Biomedical subjects

L Pei

Publications and source records attributed to L Pei.

At least 19 recordsLinked to original sources

PubMed2004

Finite-element analysis of contact between elastic self-affine surfaces.

Finite-element methods are used to study nonadhesive, frictionless contact between elastic solids with self-affine surfaces. We find that the total contact area rises linearly with the load at small loads. The mean pressure in the contact regions is independent of load and proportional to the root-mean-square slope of the surface. The constant of proportionality is nearly independent of the Poisson ratio and roughness exponent and lies between previous analytic predictions. The contact morphology is also analyzed. Connected contact regions have a fractal area and perimeter. The probability of finding a cluster of area a(c) drops as a(-tau )(c ) where tau increases with a decrease in roughness exponent. The distribution of pressures shows an exponential tail that is also found in many jammed systems. These results are contrasted to simpler models and experiments.

Journal Article↗

PubMed2001

Transcriptional repressor of vasoactive intestinal peptide receptor mediates repression through interactions with TFIIB and TFIIEbeta.

The transcriptional repressor for rat vasoactive-intestinal-polypeptide receptor 1 (VIPR-RP) is a recently characterized transcription factor that belongs to a family of proteins, which include components of the DNA replication factor C complex. In this study, I investigated the mechanisms by which VIPR-RP represses transcription. I show here that transcriptional repression by VIPR-RP is mediated by a histone deacetylase-independent mechanism. I provide evidence that VIPR-RP makes direct physical contacts with two proteins of the basal transcription apparatus, the transcription factors TFIIB and TFIIEbeta. The interaction with TFIIB is mediated by the N-terminal 180 amino acids, whereas the interactive domain with TFIIEbeta is located between residues 367 and 527 of VIPR-RP. Using gel mobility-shift assays I demonstrated that interaction between VIPR-RP and TFIIB prevents the recruitment of TFIIB into a DNA-TATA-box-binding protein complex. My results indicate that VIPR-RP mediates transcriptional repression through direct interactions with the general transcription machinery.

Animals↗

PubMed2001

Functional study of antibodies against a fibrogenin-binding protein in Staphylococcus epidermidis adherence to polyethylene catheters.

Staphylococcus epidermidis is an important pathogen in foreign body-associated infections. In a previous study, we showed that a surface-located fibrinogen-binding protein, termed Fbe, from S. epidermidis mediated the bacterial adherence to fibrinogen-coated surfaces in vitro. In the present study, we demonstrate that antibodies against Fbe can block adherence of S. epidermidis to fibrinogen-coated catheters, subcutaneously implanted catheters from rats, and peripheral venous catheters from human patients.

Animals↗

PubMed2001

Lack of fbe, the gene for a fibrinogen-binding protein from Staphylococcus epidermidis, reduces its adherence to fibrinogen coated surfaces.

The significance of Fbe, a fibrinogen-binding protein in Staphylococcus epidermidis, was investigated. A fbe mutant was constructed by allelic replacement, where a Gentamicin resistance gene replaced a portion of the A region of fbe. Adherence assay to immobilized fibrinogen on polyethylene surfaces and peripheral venous catheters from patients showed that the fibrinogen binding ability of the mutant was reduced compared to its parental strain. This shows that Fbe is a major factor involved in adherence of S. epidermidis to fibrinogen. No difference was found between the wild-type and mutant in their affinity to immobilized fibronectin.

Alleles↗

PubMed2001

Transient cerebral ischemia increases tyrosine phosphorylation of the synaptic RAS-GTPase activating protein, SynGAP.

Cerebral ischemia results in activation of the mitogen-activated protein kinase pathway and increased tyrosine phosphorylation of proteins associated with postsynaptic densities (PSDs). The authors investigated the possible relation between these events by determining the effect of ischemia on tyrosine phosphorylation of the brain-specific, PSD-enriched, Ras-GTPase activating protein, SynGAP. Transient (15 minutes) global ischemia was produced in rats by 4-vessel occlusion and PSDs prepared from forebrains immediately after ischemia or at 20 minutes, 1 hour, or 24 hours of reperfusion. Tyrosine phosphorylation of SynGAP was elevated relative to sham-operated controls by 20 minutes of reperfusion and remained elevated for at least 24 hours. Tyrosine phosphorylation of SynGAP also increased in CA1 and CA3/DG subfields of the hippocampus. Enhanced tyrosine phosphorylation of SynGAP was not accompanied by a change in PSD RasGAP activity. SynGAP bound to the SH2 domains of Src and Fyn in a tyrosine phosphorylation-dependent fashion, and this interaction increased after ischemia. SynGAP binds to the PDZ domains of PSD-95/SAP90 and coimmunoprecipitated with PSD-95. The coimmunoprecipitation of SynGAP with PSD-95 decreased after ischemia. The results indicate that changes in the properties and interactions of SynGAP may be involved in the neuropathology of ischemia.

