Biomedical subjects

Yanchun Li

Publications and source records attributed to Yanchun Li.

12 recordsLinked to original sources

PubMed2026

Effects of Moderate-Frequency Resistance Training on Cardiometabolic Risk Factors in Adults With Overweight or Obesity: A Systematic Review and Meta-Analysis.

BACKGROUND: Resistance training (RT) effectively manages cardiometabolic risk factors in adults, but the specific effects of moderate-frequency RT (2-3 sessions/week) in adults with overweight or obesity are understudied. OBJECTIVE: This study aimed to evaluate moderate-frequency RT's effects on cardiometabolic risk factors in this population and quantify effect sizes. DATA SOURCES: PubMed, Web of Science, EMBASE, and Cochrane Library searched up to July 2025. ELIGIBILITY: English randomized controlled trials (RCTs) comparing RT (≥ 7 weeks) to nonexercise control; nonathletic adults ≥ 18 years with BMI ≥ 25 kg/m2. PARTICIPANTS: 454 participants across 12 RCTs (mean age 58.93 ± 12.87 years; mean BMI 31.2 ± 3.5 kg/m2; ~50% female). RESULTS: RT significantly reduced diastolic blood pressure (MD = -1.53 mmHg; 95% CI: -2.16 to -0.91; p < 0.01), LDL-C (MD = -0.25 mmol/L; 95% CI: -0.41 to -0.08; p < 0.01), and triglycerides (MD = -0.17 mmol/L; 95% CI: -0.30 to -0.04; p = 0.01). No significant effects on systolic blood pressure, mean arterial pressure, waist circumference, glycemic markers, total cholesterol, or HDL-C. Subgroup analyses showed larger LDL-C/triglyceride improvements with concurrent dietary control. CONCLUSION: Moderate-frequency RT inconsistently improves cardiometabolic risk factors, benefiting diastolic blood pressure, LDL-C, and triglycerides but not glycemic or other parameters. Combining with dietary control may enhance benefits, supporting RT as a complementary strategy in multimodal lifestyle interventions. TRIAL REGISTRATION PROSPERO: CRD42022343167.

Humans↗

PubMed2006

Modulation of the Hering-Breuer reflex by raphe pallidus in rabbits.

Activation of the pulmonary stretch receptors by lung inflation or vagal stimulation evokes Hering-Breuer (HB) reflex, which is characterized by inspiratory inhibition and expiratory prolongation. In this work, whether the HB reflex could be modulated by the serotonergic raphe pallidus (RP) was studied by comparing the strength of this reflex before and after electrical or chemical stimulation of the RP. Experiments were performed on urethane anesthetized adult rabbits. The HB reflex was simulated with electrical stimulation of the central end of cervical vagus nerve. The RP was stimulated electrically or chemically by microinjection of glutamate. We found that after either electrical stimulation or chemical stimulation of the RP, the inspiratory inhibition and expiratory prolongation of the HB reflex were significantly attenuated. This attenuation showed post-stimulation time dependency or short-term memory, as well as RP stimulation intensity dependency. Results of the present study suggested that the serotonergic RP could exert its respiratory effects by modulating the strength of HB reflex.

Animals↗

PubMed2005

Hepatitis C virus core protein inhibits mitochondrial electron transport and increases reactive oxygen species (ROS) production.

Hepatitis C infection causes a state of chronic oxidative stress, which may contribute to fibrosis and carcinogenesis in the liver. Previous studies have shown that expression of the HCV core protein in hepatoma cells depolarized mitochondria and increased reactive oxygen species (ROS) production, but the mechanisms of these effects are unknown. In this study we examined the properties of liver mitochondria from transgenic mice expressing HCV core protein, and from normal liver mitochondria incubated with recombinant core protein. Liver mitochondria from transgenic mice expressing the HCV proteins core, E1 and E2 demonstrated oxidation of the glutathione pool and a decrease in NADPH content. In addition, there was reduced activity of electron transport complex I, and increased ROS production from complex I substrates. There were no abnormalities observed in complex II or complex III function. Incubation of control mitochondria in vitro with recombinant core protein also caused glutathione oxidation, selective complex I inhibition, and increased ROS production. Proteinase K digestion of either transgenic mitochondria or control mitochondria incubated with core protein showed that core protein associates strongly with mitochondria, remains associated with the outer membrane, and is not taken up across the outer membrane. Core protein also increased Ca(2+) uptake into isolated mitochondria. These results suggest that interaction of core protein with mitochondria and subsequent oxidation of the glutathione pool and complex I inhibition may be an important cause of the oxidative stress seen in chronic hepatitis C.

Animals↗

PubMed2005

Toll-like receptor 8-mediated reversal of CD4+ regulatory T cell function.

