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Biomedical subjects

W Ye

Publications and source records attributed to W Ye.

At least 109 records · Page 6Linked to original sources
PubMed1997

Thalidomide and thalidomide analogs reduce HIV type 1 replication in human macrophages in vitro.

Thalidomide is currently being evaluated for efficacy in alleviating some manifestations of HIV-1 infection. To determine whether thalidomide has any direct effects on HIV-1 infection, we investigated the effect of thalidomide and also of three structural analogs of thalidomide on HIV-1 replication in vitro in human monocyte-derived macrophages. The thalidomide analogs were previously shown to inhibit TNF-alpha production in vitro at much lower concentrations than thalidomide. In HIV-1-infected macrophages treated with thalidomide or thalidomide analogs, viral replication was reduced by 60 to 80% as determined by measuring viral RT activity in the culture supernatants. In all experiments the analogs inhibited HIV-1 replication more efficiently than did thalidomide. The drugs also reduced HIV-1 gag mRNA expression. Furthermore, the drugs caused a decrease in NF-kappaB-binding activity in nuclear extracts of HIV-1-infected macrophages. The role of NF-kappaB in the drug-induced inhibition of HIV-1 replication was confirmed using an NF-kappaB-defective mutant virus to infect macrophages.

Anti-HIV Agents↗
PubMed1997

Hyaluronic acid in the normal and glaucomatous optic nerve.

Eighteen normal human eye-bank eyes (age: 18-81 years), five fetal eyes (16-24 weeks), 11 primary open-angle glaucoma (POAG) eyes (age: 76-89 years), and two Schnabel's cavernous optic atrophy eyes were examined using a biotinylated-hyaluronan binding protein to study the changes in the distribution of hyaluronic acid (HA) in the fetal, adult and glaucomatous optic nerve head. The vitreous body served as a positive control. Sections treated with Streptomyces hyaluronidase were used to confirm specificity. Monoclonal antibodies to myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were used as additional controls. In fetal optic nerve, HA was localized in blood vessels, peripapillary sclera and the pial septae in the retrolaminar nerve. No staining was associated with axons. Staining for MBP was negative. In adults, HA was found surrounding the myelin sheaths in the retrolaminar nerve; staining decreased with age. In contrast, HA staining in myelinated peripheral nerves (e.g. ciliaries) remained unchanged with age. HA also was localized to the adventitia of arteries and veins throughout the posterior segment. Compared to age-matched normal eyes, HA staining was virtually absent around myelin sheaths of the retrolaminar nerve in POAG eyes. Similar changes were not found in other HA positive structures. In Schnabel's cavernous optic atrophy. HA was present in increased amount in the atrophic area, but virtually absent in the remaining retrolaminar nerve. HA staining was invariably positive in vitreous, and Streptomyces hyaluronidase treated sections were negative. In adults, staining of MBP was associated with the myelin sheath in the retrolaminar nerve. In contrast to HA, staining of MBP was unchanged with age and in POAG. In Schnabel's atrophy, MBP staining disappeared only in the atrophic area. HA in the retrolaminar optic nerve appears to be associate with the space-filling matrix between myelin sheaths. HA is not present in the axon bundles prior to myelination of the optic nerve. HA in the retrolaminar optic nerve appears to decrease with age and is further reduced in POAG; however, corresponding changes are not found in MBP or in peripheral nerves. Perhaps, decreased amounts of HA is related to a higher susceptibility to elevated intraocular pressure or to optic nerve atrophy. In Schnabel's cavernous optic atrophy, HA is present in increased amount only in the atrophic area while MBP is markedly decreased, suggesting in situ production of HA in areas of optic nerve atrophy.

Adolescent↗
PubMed1997

The non-uniform distribution of albumin in human and bovine cornea.