Animals↗

PubMed2001

Autoregulation of the human liver X receptor alpha promoter.

Previous work has implicated the nuclear receptors liver X receptor alpha (LXR alpha) and LXR beta in the regulation of macrophage gene expression in response to oxidized lipids. Macrophage lipid loading leads to ligand activation of LXRs and to induction of a pathway for cholesterol efflux involving the LXR target genes ABCA1 and apoE. We demonstrate here that autoregulation of the LXR alpha gene is an important component of this lipid-inducible efflux pathway in human macrophages. Oxidized low-density lipoprotein, oxysterols, and synthetic LXR ligands induce expression of LXR alpha mRNA in human monocyte-derived macrophages and human macrophage cell lines but not in murine peritoneal macrophages or cell lines. This is in contrast to peroxisome proliferator-activated receptor gamma (PPAR gamma)-specific ligands, which stimulate LXR alpha expression in both human and murine macrophages. We further demonstrate that LXR and PPAR gamma ligands cooperate to induce LXR alpha expression in human but not murine macrophages. Analysis of the human LXR alpha promoter led to the identification of multiple LXR response elements. Interestingly, the previously identified PPAR response element (PPRE) in the murine LXR alpha gene is not conserved in humans; however, a different PPRE is present in the human LXR 5'-flanking region. These results have implications for cholesterol metabolism in human macrophages and its potential to be regulated by synthetic LXR and/or PPAR gamma ligands. The ability of LXR alpha to regulate its own promoter is likely to be an integral part of the macrophage physiologic response to lipid loading.

3T3 Cells↗

PubMed2001

Reproductive deficiencies in transgenic mice expressing the rat inhibin alpha-subunit gene.

Inhibin is an important modulator of reproductive function at both the endocrine level, through its regulation of pituitary FSH biosynthesis, and at the paracrine and autocrine levels, as an intragonadal regulatory factor. To investigate the in vivo actions of inhibin in FSH regulation and gonadal function, transgenic mice that overexpress the rat inhibin alpha-subunit gene were generated. A transgene that includes the mouse metallothionein-I gene promoter (MT-alpha) fused to the rat inhibin alpha-subunit precursor coding sequences was used to produce three lines of transgenic mice. Transgene mRNA is expressed in numerous tissues, including the pituitary, liver, testis, ovary, and kidney. Inhibin alpha-subunit protein was also increased in transgenic pituitary and ovary. Serum inhibin alpha-subunit levels are highly increased compared with control mice. Inhibin beta(A)- and beta(B)-subunit protein amounts are lower in transgenic ovaries compared with wild type, although serum levels of activin A are not significantly reduced in transgenic female mice. FSH levels are reduced in both male and female transgenic mice, whereas LH levels are increased in MT-alpha female mice. MT-alpha transgenic females are subfertile and exhibit a 52% reduction in litter size compared with wild-type females. The smaller litter size of MT-alpha female mice was correlated with a reduction in the number of oocytes ovulated during a normal cycle. Treatment of the transgenic females with exogenous gonadotropins resulted in an ovulation rate similar to that of stimulated wild-type animals, suggesting that altered gonadotropin levels may be responsible for the decreased ovulation rates. MT-alpha transgenic male mice are fertile and sire litters of equivalent size to those sired by wild-type males, despite an approximately 50% reduction in sperm numbers. These results indicate that overexpression of the rat inhibin alpha-subunit gene in mice leads to a disruption of the normal inhibin-to-activin ratio and to reproductive deficiencies, and they support the hypothesis that inhibin and activin act to regulate FSH secretion in vivo and are essential for normal gonadal function.

Animals↗

PubMed2001

[A prospective, randomized controlled study comparing the effects of gonadotropin-releasing hormone agonist long and short protocols for in vitro fertilization].

