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J Y Wen

Publications and source records attributed to J Y Wen.

7 recordsLinked to original sources
PubMed2005

Central penetration and stability of N-terminal tripeptide of insulin-like growth factor-I, glycine-proline-glutamate in adult rat.

Insulin-like growth factor-I is a neurotrophic factor and can prevent neurons from ischemic brain injury. However, the large molecular weight and metabolic effects can be problematic in its central delivery. Glycine-proline-glutamate (GPE) is the N-terminal tripeptide of insulin-like growth factor-I, which is naturally cleaved in the plasma and brain tissues. GPE reduces neuronal loss from hypoxic-ischemic brain injury following central administration. Central penetration and the stability of GPE in the plasma and central nervous system were examined in rats using radioimmunoassay and HPLC. GPE was rapidly metabolised in the plasma (8 min) after intraperitoneal administration. Despite having a short half-life in plasma, GPE was detected in the cerebrospinal fluid up to 40 min after intraperitoneal administration. With present of peptidase inhibitors, GPE existed in the brain tissue up to 3 h after intracerebroventricular administration, suggesting a role for peptolysis in its stability. The endopeptidase inhibitors 4- (2-aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) reduced GPE metabolism in the brain tissue while acid peptidase inhibitor pepstatin-A decreased GPE metabolism in the plasma. GPE reduced neuronal loss in the CA1-2 sub-region of the hippocampus given (intraperitoneally) after 30 min of hypoxic-ischemic injury in adult rats, further suggested the effectiveness of GPE central uptake. These results indicated that GPE crosses the blood-CSF and the functional CSF-brain barriers. The longer half-life of GPE in the CNS may be due to its unique enzymatic stability.

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PubMed2004

A particle swarm optimizer with passive congregation.

This paper presents a particle swarm optimizer (PSO) with passive congregation to improve the performance of standard PSO (SPSO). Passive congregation is an important biological force preserving swarm integrity. By introducing passive congregation to PSO, information can be transferred among individuals of the swarm. A particle swarm optimizer with passive congregation (PSOPC) is tested with a set of 10 benchmark functions with 30 dimensions and compared to a global version of SPSO (GSPSO), a local version of SPSO (LSPSO), and PSO with a constriction factor (CPSO), respectively. Experimental results indicate that the PSO with passive congregation improves the search performance on the benchmark functions significantly.

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PubMed2002

Enzymatic degradation of luteinizing hormone releasing hormone (LHRH) by mucosal homogenates from the intestine of the common brushtail possum (Trichosurus vulpecula).

The peptidolytic activity of fresh and frozen mucosal homogenates from five regions (duodenum, jejunum, ileum, caecum and colon) of possum intestine from Trichosurus vulpecula towards human Luteinizing Hormone Releasing Hormone (LHRH) was investigated. The rank of order of specific peptidolytic activity of the mucosal homogenates was jejunum > ileum > caecum> duodenum = colon, with a 3 to 4 fold difference between the least and the most active segment in both frozen and fresh samples. The formation of peptides LHRH (1-3), LHRH (1-4) and LHRH (1-5) suggest endopepetidase-24.18, endopeptidase-24.15 and angiotensin converting enzyme (ACE) might be responsible for the peptide degradation in mucosal homogenates. The inhibition of LHRH degradation by mucosal homogenates was evaluated in four regions (jejunum, ileum, caecum and colon) of possum intestine. Ethylenediaminetetraacetic acid (EDTA, 5 mM), sodium deoxycholate (SDA, 10 mM) and bacitracin (3.5 or 9 mM) inhibited the degradation of LHRH in mucosal homogenates from small intestine and hindgut. However, the serine protease inhibitor, soybean trypsin-chymotrypsin inhibitor (SBTI), did not prevent degradation of LHRH. It is concluded that combining peptides with inhibitors may enhance oral delivery of bioactive peptides or proteins to possums.

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PubMed1999

Olfactory associative learning in Caenorhabditis elegans is impaired in lrn-1 and lrn-2 mutants.

The C. elegans mutants, lrn-1 and lrn-2, are impaired in associative learning using conditioned taste cues. Both mutants are defective in associative learning about appetitive and aversive events, indicating that lrn-1 and lrn-2 exert effects across motivational boundaries. In a new olfactory associative learning paradigm, in which wild type worms learn to avoid a previously attractive diacetyl odor after it has been paired with an aversive acetic acid solution, lrn-1 and lrn-2 are impaired. Although defective in associative learning using a conditioned olfactory cue, nonassociative learning (habituation and dishabituation) using this same olfactory cue is unaffected. The discovery that lrn-1 and lrn-2 are defective in associative learning with both taste and olfactory cues may suggest that associative learning in different sensory modalities converges on a common genetic pathway in C. elegans that is subserved by lrn-1 and lrn-2.

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PubMed1997

Mutations that prevent associative learning in C. elegans.

The nematode Caenorhabditis elegans offers a promising system for the reductionist study of learning and memory. In this article, classical conditioning in C. elegans is demonstrated with a variety of associative learning assays. These assays allowed for the isolation and behavioral characterization of 2 mutant C. elegans lines impaired in associative learning. Both lines show no short-term or long-term associative conditioning; however, they appear relatively normal in tests of nonassociative learning and sensorimotor function. In combination with the well-described genetics and neuroanatomy of C. elegans, the isolation of mutants selectively, yet completely, blocked in associative learning provides the basis for an effective characterization of the cellular and molecular aspects of associative learning.

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PubMed1994

Satellite cell proliferation in the adult rat trigeminal ganglion results from the release of a mitogenic protein from explanted sensory neurons.

Explant of trigeminal ganglia neurons in adult rats induces perineuronal glial proliferation of primarily satellite cells as opposed to Schwann cells. This proliferation begins at 15 h after explant culture and by 27 h there is a significant increase in glial proliferation as measured by scintillation counts of [3H]thymidine. Blocking protein synthesis between 0 and 3.5 h after explant culture (early) results in an enhanced proliferative response, while blocking protein synthesis between 3.5 and 7 h (late) causes a complete block of the proliferative response assessed at 27 h. Conditioned media experiments demonstrate that both the mitogenic and inhibitory signals are diffusible and heat labile. Finally, the addition of neurotrophic factors to rescue injured ganglionic neurons attenuates the proliferative glial response suggesting that injured neurons produce and release signals that induce glial proliferation.

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