In our previous studies, we noted a non-uniform distribution of protein tracer preferentially entering the anterior stromal lamellae of the cornea from the limbus. Given other differences reported previously between the anterior and posterior lamellae of the cornea, and the number of corneal disorders in which abnormalities are preferentially confined to either the anterior or posterior lamellae, we were prompted to examine the distribution of albumin in normal human and bovine cornea. The distribution of albumin in bovine and human cornea was studied immunohistochemically. Total soluble protein and albumin in the anterior 1/3 and posterior 2/3 of the central, middle and peripheral cornea of bovine eyes was measured biochemically. To aid in interpreting the findings, a theoretical model was developed based upon the combined effects of diffusive and convective transport. Using immunohistochemical methods, in both bovine and human eyes, intense staining of albumin was found in the anterior 1/3 of the corneal stroma. There was a gradual reduction in staining intensity from the limbus to the central cornea in the anterior corneal stroma. Less staining was found in the posterior 2/3 of corneal stroma. Additionally, a greater concentration of soluble protein and albumin was found in the anterior stroma than in the posterior stroma of the bovine eyes by biochemical analyses. The theoretical model demonstrated that this distribution of protein required a difference in excluded volume fraction between the anterior and posterior stroma and was consistent with a convective flux originating at the limbus and passing through the corneal stroma. The soluble proteins of the bovine and human cornea are preferentially concentrated in the anterior cornea and near the limbus. This distribution is likely due to differences in excluded volume fraction between the anterior and posterior stroma and a small convective flux passing through the cornea.

Albumins↗
PubMed1997

Perforin, a cytotoxic molecule which mediates cell necrosis, is not required for the early control of mycobacterial infection in mice.

Host defense against mycobacterial infection requires the participation of monocytes and T cells. Both CD4+ and CD8+ T cells have been shown to be important in resistance to mycobacterial infection in vivo. The main contribution of CD4+ T cells to the protective antituberculosis response involves the production of Th1-type cytokines, including interleukin-2 (IL-2) and gamma interferon (IFN-gamma). CD8+ T cells have been considered to be responsible primarily for cytotoxicity mediated by toxic molecules, including perforin. CD8+ T cells may also elaborate Th1-type cytokines, such as IFN-gamma, in response to the infection. To elucidate the contribution of perforin-mediated target cell death to the control of mycobacterial infection in vivo, mice with a disruption in the perforin gene (P-/-) were infected with Mycobacterium bovis BCG or M. tuberculosis Erdman for 5 and 13 weeks, respectively. At 1, 3, 5, and 13 weeks postinfection, the number of viable mycobacteria in the lungs, spleens, and livers of mice were determined by CFU assay. The infected tissues were examined histologically, and cytokine mRNA levels in the spleens of these mice were determined. Similar studies were carried out in Fas receptor-defective (CBA/lpr(cg)) mice to evaluate the contribution of this alternative cytotoxic pathway to the control of mycobacterial infection. The absence of either perforin gene function or Fas receptor gene function did not modify the course of experimental mycobacterial infection in these mice. In addition, both P-/- and Fas receptor-defective mice appeared to have a compensatory activation of cytokine genes, even in the absence of the experimental infection. P-/- mice had a mean 3.4- to 5-fold increase in mRNA levels for IL-10, IL-12p35, IL-6, and IFN-gamma. Similarly, Fas receptor-defective mice had a mean 3- to 3.6-fold increase in mRNA levels for IFN-gamma, IL-12p35, and IL-10. Our results indicate that both perforin-mediated cytotoxicity and Fas-mediated cytotoxicity do not appear to be necessary for the early control of mycobacterial infection in vivo.

Animals↗
PubMed1997

[Microbore liquid chromatography with dual electrode electrochemical detection of monoamine transmitters in brain microdialysates].

In the present work, the method of microbore liquid chromatography(MLC) with dual electrode electrochemical detection (DEED) was used to determine the monoamine transmitters and their metabolites in the striatal microdialysates from the anaesthetized rats. The potentials applied on the upstream (anodic) electrode and downstream (cathodic) electrode were set at +0.72V and +0.05V versus an Ag/AgCl reference electrode respectively. The interference of the large early-eluting peaks from brain dialysate was well eliminated on cathodic detection on the basis of electrochemical reversibility of catechol compounds. The collection efficiency of catecholamine (NA, A and DA) and DOPAC, that is the ratio of their responses in downstream electrode to those in upstream, was found to be in the range of 0.690 to 0.768, thereby providing reliable identification and measurement of early elutes. MLC-DEED is one of the best methods for the determination of monoamine transmitters at trace level. To optimize separation and detection, these adaptations were made to the system with respect to the injection valve, flow rate of the pump, connections between injector, column and detector, and cell volume of the detector. The detection limit could reach 1pg or less per injection, and the amounts, at least in the range of 2-200pg, were linearly correlated with the peak areas both at anodic detection and at cathodic detection. Prior to the collection of samples the probe recovery was measured in vitro at room temperature, and the recovery (%) for NA, DA, DOPAC, 5-HIAA, 5-HT and HVA were 19.5, 18.9, 22.1, 14,6, 16.5 and 19.3 respectively. The reported concentration of each compound was corrected according to probe recovery. The basal concentration of DA and 5-HT in striatal microdialysates was 12.5 +/- 1.8 and 5.0 +/- 0.7nmol/L. The perfussion of high K+ (100 mmol/L) through the dialysis probe induced a large increase of the concentration of NA, DA and 5-HT in microdialysates, and further increase of the concentration was observed in rat postmortem. The critical points for MLC-DEED are briefly discussed.

