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Biomedical subjects

Y M Xie

Publications and source records attributed to Y M Xie.

11 recordsLinked to original sources
PubMed2002

Effect of dietary supplemental levels of vitamin A on the egg production and immune responses of heat-stressed laying hens.

Two experiments were conducted to evaluate the effect of vitamin A supplementation of a commercial layer diet on the laying performance and immune function of heat-stressed hens. In Experiment 1, two different levels of vitamin A supplementation (3,000 and 9,000 IU/kg) were used to investigate the laying performance and antibody titer against Newcastle disease virus (NDV) of heat-stressed hens. Results showed that the high level of vitamin A supplementation (9,000 IU/kg) had a beneficial effect on the feed intake and laying rate of heat-stressed hens (P < 0.05), compared with the control group (3,000 IU/kg). The antibody titers were not influenced by the level of vitamin A (P > 0.05). In Experiment 2, the effect of four levels of vitamin A (3,000, 6,000, 9,000, and 12,000 IU/kg) on the antibody titer to NDV and T lymphocyte proportion was studied. The experimental birds were exposed to a high temperature (31.5 C) 15 d after NDV vaccination (Treatment 1) or immediately (Treatment 2). The results showed that the egg weight was increased (P < 0.01) by the high levels of vitamin A supplementation (6,000 and 9,000 IU/kg), but feed intake, laying rate, and body weight loss were not (P > 0.05). In Treatment 1, vitamin A had no significant effect on antibody titers against NDV in normal or hot environments but increased (P < 0.01) the proportion of alpha-naphthyl acetate esterase (ANAE)-positive cells. Vitamin A supplementation had a significant effect on NDV antibody titer and ANAE-positive cell proportion in Treatment 2 (P < 0.01). The results of the present study suggested that vitamin A supplementation in commercial layer diets to layer chickens under heat stress was beneficial to laying performance and immune function.

Animal Feed↗
PubMed2001

Antibody-directed targeting of retroviral vectors via cell surface antigens.

Targeted stable transduction of specific cells is a highly desirable goal for gene therapy applications. We report an efficient and broadly applicable approach for targeting retroviral vectors to specific cells. We find that the envelope of the alphavirus Sindbis virus can pseudotype human immunodeficiency virus type 1- and murine leukemia virus-based retroviral vectors. When modified to contain the Fc-binding domain of protein A, this envelope gives a significant enhancement in specificity in combination with antibodies specific for HLA and CD4 relative to that without antibody. Unlike previous targeting strategies for retroviral transduction, the virus titers are relatively high and stable and can be further increased by ultracentrifugation. This study provides proof of principle for a targeting strategy that would be generally useful for many gene therapy applications.

Animals↗
PubMed2001

Inhibiting effect of antisense oligonucleotides phosphorthioate on gene expression of TIMP-1 in rat liver fibrosis.

AIM: To observe the inhibition of antisense oligonucleotides (asON) phosphorthioate to the tissue inhibitors metalloproteinase-1 (TIMP-1) gene and protein expression in the liver tissue of immunologically induced hepatic fibrosis rats. The possibility of reversing hepatic fibrosis through gene therapy was observed. METHODS: Human serum albumin (HSA) was used to attack rats, as hepatic fibrosis model, in which asONs were used to block the gene and protein expressing TIMP-1. According to the analysis of modulator, structure protein, coding series of TIMP-1 genome, we designed four different asONs. These asONs were injected into the hepatic fibrosis models through coccygeal vein. The results was observed by RT-PCR for measuring TIMP-1 mRNA expression, immunohistochemistry and in situ hybridization for collagen I, II, special staining of collagen fiber, and electron microscopic examination. RESULTS: Hepatic fibrosis could last within 363 days in our modified model. The expressing level of TIMP-1 was high during hepatic fibrosis process. It has been proved by the immunohistochemical and the electron microscopic examination that the asON phosphorthioate of TIMP-1 could exactly express in vivo. The effect of colchicine was demonstrated to inhibit the expressing level of mRNA and the content of collagen I, III in the liver of experimental hepatic fibrosis rats. However, the electron microscopy research and the pathologic grading of hepatic fibrosis showed that there was no significant difference between the treatment group and the model group (P> 0.05). CONCLUSION: The experimental rat model of hepatic fibrosis is one of the preferable models to estimate the curative effect of anti-hepatic fibrosis drugs. The asON phosphorthioate of TIMP-1 could block the gene and protein expression of TIMP-1 in the liver of experimental hepatic fibrosis rats at the mRNA level. It is possible to reverse hepatic fibrosis, and it is expected to study a new drug of antihepatic fibrosis on the genetic level. Colchicine has very limited therapeutic effect on hepatic fibrosis, furthermore, its toxicity and side effects are obvious.

