Long-term endurance training or physical activity has been confirmed not only to improve physical performance, but to bring about an obvious beneficial effect on human health; however, the mechanism of this effect is not clear. The most studied health adaptations in skeletal muscle response to endurance exercise are increased muscle glycogen level and insulin sensitivity, fiber type transformation toward oxidative myofibers, and increased mitochondrial content/function. Mitochondria are dynamic organelles in eukaryotic cells critical in physical performance and disease occurrence. The mitochondrial life cycle spans biogenesis, maintenance, and clearance. Exercise training may promote each of these processes and confer positive impacts on skeletal muscle contractile and metabolic functions. This review focused on the regulation of these processes by endurance exercise and discussed its potential benefits in health and disease. We presented evidence suggesting that exercise training potentiates not only the biogenesis of mitochondria but also the removal of old and unhealthy mitochondria through mitochondrial quality control.
Adaptation, Physiological ; Exercise ; Humans ; Mitochondria ; physiology ; Muscle Contraction ; Muscle, Skeletal ; physiology

Objective NKT cells are very important as a kind of non-specific immune cells. Much attention in antitumor significance has been received in the study of its effect on malignant diseases. The aim of this study was to detect the expression of NKT cells and its CD+8 NKT subsets in peripheral blood of esophageal patients and normal person, and to analyze the changes in the expression of NKG2D and NKG2A receptorsand its clinical pathological factors. Methods By flow cytometric analysis, 53 patients with esophageal carcinoma and 39 normal controls were analysed for peripheral blood of NKT cells and CD+8 NKT subsets, and the expression of NKT cells NKG2A and expression of NKG2D receptor. The clinical pathological factors were collected for the comparative analysis. Results Compared with the normal control group, the expression of NKT cells in peripheral blood of esophageal patients increased [(4.32±0.73) %, (5.97±1.29) %] (t =3.562, P <0.01), and the expression level of its surface receptor NKG2D reduced [(17.56±5.92) %, (15.12±1.56) %] (t =3.892, P <0.05), but the express levels of NKG2A [(4.02±1.41) %, (5.99±4.59) %] in creased (r = 4.015, P <0.05), those expression change with the development of the esophageal cancer. Conclusion The increased expression of NKT cells and CD+8 NKT subsets in the peripheral blood of patients with esophageal carcinoma refletcs that the immune feedback of patients' antineoplastic effect is strengthened. The decresed expression of the active receptor NKG2D and the increased expression of the inhibitory receptor NKG2A on NKT cells might be one of mechanisms leading to the reduction of NKT cell activity and immune escape of patients with esophageal carcinoma. The changes of surface receptors of NKT cells may be associated with the development of the esophageal cancer.

Objective To analyze CD+4 CDHi25 CDLo127 regulatory T cells (Treg) in peripheral blood of patients with thyroid nodules and differentiated thyroid cancer and their change regularity, and to investigate the immunosuppression mechanism. Methods The peripheral blood was collected from 175 patients with thyroid nodules, including 43 patients with differentiated thyroid cancer and 132 patients with nodular goiter.By using monoclonal antibodies, the blood samples were evaluated with the flow cytomertry for lymphocyte subsets and Treg cells. Results The results showed the prevalence of the CD+4 CDHi25 CDLo127 Treg in differentiated thyroid cancer group [(6.48±1.49) %] and nodular goiter group [(6.23+1.67) %] was higher than those in the healthy group [(5.62±1.48) %], and the difference was significant(P < 0.005), but there was no significant difference between the nodular goiter group and differentiated thyroid cancer group (P >0.005).Conclusion It is concluded that the relative increase of CD+4 CDHi25 CDLo127 Treg in peripheral blood of patients with nodular goiter and differentiated thyroid cancer may be related to immunosuppression and tumor progression.

Objective To investigate the neuropathic pain (NP) accompanying spinal cord injury (SCI),and to analyze the related factors to provide references for its prevention and treatment.Methods Seventy SCI patients with NP were selected using the DN4 scale.Their age,gender,occupation,education level,monthly income,injury position,marital status and other data were surveyed using a general questionnaire.Their NP situation was surveyed using a simplified McGill pain questionnaire (SF-MPQ).Results The patients' average visual analogous scale (VAS) score was 4.37.Their average pain rating index (PRI) according to the SF-MPQ was 8.23,with the PRI-sensory and PRI-emotional components 5.23 and 3.00 respectively.The average degree of present pain intensity was 1.86,between mild pain and discomfort,and discomfort was the description most commonly used.The most common pain descriptor was prickling pain,followed by burning pain and bulge pain.85.7％ of the patients felt that their pain had an adverse effect on their affective state,and exhaustion occurred more often than any other descriptive words.Univariant analysis showed that the degree of injury,education level,marital status,monthly income,family support and medication history were all factors correlated with NP perceptions.Multi-variate logistic regression analysis showed that being unmarried and severity of injury were independent protective factors against NP.No family support,no medication and low income were independent risk factors for NP.Conclusion The type of neuropathic pain varies in patients with spinal cord injury.The intensity of the pain is mostly at a medium level.The emotional state of most patients was affected.Neuropathic pain involves many factors.Being unmarried and severely injured are independent protective factors,while lack of family support,no medication,and having low income were independent risk factors.