Animals↗
PubMed1997

Interendothelial junctions in normal human Schlemm's canal respond to changes in pressure.

PURPOSE: To determine if changes in the structure and complexity of junctions between endothelial cells lining Schlemm's canal (SC) occur in normal human eyes with changes in perfusion pressure. METHODS: Twelve normal human eyes were either perfusion-fixed (at 15 or 45 mm Hg) or immersion-fixed (0 mm Hg) in modified Karnovsky's fluid. 'Outflow facility was measured continually during the perfusion fixation. The intercellular junctions of the endothelial cells of SC were ultrastructurally examined in thin sections, including serial sections and freeze-fracture replicas. Morphometric data on the number of junctional strands per total length of tight junction were documented and categorized by the number of strands (one, two, or three or more). The length of endothelial cell overlap was measured on thin sections. RESULTS: In freeze-fracture replicas, perfusion-fixed eyes demonstrated less complex junctions. At 15 mm Hg, 18.06% of the total junctional length was represented by three or more strands; at 45 mm Hg, this percentage decreased to 8.59%. In immersion-fixed eyes, 24.17% of the total junctional length was represented by three or more strands. These differences were statistically significant (P < 0.0012). In sections, the amount of endothelial cell overlap, and thus the length of paracellular pathway, was reduced in perfusion-fixed versus immersion-fixed eyes (P < 0.02). Extensive serial sectioning demonstrated that giant vacuoles were formed, either by individual endothelial cells or by two or more adjacent endothelial cells. CONCLUSIONS: When compared with specimens fixed at zero pressure, overlap between endothelial cells of SC is reduced significantly when this cell layer is under conditions of flow similar to those encountered in vivo. The tight junctions between cells of the inner wall of SC become less complex with increasing pressure. Our data suggest that the paracellular pathway into SC in the normal eye is sensitive to modulation within a range of physiologically relevant pressures.

Aged↗
PubMed1997

Ribosomal binding of modified tRNA anticodons related to thermal stability.

The physicochemical contributions of modified nucleosides to tRNA functions are not well understood. In order to determine the contributions of specific modifications to tRNA stability as well as to ribosomal binding, ten variously modified yeast tRNA(Phe) anticodon stems and loops (tRNA(Phe)AC) were synthesized. Thermal denaturation studies on these synthetic 17mers show dramatic stabilization (or destabilization) by the presence of the various naturally occurring nucleoside modifications. Adapting a novel molecular biology approach (initially pioneered by Moazed and Noller), the interactions of these variously modified anticodons with the E. coli 16S rRNA "P-site" residues are being quantitated. The binding (affinity) constant (kD) of the tRNA(Phe)AC to the 8 of the ten 16S rRNA nucleosides that interact with tRNA and synthetic anticodons are being examined. We postulate that the "stabilizing" modifications (m1G37, psi 39, and m5C40) in the presence of an "open loop" will dramatically increase the binding affinity of the tRNA(Phe)AC to the 30S E. coli ribosomal subunit when compared to unmodified tRNA(Phe)AC. On the other hand, "destabilizing" modifications are expected to reduce the binding affinity of the tRNA(Phe)AC to the E. coli 30S ribosomal subunit. The results from these experiments have demonstrated the importance of nucleoside modifications to tRNA stability and ribosomal binding affinity, and will relate the structural contributions of nucleoside modifications to tRNA function.

Anticodon↗
PubMed1997

Percutaneous transluminal coronary angioplasty for acute myocardial infarction: initial experience in 43 cases.