Animals↗
PubMed1999

The presence of human immunodeficiency virus type 1 Vpr correlates with a decrease in the frequency of mutations in a plasmid shuttle vector.

The human immunodeficiency virus type 1 (HIV-1) Vpr protein induces cell cycle arrest at the border of G(2) and M similar to the arrest caused by agents which damage DNA. We determined whether the presence of Vpr would affect the ability of cells to repair DNA. We developed a shuttle vector system to analyze the effect of Vpr upon the repair of UV-damaged DNA. Our results demonstrated that the presence of Vpr decreased the rate of deletions in this system. Of note, cells arrested in G(2) by other genotoxic agents also increased the frequency of DNA repair of UV-damaged shuttle vectors. We did not observe any direct effect of Vpr upon the rate of double-strand break repair and/or nucleotide excision repair of genomic DNA in cells. Our results suggest a role for HIV-1 Vpr in altering the frequency of DNA repair, a property which may have importance for HIV-1 replication and pathogenesis.

Animals↗
PubMed1997

Synthetic NGF peptide derivatives prevent neuronal death via a p75 receptor-dependent mechanism.

Cyclized peptides corresponding to beta-loop regions of NGF were purified by HPLC and assayed for neurotrophic activity using DRG neurons. Peptides with the highest activity corresponded to loop region 29-35, a domain likely to interact with the p75 receptor. Unexpectedly, activity was confined to late-eluting HPLC fractions containing peptide multimers and primarily promoted neuronal survival without neurite outgrowth. Directed synthesis of dimer and monomer cyclized peptides demonstrated that dimers acted as partial NGF agonists in that they had both survival-promoting and NGF-inhibiting activity while monomer and linear peptides were inactive. Dimer activity was not affected by the Trk inhibitor K252a but was blocked by p75 receptor antibody and absent using p75 null mutant neurons. These studies suggest that region 29-35 peptide derivatives inhibit neuronal death via a structure- and p75-dependent mechanism.

Animals↗
PubMed1997

Human immunodeficiency virus type 1 Vpr interacts with HHR23A, a cellular protein implicated in nucleotide excision DNA repair.

The human immunodeficiency virus type 1 (HIV-1) vpr gene is an evolutionarily conserved gene among the primate lentiviruses HIV-1, HIV-2, and simian immunodeficiency viruses. One of the unique functions attributed to the vpr gene product is the arrest of cells in the G2 phase of the cell cycle. Here we demonstrate that Vpr interacts physically with HHR23A, one member of an evolutionarily conserved gene family involved in nucleotide excision repair. Interaction of Vpr with HHR23A was initially identified through a yeast two-hybrid screen and was confirmed by the demonstration of direct binding between bacterially expressed recombinant and transiently expressed or chemically synthesized protein products. Visualization of HHR23A and Vpr by indirect immunofluorescence and confocal microscopy indicates that the two proteins colocalize at or about the nuclear membrane. We also map the Vpr-binding domain in HHR23A to a C-terminal 45-amino-acid region of the protein previously shown to have homology to members of the ubiquitination pathway. Overexpression of HHR23A and a truncated derivative which includes the Vpr-binding domain results in a partial alleviation of the G2 arrest induced by Vpr, suggesting that the interaction between Vpr and HHR23A is critical for cell cycle arrest induced by Vpr. These results provide further support for the hypothesis that Vpr interferes with the normal function of a protein or proteins involved in the DNA repair process and, thus, in the transmission of signals that allow cells to transit from the G2 to the M phase of the cell cycle.

