Humans ; Maxillary Sinus Neoplasms ; pathology ; Myoepithelioma ; pathology ; Paranasal Sinuses ; pathology

Humans ; Imaging, Three-Dimensional ; Neoplasms ; radiotherapy ; surgery ; Radiosurgery ; instrumentation ; methods ; Tomography, X-Ray Computed

Adult ; Blood Glucose ; metabolism ; Female ; Herbicides ; poisoning ; Humans ; Liver ; physiopathology ; Male ; Middle Aged ; Paraquat ; poisoning

The Tongmai Yangxin pill (TMYX) has potential clinical effects on no-reflow (NR); however, the effective substances and mechanisms by which this occurs remain unclear. This study evaluates the cardioprotective effects and molecular mechanisms of TMYX against NR. We used a myocardial NR rat model (2 h after myocardial ischemia and 2 h after reperfusion) to confirm the effect and mechanism of action of TMYX in alleviating NR. In vitro studies in isolated coronary microvasculature of NR rats and in silico network pharmacology analyses were performed to reveal the underlying mechanisms of TMYX and determine the main components, targets, and pathways of TMYX, respectively. The experiment was approved by the Ethics Committee of Hunan University of Chinese Medicine (LLBH-202212160001). TMYX showed therapeutic effects on NR by improving cardiac structure and function, reducing NR, ischemic areas, and cardiomyocyte injury, and decreasing the content of cardiac troponin I (cTnI). Moreover, the mechanism of TMYX predicted by network pharmacology is related to the hypoxia inducible factor-1 (HIF-1), nuclear factor kappa-B (NF-κB), and tumor necrosis factor (TNF) signaling pathways. TMYX increased the expression of G protein-coupled estrogen receptor (GPER), phospho-extracellular signal-regulated kinase (p-ERK), and HIF-1α. In vitro, TMYX enhanced the diastolic function of coronary microvascular cells; however, this effect was inhibited by GPER inhibitor (G-15), eNOS inhibitor (L-NAME), and sGC inhibitor (ODQ). This study integrates pharmacology and experimental evaluation to reveal that TMYX activates HIF-1α/eNOS signaling pathway by upregulating GPER to relax coronary microvessels, thereby significantly alleviating NR.

OBJECTIVETo investigate development of a cell extraction process for preparing human meniscus acellular matrix, and morphology and biomechanical properties.

METHODSHuman meniscus were subjected to modified eight-step detergent, then, the specimens were assessed by staining with haematoxylin-eosin, toluidine blue, sirius red, saffron O, alcain blue and hoechst-33258, et al. The ultrastructure of the specimens was observed with scanning electron microscope. Transient recovery rate of deformation, maximal recovery rate of deformation and maximal compressive strength were tested to determine the biomechanical properties of the scaffold.

RESULTSEvery stain confirmed that the celluar constituents of the specimens were removed. The specimens stained positively by staining with sirius red. Lacuna were found irregularly not only on the surface of the meniscus,but also in the meniscus with scanning electron microscope. Pores in the specinmens were large, the diameter of pores was 80 to 760 microm, porosity was over 67%. The transient recovery rate of deformation was (89.62 +/- 1.04)%, the maximal recovery rate of deformation was 100% and the maximal compressive strength was (3.04 +/- 0.13)N, when the specimens were compressed 30%.

CONCLUSIONThe modified eight-step detergent can remove the immunogenic cell components from human meniscus, in addition, 3D extracellular matrix can be retained. The scaffold has good biomechanical properties. This scaffold stands a good chance to be an implant for future tissue engineering of the human meniscus.

Adult ; Cell Separation ; methods ; Cells ; chemistry ; cytology ; Cells, Cultured ; Humans ; Male ; Menisci, Tibial ; cytology ; Staining and Labeling

Objective:To evaluate the fit of titanium alloy removable partial denture framework fabricated by selective laser melting(SLM) technique.Methods:7 Kennedy Ⅲ Ti-6Al-4V removable titanium alloy partial denture frameworks were fabricated by SLM technology.An optical scanner was used to scan the gypsum model adhered with the silicone rubber film obtained by the impression method before and after removal of the film.Geomagic Qualify 2013 software was used to analyze the gap between the model and the tissue surface of the major connector of the framework,the fit of the frame work was evaluated.Results:The overall 3D deviation between the titanium alloy frameworks and the gypsum model was (0.221 9±0.07) mm.Conclusion:The fit of the titanium alloy removable partial denture framework made by SLM technology can basically met the clinical requirements.