OBJECTIVE: To evaluate the initial experience with the use of percutaneous transluminal coronary angioplasty (PTCA) in the set of acute myocardial infarction (AMI). METHODS: Between October 1993 and April 1996, PTCA was performed in 43 patients (34 male, 9 female) with initial onset of AMI. These patients ranged in age from 40 to 74 years (mean +/- SD, 60.3 3 +/- 9.2). Primary PTCA was performed in 16, rescue PTCA in 8, and semi-elective PTCA in 19 patients. RESULTS: The initial success was achieved in 95.3% (41/ 43). Failed angioplasty occurred in 2 patients, with acute reocclusion after rescue PTCA (this patient died of cerebral stroke 3 days later) in one patient, and small local intimal dissection during semi-elective PTCA in another patient. CONCLUSION: PTCA was a safe and effective approach in the treatment of AMI in the present study patients, with a high primary success and low acute complication rate.

Adult↗
PubMed1996

The involvement of interleukin (IL)-15 in regulating the differentiation of granulated metrial gland cells in mouse pregnant uterus.

Previous studies have suggested that granulated metrial gland (GMG) cells are bone marrow-derived lymphoid cells, which differentiate in situ in the mouse pregnant uterus into natural killer (NK)-like cells. Similar to NK cells, GMG cells express an abundant level of cytolytic mediators such as perforin. The factor(s) regulating the differentiation of GMG cells remain(s) to be identified, although cytokines previously implicated in the stimulation/activation of NK cells (e.g., IL-2, IL-6, IL-7, and IL-12) can be considered as potential candidates. Recently, IL-15, a novel cytokine, which displays biological activities similar to IL-2, has also been shown to be capable of activating NK cells. Using reverse transcription-polymerase chain reaction (RT-PCR) analysis, we have demonstrated in the present study that IL-15 and its cognate receptor, but not the other cytokines, are expressed in the mouse pregnant uterus, with a time course concomitant with those of cytolytic mediators in differentiated GMG cells. Moreover, IL-15, though not IL-2, is capable of inducing the expression of perforin and granzymes in pregnant uterine tissues explanted in vitro. Data obtained from in situ hybridization study have suggested that the macrophages present in the pregnant uterus may be responsible for the production of IL-15. These results suggest that IL-15 is involved in regulating the differentiation of GMG cells during mouse pregnancy.

Animals↗
PubMed1996

Interleukin-15 induces the expression of mRNAs of cytolytic mediators and augments cytotoxic activities in primary murine lymphocytes.

Interleukin-15 (IL-15) is a novel cytokine displaying biological activities that overlap those of interleukin-2 (IL-2). Like IL-2, IL-15 has been shown to be capable of stimulating the proliferation of human natural killer cells and PHA-treated T lymphocytes and of generating cytotoxic activity in stimulated lymphocyte populations. Using primary murine lymphocytes as a model in the present study, we have investigated the effects of IL-15 on the induction of the expression of mRNAs encoding different lymphocyte cytolytic mediators and the enhancement of cytolytic activities. Using reverse transcription-polymerase chain reaction analysis, both IL-15 and IL-2 have been shown to induce the expression of mRNAs for perforin, granzymes A and B, interferon-gamma, and Fas ligand in primary murine splenic lymphocytes. The induction effect of IL-15 has been shown to be at least partially independent of cell proliferation. Although IL-15 and IL-2 appear to be comparably effective in inducing the expression of cytolytic mediator mRNAs, the former is less potent in eliciting functional cytolytic activity in stimulated lymphocyte populations. The inadequate cytolytic activity of IL-15-stimulated lymphocytes may in part be due to the less efficient production of cytolytic mediator proteins, e.g., perforin and granzyme A, in these cells.

Animals↗
PubMed1996

[Effect of the T4 on the viscera and embryo of perinatal mice].

58 Female Kun Ming mice of perinatal stage (from the 15th day of pregnacy to the 21th day after birth) were fed with Tripcholorolide (T4) isolated from multiglycosides of Tripterygium wilfordii (GTW) at a doze of 0.6 mg/kg for group 1 or 0.3 mg/kg for group 2 per day for 4 weeks. Lactation was decreased in some females and some F1 off spring died. The succinic dehydrogenase (SDH) activity of the mice liver were increased due to the destruction of its mitocondian. Liver cells degenerated and glycogen decreased. Distal tubules of kidney degenerated. Heart and spleen were normal. T4 was also fed to 10 female mice from the 5th to 17th day of pregnacy. However, neither the absorbed fetus nor dead fetus increased.