Amino Acid Sequence↗
PubMed1997

[Clinical study of bugu shengsui capsule in treating primary osteoporosis with kidney-yang deficiency syndrome].

OBJECTIVE: To assess the effect of Bugu Shengsui capsule (BGSSC) in treating primary osteoporosis. METHODS: Using double energy X-ray bone densimeter and radioimmunoassay (RIA), the effect of BGSSC in treating primary osteoporosis (OP) with Kidney-Yang Deficiency syndrome. RESULTS: The clinical markedly effective and total effective rates of BGSSC were 46% and 82%, respectively. The rate of TCM group is significantly higher than that of the control group (Vitamin D plus calcium). BGSSC could improve bone mineral density by the verification of double energy X-ray bone dansity (DEXA). It could also increase the level of serum calcitonin, luteinizing hormone and calcium, decrease the activity of parathyroid hormone. CONCLUSIONS: The effects of BGSSC on primary OP included increasing patient's bone mineral density, depressing bone resorption and decreasing bone loss.

Aged↗
PubMed1995

[Clinical and laboratory studies of effect of longevity-antihypertensive-mixture on elderly hypertension with kidney deficiency].

UNLABELLED: Longevity-Antihypertensive-Mixture (LAM) is a Chinese herbal drug, which could tonify Kidney in treating the hypertension with Kidney Deficiency in aged patients. RESULTS: 302 patients were randomly divided into three group: The treated group was subdivided into group I (107 Kidney Yin Deficiency patients) and group II (96 non-Kidney Yin Deficiency cases) and group III (99, control group). After treatment of LAM for 8 weeks, the rate of normalizing the blood pressure was 92.52% in group I while in group II, it was 84.43%, the symptoms were also significantly alleviated, and in group III, the rate was 70.71% only. The aorta compliance in group I significantly improved after LAM treatment (P < 0.025), the quality index of left ventricle reduced in treated group, and there was significant difference between treated and control groups. After treatment, LAM could shorten the length of extracorporal thrombus in group. The study showed that LAM could treat hypertension through LAM, administration with good effect.

Aged↗
PubMed1991

The Rex proteins of human T-cell leukemia virus type II differ by serine phosphorylation.

The Rex proteins of human T-cell leukemia virus types I and II (HTLV-I and HTLV-II) induce cytoplasmic expression of unspliced gag-pol mRNA and singly spliced env mRNA and are critical for virus replication. Two rex gene products, p27rex and p21rex of HTLV-I and p26rex and p24rex of HTLV-II, have been detected in HTLV-infected cells; however, the structural and biological relationship of the proteins has not been clearly elucidated. Endoproteinase digestion and phosphoamino acid analysis of HTLV-II Rex indicated that p24rex has the same amino acid backbone as p26rex and that the larger apparent molecular size of p26rex is attributable to serine phosphorylation.

Amino Acid Sequence↗
PubMed1990

The internal methionine codons of human T-cell leukemia virus type II rex gene are not required for p24rex production or virus replication and transformation.

Human T-cell leukemia virus types I (HTLV-I) and II (HTLV-II) have two nonstructural trans-acting regulatory genes, tax and rex, located in the 3' region of the viral genome. The tax gene product (HTLV-I p40tax and HTLV-II p37tax) is the transcriptional activator of the viral long terminal repeat. The rex gene encodes two protein products, p27rex/p21rex and p26rex/p24rex in HTLV-I and HTLV-II, respectively. Rex acts posttranscriptionally to facilitate accumulation of full-length gag/pol and singly spliced env mRNA in the cytoplasm of HTLV-infected cells. Previous studies showed that the first ATG of the rex gene is critical for Rex production and function. The importance of the internal ATGs to Rex function is not known. However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex, and by analogy HTLV-II p24rex, results from initiation at an internal AUG of the tax/rex mRNA. By using an infectious molecular clone of HTLV-II, we investigated the importance of the internal ATGs of the rex gene on Rex protein production and function. Our results indicate that p24rex of HTLV-II is not initiated at an internal AUG and that the internal methionine codons are not crucial to the function of the rex gene and, ultimately, the transforming properties of the virus.

Cell Line↗