/L AVP in the presence of simvastatin (Sim) with varied concentrations. MTT assay was employed to measure CFs proliferation and determine the cell number, and the cell cycle distribution was determined with flow cytometer (FCM). RESULTS: With the increase of Sim concentration, D490 of CFs as shown by MTT assay gradually decreased, and for the cells treated with 1x10-6 mol/L Sim or 1x10-5 mol/L Sim, D490 (0.215+/-0.041and 0.163+/-0.018, respectively) was significantly lower than that of the control (0.939+/-0.048, P<0.01). In a dose-dependent manner, Sim decreased the cell percentage at S stage and the proliferation index (PI) as its concentration increased, but acted to the contrary effect with the percentage of cells at G0/G1 stage, and in CFs treated with 1x10-5 mol/L or 1x10-6 mol/l Sim, the 3 parameters were significantly different from those measured in the CFs with 1x10-7 mol/L AVP treatment (P<0.01). CONCLUSION: The results indicate that Sim can inhibit the proliferation of CFs induced by AVP, possibly through the mechanism of regulating the cell cycle distribution.

Journal Article↗
PubMedDate not supplied

Primary functioning hepatic paraganglioma: a case report.

An extra-adrenal pheochromocytoma is known as a paraganglioma. This report describes a patient with a rare primary functioning hepatic paraganglioma that resulted in hypertension. Computed tomography showed a highly vascular lesion located in segment 6 of the liver; it measured 6 x 5.5 cm. A right hemihepatectomy was subsequently performed; this was followed by an uneventful recovery and the disappearance of hypertension. The imaging characteristics and therapeutic principles of this rare tumor were gleaned from a review of the literature. Identification of this malignant tumor or possible recurrence is difficult, so longterm follow-up is recommended.

Adult↗