OBJECTIVE: To compare the effects of gonadotropin-releasing hormone agonist (GnRH-a) long and short protocols as part of in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) treatment. METHODS: One hundred and nine infertile couples accepted a prospective, randomized comparative study for IVF or ICSI treatment were divided into GnRH-a long protocol group (55 cases) and GnRH-a short protocol group (54 cases). GnRH-a long protocol group: GnRH-a was taken by nasal spray 0.9 mg/day starting on day 21 of the previous menstrual cycle. Once the patient was down regulated, gonadotropin (Gn) injection was started. GnRH-a short protocol group: GnRH-a was taken by nasal spray 0.45 mg/day starting on day 2 of the menstrual cycle, and Gn was started on the same day. Two groups had human chorionic gonadotrophin (hCG) administered when the leading follicle was at least 18 mm in diameter. Oocytes were retrieved 36 hours after hCG administration guided by transvaginal ultrasounography. IVF/ICSI were performed as routine. RESULTS: Serum follicle stimulating hormone and luteinizing hormone (LH) levels on the day of starting Gn were lower in the long protocol group comparing with the short protocol group [(4.4 +/- 1.2) IU/L Vs (6.3 +/- 1.7) IU/L, (2.7 +/- 1.5) IU/L Vs (4.4 +/- 2.8) IU/L, P < 0.01 respectively]. The levels of serum estradiol (E2), LH and E2 per oocyte on the day of hCG injection were lower in the long protocol group comparing with the short protocol group [(7,119 +/- 3,584) pmol/L Vs (9,523 +/- 3,587) pmol/L, (1.0 +/- 1.0) IU/L Vs (4.0 +/- 3.4) IU/L, (610 +/- 315) pmol/L Vs (935 +/- 450) pmol/L, P < 0.01 respectively]. Patients treated with short protocol were stimulated for a shorter period, required fewer Gn ampoules than the long protocol group [(10.1 +/- 1.5) d Vs (11.1 +/- 1.2) d, (23.4 +/- 8.7) Amps Vs (28.0 +/- 8.6) Amps, P < 0.01 respectly]. There are no statistically differences between the two groups in the numbers of oocytes retrieved, metaphase of second meiosis oocytes, fertilized oocytes, cleaved embryos, high quality embryos and pregnancy rates. CONCLUSIONS: The GnRH-a long and short protocols have equal effects on controlled ovarian hyperstimulation for in vitro fertilization. Patients who received GnRH-a short protocol required fewer ampoules of gonadotrpins and shorter period of treatment than those who received the GnRH-a long protocol.

Adult↗

PubMed2000

Identification of c-myc as a down-stream target for pituitary tumor-transforming gene.

Pituitary tumor-transforming gene (PTTG) encodes a protein implicated in cellular transformation and transcriptional regulation. To identify downstream target genes, I established cell lines with tightly regulated inducible expression of PTTG. DNA arrays were used to analyze gene expression profiles after PTTG induction. I identified c-myc oncogene as a major PTTG target. Induction of PTTG resulted in increased cell proliferation through activation of c-myc. I showed that PTTG activates c-myc transcription in transfected cells. PTTG binds to c-myc promoter near the transcription initiation site in a protein complex containing the upstream stimulatory factor (USF1). I have defined the PTTG DNA-binding site and mapped PTTG DNA binding domain to a region between amino acids 61 and 118. Furthermore, I demonstrated that PTTG DNA binding is required for its transcriptional activation function. These results definitively established the role of PTTG as a transcription activator and indicate that PTTG is involved in cellular transformation and tumorigenesis through activation of c-myc oncogene.

Binding Sites↗

PubMed2000

Activation of mitogen-activated protein kinase cascade regulates pituitary tumor-transforming gene transactivation function.