Animals↗
PubMed1996

[Reversal of adriamycin or vincristine resistance by tetrandrine in human cancer cells in vitro].

In an in vitro culture system of human cancer cells MCF-7 and its adriamycin-resistant line MCF-7/Ad or KB and its vincristine-resistant line KBv200, tetrandrine was found to exhibit significantly selective anticancer activity against the drug-resistant cancer cell MCF-7/Ad. In addition, essentially complete reversal effects of tetrandrine on drug resistance were observed in MCF/Ad or KBv200.

Alkaloids↗
PubMed1995

An STS-based map of the human genome.

A physical map has been constructed of the human genome containing 15,086 sequence-tagged sites (STSs), with an average spacing of 199 kilobases. The project involved assembly of a radiation hybrid map of the human genome containing 6193 loci and incorporated a genetic linkage map of the human genome containing 5264 loci. This information was combined with the results of STS-content screening of 10,850 loci against a yeast artificial chromosome library to produce an integrated map, anchored by the radiation hybrid and genetic maps. The map provides radiation hybrid coverage of 99 percent and physical coverage of 94 percent of the human genome. The map also represents an early step in an international project to generate a transcript map of the human genome, with more than 3235 expressed sequences localized. The STSs in the map provide a scaffold for initiating large-scale sequencing of the human genome.

Animals↗
PubMed1995

Clathrin binding and assembly activities of expressed domains of the synapse-specific clathrin assembly protein AP-3.

We separately expressed the 58-kDa C-terminal, 42-kDa middle, 16-kDa C-terminal, and 33-kDa N-terminal regions of AP-3 (also called F1-20, AP180, NP185, and pp155), and determined their clathrin binding and assembly properties. The 58-kDa C-terminal region of AP-3 is able to bind to clathrin triskelia and assemble them into a homogeneous population of clathrin cages and will also bind to preassembled clathrin cages. The 42-kDa central region of AP-3 can bind to both clathrin triskelia and to clathrin cages, but cannot assemble clathrin triskelia into clathrin cages. The 16-kDa C-terminal region of AP-3 can bind to clathrin cages, but cannot bind to clathrin triskelia or assemble clathrin triskelia into clathrin cages. The clathrin binding activities of the 42-kDa central region and 16-kDa C-terminal region are weaker than the corresponding activity of either the 58-kDa C-terminal region or full-length AP-3. Previous efforts had mapped a clathrin binding site within the N-terminal 33 kDa of AP-3 (Murphy, J. E., Pleasure, I. T., Puszkin, S., Prasad, K., and Keen, J. H. (1991) J. Biol. Chem. 266, 4401-4408; Morris, S. A., Schroder, S., Plessmann, U., Weber, K., and Ungewickell, E. (1993) EMBO J. 12, 667-675). However, although the N-terminal 33 kDa of AP-3 is able to bind to clathrin triskelia (Murphy, J. E., Pleasure, I. T., Puszkin, S., Prasad, K., and Keen, J. H. (1991) J. Biol. Chem. 266, 4401-4408; Ye, W., and Lafer, E. M. (1995) J. Neurosci. Res. 41, 15-26), it does not promote their assembly into clathrin cages (Murphy, J. E., Pleasure, I. T., Puszkin, S., Prasad, K., and Keen, J. H. (1991) J. Biol. CHem. 266, 4401-4408; Ye, W., and Lafer, E. M. (1995) J. Neurosci. Res. 41, 15-26) or bind to preassembled clathrin cages (Ye, W., and Lafer, E. M. (1995) J. Neurosci. Res. 41, 15-26). It appears that the smallest functional unit that carries out all of the reported clathrin binding and assembly properties of AP-3, essentially as well as the full-length protein, is the 58-kDa C-terminal region.

Adaptor Proteins, Vesicular Transport↗
PubMed1995

Bacterially expressed F1-20/AP-3 assembles clathrin into cages with a narrow size distribution: implications for the regulation of quantal size during neurotransmission.