Isoliquiritigenin (ISL) is an active chalcone compound isolated from licorice. It possesses anti-inflammatory and anti-oxidative activities. In our previous study, we uncovered a great potential of ISL in treatment of type 2 diabetes mellitus (T2DM). Therefore, this study aims to reveal the mechanism underlying the alleviatory effects of ISL on T2DM-induced glycolipid metabolism disorder. High-fat-high-sugar diet (HFD) combined with intraperitoneal injection of streptozotocin (STZ) were used to establish T2DM mice model. All animal experiments were carried out with approval of the Committee of Ethics at Beijing University of Chinese Medicine. HepG2 cells were used in in vitro experiments, and sodium palmitate (SP) was applied to establish insulin resistance (IR) model cells. The effects of ISL on body weight, fasting blood glucose levels, and pathological changes in the livers of mice were examined. Enzyme-linked immune sorbent assay (ELISA) and real-time quantitative PCR (RT-qPCR) were applied to detect the regulatory effects of ISL on key targets involved in glucolipid metabolism. Additionally, molecular docking and analytical dynamics simulation methods were used to analyze the interaction between ISL and key target protein. The results indicate that ISL significantly downregulates the transcriptional levels and inhibits the activities of key enzymes involved in gluconeogenesis, including pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK), and fructose-1, 6-bisphosphatase (FBP). It also downregulates the transcriptional and protein levels of hepatocyte nuclear factor 4α (HNF4α) and cAMP response element binding protein (CREB), the two transcriptional factors involved in gluconeogenesis. Thus, ISL inhibits hepatic gluconeogenesis in T2DM mice. In addition, ISL reduces total cholesterol (TC) and triglyceride (TG) levels in the livers of T2DM mice. Moreover, ISL downregulates the mRNA levels of lipogenesis genes and upregulates those of genes involved in fatty acid oxidation, lipid uptake, and lipid export. In conclusion, ISL suppresses hepatic gluconeogenesis, promotes lipolysis, and restrains lipogenesis in T2DM mice, thereby improving the abnormal glycolipid metabolism caused by T2DM.

Isoliquiritigenin (ISL) is a flavonoid compound isolated from licorice. It possesses excellent antioxidant and anti-diabetic activities. This study aims to investigate the molecular mechanism underlying the alleviatory effect of ISL on energy metabolism imbalance caused by type 2 diabetes mellitus (T2DM). 8-week-old male C57BL/6J mice were used in in vivo experiments. The high-fat-high-glucose diet combined with intraperitoneal injection of streptozotocin was applied to establish T2DM animal model. All animal experiments were performed in accordance with the Institutional Guidelines of Laboratory Animal Administration issued by the Committee of Ethics at Beijing University of Chinese Medicine. HepG2 cells were used in in vitro experiments. Enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (RT-qPCR) were used to examine the protein and mRNA levels of mitochondrial function-related targets. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) in HepG2 cells were measured by the flow cytometry. Additionally, the molecular docking of ISL and key target proteins was analyzed. It was found that ISL significantly inhibited the activity of mitochondrial respiratory chain complex I and increased the protein levels of uncoupling protein 2 (UCP2) in the livers of mice and HepG2 cells. It also obviously decreased the ROS levels and increased the MMP levels in cultured HepG2 cells. In addition, ISL promoted mitochondrial biogenesis by activating proliferator-activated receptor gamma co-activator 1α (PGC-1α) and enhanced mitophagy by upregulating Parkin. It also improved mitochondrial fusion by increasing the mRNA and protein levels of mitofusin 2 (MFN2). In conclusion, ISL alleviates energy metabolism imbalance caused by T2DM through suppression of excessive mitochondrial oxidative phosphorylation and promotion of mitochondrial biogenesis, mitophagy, and fusion.