Pituitary tumor-transforming gene (PTTG) is a recently characterized oncogene that can act as a transcriptional activator. In this study, we have characterized the transactivation domain of PTTG. Transient transfection of fusion constructs containing GAL4 DNA-binding domain and different parts of PTTG indicated the transactivation domain of PTTG is located between amino acids 119 and 164. Mitogen-activated protein (MAP) kinase cascade is important in the regulation of cell growth, apoptosis, and differentiation. Therefore, we have explored the possibility that this kinase cascade plays a role in regulating PTTG transactivation function. Activation of the MAP kinase cascade by epidermal growth factor or an expression vector for a constitutively active form of the MAP kinase kinase (MEK1) led to stimulation of PTTG transactivation activity. We showed that PTTG is phosphorylated in vitro on Ser(162) by MAP kinase and that this phosphorylation site plays an essential role in PTTG transactivation function. We demonstrated that PTTG interacts directly with MEK1 through a putative SH3 domain-binding site located between amino acids 51 and 54 and that this interaction is crucial for PTTG transactivation function. In addition, we showed that activation of MAP kinase phosphorylation cascade resulted in nuclear translocation of PTTG. Together, our data establish that a growth factor-stimulated MAP kinase plays an important role in modulating PTTG function.

3T3 Cells↗

PubMed2000

A novel binding factor facilitates nuclear translocation and transcriptional activation function of the pituitary tumor-transforming gene product.

Pituitary tumor-transforming gene (PTTG) is a recently characterized oncogene whose expression product contains a transcriptional activation domain at the C terminus. To understand the mechanisms involved in PTTG biological functions, we used yeast two-hybrid screening to identify proteins that interact with PTTG. This study reports the isolation and characterization of a novel PTTG-binding factor (PBF). PBF contains an open reading frame of 179 amino acids with a predicted molecular mass of 22 kDa. In Northern blot analyses, PBF mRNA was ubiquitously expressed in human tissues. Glutathione S-transferase pull-down and co-immunoprecipitation assays demonstrate that PBF interacts specifically with PTTG under both in vitro and in vivo conditions. The PTTG binding domain in PBF was located within the C-terminal 30-amino acid region that contain a nuclear localization signal. Immunofluorescence and subcellular fractionation studies showed that PTTG is predominantly expressed in the cytoplasm with partial nuclear localization, whereas PBF is localized both in the cytoplasm and the nucleus. The interaction between PBF and PTTG facilitated PTTG translocation from the cytoplasm to the nucleus. Furthermore, PBF is required for transcriptional activation of basic fibroblast growth factor by PTTG. In summary, we have characterized a novel PTTG-binding protein that facilitates PTTG nuclear translocation and potentiates its transcriptional activation function.

Amino Acid Sequence↗

PubMed2000

Phosphorylation modulates the function of the vasoactive intestinal polypeptide receptor transcriptional repressor protein.

The transcriptional repressor for rat vasoactive intestinal polypeptide receptor 1 (VIPR-RP) is a recently isolated transcription factor. In this study, we have characterized the functional domains of VIPR-RP and the importance of phosphorylation on VIPR-RP function. Using various regions of VIPR-RP in gel mobility shift assays, we show that the amino acid sequences between positions 367 and 475 play an essential role for VIPR-RP DNA binding. Transient transfection of fusion constructs containing GAL4 DNA binding domain and different parts of VIPR-RP indicated that there are two separate transcriptional repression domains in VIPR-RP, located between amino acids 50 and 101 and between 469 and 527. We demonstrated that VIPR-RP is phosphorylated in vitro by casein kinase II on Ser-69/71 and Thr-110, and by cAMP-dependent kinase on Ser-245/361. Furthermore, by site-directed mutagenesis, we show that phosphorylation of the casein kinase II sites potentiates VIPR-RP transcriptional repression activity by enhancing its nuclear translocation, and that phosphorylation by cAMP-dependent kinase inhibits VIPR- RP transcriptional repression function without affecting its subcellular localization. These observations suggest that phosphorylation plays an important role in regulating VIPR-RP function.

Amino Acid Sequence↗

PubMed2000

Long circulating liposomes encapsulating organophosphorus acid anhydrolase in diisopropylfluorophosphate antagonism.

These studies are focused on antagonizing organophosphorous (OP) intoxications by a new conceptual approach using recombinant enzymes encapsulated within sterically stabilized liposomes to enhance diisopropylfluorophosphate (DFP) degradation. The OP hydrolyzing enzyme, organophosphorous acid anhydrolase (OPAA), encapsulated within the liposomes, was employed either alone or in combination with pralidoxime (2-PAM) and/or atropine. The recombinant OPAA enzyme, from the ALTEROMONAS: strain JD6, has high substrate specificity toward a wide range of OP compounds, e.g., DFP, soman, and sarin. The rate of DFP hydrolysis by liposomes containing OPAA (SL)* was measured by determining the changes in fluoride-ion concentration using a fluoride ion-selective electrode. This enzyme carrier system serves as a biodegradable protective environment for the OP-metabolizing enzyme (OPAA), resulting in an enhanced antidotal protection against the lethal effects of DFP. Free OPAA alone showed some antidotal protection; however, the protection with 2-PAM and/or atropine was greatly enhanced when combined with (SL)*.