F1-20/AP-3 is a synapse-specific phosphoprotein. In this study we characterize the ability of bacterially expressed F1-20/AP-3 to bind and assemble clathrin cages. We find that both of two bacterially expressed alternatively spliced isoforms of F1-20/AP-3 can bind and assemble clathrin as efficiently as preparations of F1-20/AP-3 from bovine brain. This establishes that the clathrin assembly activity found in F1-20/AP-3 preparations from brain extracts is indeed encoded by the cloned gene for F1-20/AP-3. It also demonstrates that post-translation modification is not required for activation of the clathrin binding or assembly function of F1-20/AP-3. Ultrastructural analyses of the clathrin cages assembled by bacterially expressed F1-20/AP-3 reveals a strikingly narrow size distribution. This may be important for the regulation of quantal size during neurotransmission. We also express the 33 kD NH2-terminus of F1-20/AP-3 in E. coli, and measure its ability to bind to clathrin triskelia, to bind to clathrin cages, and to assemble clathrin triskelia into clathrin cages. It has been suggested that the 33 kD NH2-terminus of F1-20/AP-3 constitutes a clathrin binding domain. We find that the bacterially expressed 33 kD NH2-terminus of F1-20/AP-3 binds to clathrin triskelia, fails to bind to preassembled clathrin cages, and is not sufficient for clathrin assembly. The finding that the 33 kD NH2-terminus of F1-20/AP-3 binds to clathrin triskelia but fails to assemble clathrin triskelia into clathrin cages is consistent with the published proteolysis studies. The finding that the 33 kD NH2-terminus of F1-20/AP-3 fails to bind to clathrin cages is novel and potentially important. It is clear from these experiments that the 33 kD NH2-terminus of F1-20/AP-3 is sufficient to carry out some aspects of clathrin binding; however it appears that defining the regions of the protein involved in clathrin binding and assembly may be more complex than originally anticipated.

Adaptor Proteins, Vesicular Transport↗
PubMed1995

Inhibition of clathrin assembly by high affinity binding of specific inositol polyphosphates to the synapse-specific clathrin assembly protein AP-3.

Bacterially expressed synapse-specific clathrin assembly protein, AP-3 (F1-20/AP180/NP185/pp155), bound with high affinity both inositol hexakisphosphate (InsP6) (Kd = 239 nM) and diphosphoinositol pentakisphosphate (PP-InsP5) (Kd = 22 nM). The specificity of this ligand binding was demonstrated by competitive displacement of bound [3H]InsP6. IC50 values were as follows: PP-InsP5 = 50 nM, InsP6 = 240 nM, inositol-1,2,4,5,6-pentakisphosphate (Ins(1,2,4,5,6)P5) = 2.2 microM, inositol-1,3,4,5,6-pentakisphosphate (Ins(1,3,4,5,6)P5) = 5 microM, inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4) > 10 microM, inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) > 10 microM. Moreover, 10 microM inositol hexasulfate (InsS6) displaced only 15% of [3H]InsP6. The physiological significance of this binding is the ligand-specific inhibition of clathrin assembly (PP-InsP5 > InsP6 > Ins(1,2,4,5,6)P5); Ins(1,3,4,5,6)P5 and InsS6 did not inhibit clathrin assembly. We also observed high affinity binding of InsP6 to purified bovine brain AP-3. We separately expressed the 33-kDa amino terminus and the 58-kDa carboxyl terminus, and it was the former that contained the high affinity inositol polyphosphate binding site. These studies suggest that specific inositol polyphosphates may play a role in the regulation of synaptic function by interacting with the synapse-specific clathrin assembly protein AP-3.

Adaptor Proteins, Vesicular Transport↗
PubMed1995

[Effect of Astragalus membranaceus on T-lymphocyte subsets in patients with viral myocarditis].

The efficacy of Astragalus membranaceus (AM) oral liquor combined with routine therapy and routine therapy alone on T-lymphocyte subsets of peripheral blood in viral myocarditis patients have been studied. The results showed that the T-lymphocyte subsets profile and OKT4/OKT8 ratio of peripheral blood were significantly lower in viral myocarditis patients than that in healthy control (P < 0.05, 0.01). Routine therapy combined with AM could significantly enhance OKT3, OKT4 and OKT4/OKT8 ratio in the above-mentioned patients (P < 0.05, 0.01). The possible pharmacodynamic mechanism of improved cell immunity in viral myocarditis patients by combining routine therapy with AM was discussed.

Adolescent↗