CD4+ regulatory T (Treg) cells have a profound ability to suppress host immune responses, yet little is understood about how these cells are regulated. We describe a mechanism linking Toll-like receptor (TLR) 8 signaling to the control of Treg cell function, in which synthetic and natural ligands for human TLR8 can reverse Treg cell function. This effect was independent of dendritic cells but required functional TLR8-MyD88-IRAK4 signaling in Treg cells. Adoptive transfer of TLR8 ligand-stimulated Treg cells into tumor-bearing mice enhanced anti-tumor immunity. These results suggest that TLR8 signaling could play a critical role in controlling immune responses to cancer and other diseases.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Functional characterization of EBV-encoded nuclear antigen 1-specific CD4+ helper and regulatory T cells elicited by in vitro peptide stimulation.

CD4(+) helper and regulatory T (Treg) cells play important but opposing roles in regulating host immune responses against cancer and other diseases. However, very little is known about the antigen specificity of CD4(+) Treg cells. Here we describe the generation of a panel of EBV-encoded nuclear antigen 1 (EBNA1)-specific CD4(+) T-cell lines and clones that recognize naturally processed EBNA1-P(607-619) and -P(561-573) peptides in the context of HLA-DQ2 and HLA-DR11, -DR12, and -DR13 molecules, respectively. Phenotypic and functional analyses of these CD4(+) T cells revealed that they represent EBNA1-specific CD4(+) T helper as well as Treg cells. CD4(+) Treg cells do not secrete interleukin (IL)-10 and transforming growth factor beta cytokines but express CD25, the glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR), and Forkhead Box P3 (Foxp3), and are capable of suppressing the proliferative responses of naive CD4(+) and CD8(+) T cells to stimulation with mitogenic anti-CD3 antibody. The suppressive activity of these CD4(+) Treg cells is mediated via cell-cell contact or in part by a cytokine-dependent manner. Importantly, these Treg cells suppress IL-2 secretion by CD4(+) effector T cells specific for either EBNA1 or a melanoma antigen, suggesting that these CD4(+) Treg cells induce immune suppression. These observations suggest that the success of peptide-based vaccines against EBV-associated cancer and other diseases may likely depend upon our ability to identify antigens/peptides that preferentially activate helper T cells and/or to design strategies to regulate the balance between CD4(+) helper and Treg cells.

Amino Acid Sequence↗

PubMed2005

Mitochondrial dysfunction in hepatitis C.

Chronic hepatitis C induces a state of hepatic oxidative stress that is more pronounced than that present in many other inflammatory liver diseases. This review summarizes recent information that the hepatitis C virus (HCV) core protein plays an important role in this phenomenon. Core protein localizes to mitochondria, particularly at the points of contact between mitochondrial outer membrane and endoplasmic reticulum. Its expression causes inhibition of electron transport at complex I, increased complex I reactive oxygen species (ROS) production, decreased mitochondrial glutathione, and increased mitochondrial permeability transition in response to exogenous oxidants and tumor necrosis factor-alpha. Possible mechanisms of the core protein effects include direct interaction with electron carriers and indirect effects mediated by changes in mitochondrial calcium. These results suggest that antioxidant approaches may prove beneficial for patients with chronic hepatitis C.

Hepacivirus↗

PubMed2005

[The effect of bamboo leaves extract on hemorheology of normal rats].

Sixty rats were randomly divides into six groups. Blood stasis model was set up by sc isoprenaline, and different dose of BLE (15 mg/kg, 30 mg/kg and 60 mg/kg) were iv. The effects of BLE on rat's blood viscosity, plasma viscosity, FIB, ESR, TK, electrophoresis times and HCT were measured by automatic analysis system. Sixty mice were randomly divided into six groups, and the serum cholesterol of the high cholesterol's mice was obtained by eyepit vein and measured. The results showed that BLE (15 mg/kg, 30 mg/kg and 60 mg/kg) could reduce blood viscosity, plasma viscosity, FIB, ESR, TK, HCT and increase the speed of electrophoresis time in blood adhesion model, and BLE (22.5 mg/kg, 45 mg/kg, 90 mg/kg) could significantly reduce serum cholesterol of the high cholesterol's mice.

Animals↗

PubMed2004

Modulation of inspiratory inhibition of the Bötzinger complex by raphe pallidus and locus coeruleus in rabbits.

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Animals↗

PubMed2004

Tumor-specific human CD4+ regulatory T cells and their ligands: implications for immunotherapy.