Animals↗

PubMed2000

Molecular characterization of the VIP receptor transcriptional repressor protein.

The rat type 1 VIP receptor transcriptional repressor protein (VIPR-RP) is a recently isolated novel transcription factor. In the study reported here, the functional domains of VIPR-RP were characterized. To map the DNA binding domain, various regions of VIPR-RP were either transcribed and translated in vitro or expressed in and purified from E. Coli as a glutathione S-transferase (GST) fusion. The ability of the truncated proteins to bind to VIPR-RP specific binding sequence was tested by gel mobility shift assays. The results indicated that the amino acid sequences between 367 and 475 play an essential role for VIPR-RP DNA binding. To determine the amino acid sequences required for transcriptional repression, fusion proteins containing the GAL4 DNA binding domain and various parts of VIPR-RP were constructed, and their ability to repress transcription of the reporter gene containing GAL4 DNA binding sequences were tested in transiently transfected COS7 cells. The results showed that VIPR-RP contains two separate transcriptional repression domains located between amino acids 50 to 101 and 470 to 527.

Animals↗

PubMed2000

[Effects of tumor necrosis factor-alpha on proliferation and intracellular free calcium concentration in endothelium of human umbilical vein endothelial cells].

OBJECTIVE: To Observe the effects of tumor necrosis factor-alpha (TNF-alpha) on cell proliferation and Intracellular free calcium concentration ([Ca2+]i) in endothelium of human umbilical vein endothelial cells (HUVEC) and investigate the pathogenesis of pregnancy induced hypertension syndrome (PIH). METHODS: Confluent monolayer of HUVEC was directly incubated with TNF-alpha at following final concentrations: 500, 1,000, 2,000 U/ml for 24 hours. The percentages of different cellcycles and [Ca2+]i were measured by flow cytometry and fluorospectrophotmetry. RESULTS: Incubated with TNF-alpha, the endothelial cells were elongated and transformed into fibroblast-like cells. Border of nucleus was sharp, clarity, and cells were in regular shape. But there were abnormal granules in cytoplasma and some cells detached at the concentrotion of 2,000 U/ml of TNF-alpha. Stimulated by TNF-alpha, the percentage of cellcycles from phase G0 + G1 to S and G2 + M decreased significantly and it was dose-dependent [Ca2+]i increased significantly and dose-dependent as well. CONCLUSION: TNF-alpha may injure endothelium directly and inhibit its proliferation and repair through the changes of [Ca2+]i level. It may play an important role in the pathogenesis of PIH.

Calcium↗

PubMed2000

Mechanisms of regulation of tyrosine phosphorylation of NMDA receptor subunit 2B after cerebral ischemia/reperfusion.

AIM: To study the mechanisms of the regulation of the tyrosine phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunit 2B(NR2B) in the gerbil hippocampal synaptosomes following ischemia/reperfusion (I/R). METHODS: Transient (15 min) cerebral ischemia was produced by bilateral carotid artery occlusion procedure. The tyrosine phosphorylation of NR2B was analyzed by immunoprecipitation and immunoblot assay. RESULTS: Transient forebrain ischemia for 15 min caused a marked decrease in the levels of tyrosine phosphorylation of many protein bands including 180 kDa protein. Transient ischemia followed by reperfusion induced rapid (within 15 min of reperfusion), and sustained (for at least 48 h) increase in the tyrosine phosphorylation of many protein bands including 180 kDa protein. Immunoprecipitation and immunoblot confirmed that NR2B is among the phosphorylated 180 kDa protein. Maximal phosphorylation of 180 kDa band corresponding to NR2B (1.8 fold relative to sham-operated controls) was reached at 6 h of reperfusion following 15 min of cerebral ischemia. But the level of protein expression of NR2B did not change. Administration of ketamine (KT), a non-competitive NMDA receptor antagonist, or nifedipine (ND), an L-type voltage gated calcium channel (L-type VGCC) blocker, 20 min before ischemia attenuated stimulation of the tyrosine phosphorylation of NR2B without affecting the level of protein expression of NR2B. Under these conditions, non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) had no effect on the level of tyrosine phosphorylation. Protein tyrosine phosphatase (PTP) inhibitor vanadate and protein tyrosine kinase (PTK) inhibitor genestein resulted in the increase and the decrease of the tyrosine phosphorylation of NR2B, respectively. Src coprecipitated with NR2B protein. CONCLUSION: The increase of the tyrosine phosphorylation of NR2B induced by I/R has relation to NR and L-type VGCC; PTK and PTP participate in the regulation of the tyrosine phosphorylation of NR2B during I/R. Src that associates with NR2B may play an important role in the regulation of the tyrosine phosphorylation of NR2B during I/R.