(3S)-Linalool synthase (LIS) is a key enzyme involved in the monoterpene biosynthetic pathway. Based on our previous transcriptome study, the expression level of LIS gene was exceedingly related to glycyrrhizic acid (GA) biosynthesis. Therefore, we used hairy root culturing to further investigate the effect of LIS on the GA biosynthesis. A LIS gene (GenBank accession number: MZ169552) was cloned from Glycyrrhiza uralensis. The plant binary overexpression vector pCA-LIS was constructed by gene fusion. G. uralensis hairy roots overexpressing LIS were induced by the Agrobacterium rhizogenes ATCC15834. The expression levels of LIS were analyzed by real-time quantitative PCR (RT-qPCR) and the contents of GA in hairy root lines were determined by UPLC. It was found that in the hairy root lines overexpressing LIS, the expression levels of LIS were significantly higher than that in the wild type, while the contents of GA were remarkably lower than those in the wild type and negative control. These findings indicate that the expression level of LIS is negatively correlated with the accumulation of GA. In this study, LIS was cloned from G. uralensis for the first time and the negative regulatory effect of LIS on GA biosynthesis was confirmed by reverse genetics. This work provides support for further improvement of the molecular regulatory network of GA biosynthesis in G. uralensis.

BackgroundRetinal pigment epithelial(RPE) cells can secrete platelet-derived growth factor (PDGF) and PDGF receptor(PDGFR).Studies have shown that PDGF plays a key role in the formation of proliferative vitreous retinopathy(PVR). ObjectiveThis study was to investigate the proliferation and apoptosis changes of RPE after blockage of the PDGFR-α expression by antisense oligonucleotide ( ASODN ) in vitro. Methods Human RPE cells strain was cultured in low glucose DMEM with 10％ fetal bovine serum.Logarithmic phase cells were collected and incubated in 96-well plate at the density of 5 × 105 cells/hole.PDGFR-α ASODN was transfected into RPE cells at different concentrations for 48 hours.The cells of the blank control group were regularly cultured without any transfection.The changes of PDGFR-α expression were detected by reverse transcription-polymerase chain reaction(RT-PCR),and the proliferation of RPE was detected by MTT as the A490 value.Hoechst 33258 fluorescence staining was used to determine the apoptosis of RPE.Flow cytometry method (FCM) was applied to detect the change of cell cycle and apoptosis rate of RPE cells. ResultsThe A490 values of RPE cells were 1.45±0.12,1.07±0.06,0.65±0.05 in blank control group,1.0 μmol/L Lipo-ASODN group and 2.0 μmol/L Lipo-ASODN group with the significant difference(P=0.00 ),and that of 1.0 μmol/L Lipo-ASODN group and 2.0 μ mol/L Lipo-ASODN group were significantly lower than the blank control group ( P =0.00,0.00).Hoechst 33258 staining showed that the apoptosis cells were obviously more in Lipo-ASODN group compared with blank control group.PDGFR-α ASODN transfection induced an increase of percentage of RPE cells in G0/G1 phase( F =206.70,P =0.00),and the apoptosis rates in 1.0 μmol/L Lipo-ASODN group and 2.0 μmol/L Lipo-ASODN group were significantly enhanced in comparison with blank control group ( 37.8 ± 1.3 vs 10.5 ± 0.1,61.2 ± 1.9 vs 10.5 ± 0.1 ) ( F =1808.90,P =0.00 ).Expression intensity of PDGFR-α mRNA in RPE cells in Lipo-ASODN groups was lower. ConclusionsBlocking the PDGFR-α expression with ASODN technology can suppress proliferation and induce apoptosis of RPE cells.Intensity of PDGFR-α mRNA expression in RPE cells is ASODN dose-dependent.ASODN targeted to PDGFR-α offers an experimental basis of the gene therapy for PVR.

Objective To study the possible relationship between the psychological health of children with hematuria and their mothers.Methods Sixty children with hematuria were tested with podiatric symptom checklist(PSC),and the findings were compared with 60 healthy children.The mothers of the patients were assessed by self-rating anxiety scale(SAS),compared with the mothers of healthy children.Results The scores of PSC in patients were higher than those in healthy children(P

Objective To construct a recombinant expression vector for expression of the function-al domains of dengue virus serotype 1 ( DENV1 ) envelope ( E ) protein in native soluble form. Methods The genes encoding the functional domains of DENV1-E protein (1-394 aa) were amplified with PCR and then cloned into the Psectag2B-Fc eukaryotic expression vector.The 293T cells were transfected with the recombinant vector by cationic lipid-based delivery.The cell clones expressing the fusion DENV1-E-Fc protein were screened out with 2 mg/ml of Zeocin.Immunofluorescence assay ( IFA) was performed to analyze the antigenicity and integrity of the fusion protein.The fusion proteins were purified from cell lysate with Protein-G and further identified by Western blot assay.Results The soluble form of fusion protein with a molecular weight of about 90×103 was obtained at a yield of about 25 μg per 1×107 cells.The results of IFA indicated that the fusion protein kept its integrity with right conformational epitopes.The fusion protein was successfully expressed with the advantage of good specificity as indicated by IFA and Western blot assay. Conclusion The recombinant fusion protein in soluble form was successfully expressed in eukaryotic ex-pression system, which paved the way for further investigation on the function of DENV1 E protein and its protective epitopes.