Regulatory T cells play an important role in the maintenance of immunological self-tolerance by suppressing immune responses against autoimmune diseases and cancer. Little is known, however, about the nature of the physiological target antigens for CD4(+) regulatory T (Treg) cells. Here we report the identification of the LAGE1 protein as a ligand for tumor-specific CD4(+) Treg cell clones generated from the tumor-infiltrating lymphocytes (TILs) of cancer patients. Phenotypic and functional analyses demonstrated that they were antigen-specific CD4(+) Treg cells expressing CD25 and GITR molecules and possessing suppressive activity on the proliferative response of naive CD4(+) T cells to anti-CD3 antibody stimulation. Ligand-specific activation and cell-cell contact were required for TIL102 Treg cells to exert suppressive activity on CD4(+) effector cells. These findings suggest that the presence of tumor-specific CD4(+) Treg cells at tumor sites may have a profound effect on the inhibition of T cell responses against cancer.

Antigens, Neoplasm↗

PubMed2003

Interaction mechanism of in-situ nano-TiN-AlN particles and solid/liquid interface during solidification.

This paper deals with the interaction mechanism between in situ nanometer-grade TiN-AlN particles and the solid/liquid (S/L) interface during the solidification of an in situ TiN-AlN/Al composite. According to the setting of a force balance for the particles in front of the S/L interface during solidification, F = F(buoyant) + F(repulsive) + F(viscous). We obtained the relationship between the critical cooling velocity of the liquid composite, Vr, and the size of the ceramic particle, rp. By this relationship formula, we can know that the S/L interface engulfs particles or pushes them to the crystal grain boundary during the solidification of a TiN-AlN/Al composite. It is found that Vr is proportional to the radius of ceramic particles by transmission electron microscope (TEM) observation. The TEM test indicates that the smaller the particle is, the more easily the S/L interface engulfs particles.

Aluminum Compounds↗

PubMed2003

Expression of adenovirus type 5 E1A in the methylotrophic yeast Pachia pastoris and the inhibitory effect on S-180 tumor growth.

The human adenovirus type 5 (Ad5) early-region 1A (E1A) proteins have been shown to have strong tumor-suppressive activities in human tumor cells and to enhance the sensitivity of a variety of malignant tumors to apoptosis induced by ionizing radiation and chemotherapeutic agents. However, the inherent limitations of E1A gene therapy prevent its application, such as the efficiency of expression, precision of targeting, and toxicity of vector. This prompted us to construct an E1A expression vector (pPIC9/E1A) and express the E1A protein in the methylotrophic yeast Pichia pastoris. The E1A protein was purified using two steps of ion-exchange column chromatography on HiTrap Q and HiTrap SP. The analysis indicated that the E1A protein/liposome inhibited S-180 tumor growth and also rendered the S-180 tumor strongly susceptible to the anticancer drug bleomycin in vivo. Furthermore, tunnel assay clearly revealed that the mechanism was induction of cellular apoptosis. Importantly, the E1A protein overcame the limitations of gene therapy. Thus the E1A protein may be a useful therapeutic agent for some malignant tumors.

Adenovirus E1A Proteins↗

PubMed2002

[Effect of hormone replacement therapy on homocysteine and echocardiography in postmenopausal women].

OBJECTIVE: To observe the effects of hormone replacement therapy (HRT) on fasting total plasma homocysteine levels and echocardiography in postmenopausal women. METHODS: Subjects were assigned to four groups. Group I: 30 postmenopausal women were assigned to sequentially combined daily 0.625 mg conjugated equine estrogen (CEE) plus 2 mg medroxyprogesterone acetate (MPA) or plus 4 mg MPA daily for 14 days in a 28 day cycle for 3 months. Group II: 30 postmenopausal women did not received HRT. Group III: 20 postmenopausal women who took HRT for 1.5 years. Group IV: 20 postmenopausal women who never took HRT. Measurement of fasting total plasma homocysteine was performed before and after 3 months treatment in group I and group II. Fasting total plasma homocysteine was determined and echocardiography was taken in group III and group IV. RESULTS: Fasting total plasma homocysteine concentrations were not altered significantly after 3 months in group I and group II [before HRT: (9.3 +/- 2.5) micro mol/L, (9.4 +/- 2.9) micro mol/L; after HRT: (9.1 +/- 2.8) micro mol/L, (9.8 +/- 3.6) micro mol/L, respectively (P > 0.05)]. Compared with women of group III, women of group IV had statistically significant lower plasma homocysteine [(8.0 +/- 1.3) micro mol/L, (10.3 +/- 3.2) micro mol/L, respectively (P < 0.05)]. Echocardiography was not found any difference between those two groups. CONCLUSIONS: Three months HRT has no effect on plasma homocysteine levels in postmenopausal women but the postmenopausal women using HRT 1.5 years have lower plasma homocysteine levels than those who never received HRT. Echocardiography showed no detectable changes between women received 1.5 years HRT and those who received no HRT.

Adult↗