Animals↗

PubMed2000

Changes and mechanisms of protein-tyrosine kinase and protein-tyrosine phosphatase activities after brain ischemia/reperfusion.

AIM: To study the changes and mechanisms of protein-tyrosine kinase (PTK) and protein-tyrosine phosphatase (PTP) activities in the hippocamal synaptosome following cerebral ischemia/reperfusion (I/R) in gerbil. METHODS: Transient (15 min) global ischemia was produced by bilateral carotid artery occlusion. Total PTK and PTP activities were measured by [r-32P] incorporation and colorimetric analysis, respectively. Src and proline-rich tyrosine kinase2 (PYK2) activities were measured by immunoprecipitation and [r-32P] incorporation. RESULTS: Total PTK activity increased significantly after I/R, but the PTP activity did not change. The Src activity was much higher than PYK2 activity in sham-operated controls. I/R mainly caused a pronounced increase in Src activity, but not PYK2 activity. The increase in Src activity had no relation to the expression of Src protein. Administration of ketamine (KT) or nifedipine (ND) 20 min before ischemia caused a decrease in total PTK and Src activities, and no change in the PYK2 and PTP activities. CONCLUSION: The increase in PTK activity caused by I/R may be mainly due to the increase in Src activity. This increase in Src activity has no relation to the expression of Src protein. But it is related to the activation of NMDA (N-methyl-D-aspartate) receptor (NR) and L-type voltage-gated calcium channel (L-type VGCC). In other words, the increase in total PTK and Src activities induced by I/R may be mediated via NR and L-type VGCC. The PTP activity did not change during I/R.

Animals↗

PubMed2000

[Mechanism of Se-Indocalamus tessdatus polycassine(S-ITPS) against human immunodeficiency virus type 1 (HIV-1)].

OBJECTIVE: To study the mechanism of Se- Indochalamus tessdatus polycassine (S-ITPS) against HIV-1 and to provide a theoretical support for developing the anti-HIV drugs. METHODS: S-ITPS was added to MT4 cells before viral inoculation, at the same time of viral inoculation, then the cells were cultured with or without S-ITPS for 1-4 weeks, finally, cytopathic effect (CPE), MTT staining method for viable cells(MTT assay),p24 antigen titer (ELISA), or infectivity (TCID50 assay) of the cultural supernatants were used as markers to monitor the virus growth. RESULTS: S-ITPS can inhibit HIV-induced CPE (1C50 = l0microg/ml)and viral replication (1C50 = 156 microg/ml)in dose dependent manner. The virus infectivity in the presence of S-ITPS was greatly decreased than that of the control. The virus inhibition was enhanced under the presence of noncytotoxic drug concentration of <1250 microg/ml in cell culture, inhibition of viral replication by S-ITPS was 73.7%, 63.5%, 87.7% and 95.4% at week 1, week 2, week 3 and week 4 of cultured cells respectively. It can also inhibit absorption of HIV-1 to MT-4 cells, but no inhibition of HIV-1 was seen when MT-4 cells were pretreated with S-ITPS. Virus can be inactivated by the agent also. CONCLUSIONS: S-ITPS is a potent anti-HIV- 1 agent in MT-4 /HIV- 1 cultural system, at least two mechanisms were included inhibition both of HIV-1 absorption to MT-4 cells and viral replication in HIV-infected cells. S-ITPS inhibition of CPE is stronger than that of p24 antigen production.

Anti-HIV Agents↗