AIM:To detect the activation of macrophage autophagy caused by lipopolysaccharide ( LPS) and the possible related signaling pathways .METHODS:The macrophage cell line RAW264.7 cultured in vitro was divided into 5 groups according to the culture environment , including normal culture group , starvation-activated sautophagy group , LPS group, LPS+PI3K inhibitor (hVps34) group and LPS+mTOR inhibitor (rapamycin) group.Fluorescent expression vector pcDNA3.1-GFP-LC3 constructed in previous work was transfected into the macrophages .The fluorescence microscopy was used to detect the formation of autophagosome .The mRNA expression of autophagy-associated genes Atg5, Atg7, LC3-II and Bnip3 in the macrophages was detected by qRT-PCR.The protein levels of LC3-II, p-Akt and p-mTOR were deter-mined by Western blotting , so as to evaluate the molecular pathways of autophagy in LPS-activated macrophages .RE-SULTS:The macrophages stably expressing GFP-LC3 were successfully established , which were used to observe the auto-phagy under fluorescence microscope .Compared with normal culture group , the autophagy in starvation group , LPS +hVps34 group and LPS+rapamycin group was significantly increased .The mRNA expression levels of Atg5, LC3-II and Bnip3 were significantly increased in starvation group , LPS+hVps34 group and LPS +rapamycin group , while in LPS group, those decreased slightly .The protein level of p-Akt in starvation group , LPS group and LPS+rapamycin group was significantly increased , while p-mTOR in starvation group , LPS+hVps34 group and LPS+rapamycin group significantly declined .LC3-II expression level in starvation group , LPS+hVps34 group and LPS+rapamycin group was higher than that in control group and LPS group .CONCLUSION: LPS regulates macrophage autophagy , and its possible pathway is the PI3K/Akt/mTOR pathway, but there are some other effective regulatory pathways .

Objective To compare the effects of short- term high- intensity interval training (HIT) and moderate continuous training (MCT) on inflammatory mediators for healthy young males. Methods 19 healthy young male volunteers were randomized into HIT group (n=6), MCT group (n=7) and no training control (CON, n=6) group. The groups of HIT and MCT accepted treadmill exercise once per 2 days to 6 times (2 weeks), and the CON group did not accepted treadmill exercise. The levels of high-sensitive C-reactive protein (hs-CRP), interleukin (IL) -1α, IL-6 and tumor necrosis factor α (TNF-α) were detected 3 days before exercise, immediately after the first exercise, 3 days after the course. Results There was no difference among groups in the level of hs-CRP, IL-1α, IL-6 and TNF-α in all the time (P>0.05). The concentration of IL-1α increased in the MCT group after the first exercise (P<0.01), and also the concentration of IL-6 in the CON group after the course (P<0.05). Conclusion It needs further srudy for the significance of HIT and MCT in the levels of inflammatory media.

Our previous results have demonstrated that insulin reduces myocardial ischemia/reperfusion (MI/R) injury and increases the postischemic myocardial functions via activating the cellular survival signaling, i.e., phosphatidylinositol 3-kinase (PI3-K)-Akt-endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) cascade. However, it remains largely controversial whether c-Jun NH2-terminal kinase (JNK) is involved in the effects of insulin on MI/R injury. Therefore, the aims of the present study were to investigate the role of JNK, especially the cross-talk between JNK and previously expatiated Akt signaling, in the protective effect of insulin on I/R myocardium. Isolated hearts from adult Sprague-Dawley rats were subjected to 30 min of regional ischemia and followed by 2 or 4 h of reperfusion (n=6). The hearts were pretreated with PI3-K inhibitor LY294002, or phosphorylated-JNK inhibitor SP600125, respectively, then perfused retrogradely with insulin, and the mechanical functions of hearts, including the heart rate (HR), left ventricular developed pressure (LVDP) and instantaneous first derivation of left ventricular pressure (+/-LVdp/dt(max)) were measured. At the end of reperfusion, the infarct size (IS) and apoptotic index (AI) were examined. MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with the control group, insulin treatment in MI/R rats exerted protective effects as evidenced by reduced myocardial IS [(28.9 +/- 2.0)% vs (45.0 +/- 4.0) %, n=6, P<0.01], inhibited cardiomyocyte apoptosis [decreased AI: (16.0 +/- 0.7) % vs (27.6 +/- 1.3) %, n=6, P<0.01] and improved recovery of cardiac systolic/diastolic function (including LVDP and +/-LVdp/dt(max)) at the end of reperfusion. Moreover, insulin resulted in 1.7-fold and 1.5-fold increases in Akt and JNK phosphorylation in I/R myocardium, respectively (n=6, P<0.05). Inhibition of Akt activation with LY294002 abolished, and inhibition of JNK activation with SP600125 enhanced the cardioprotection by insulin, respectively. And the abolishment by LY294002 could be partly converted by SP600125 pretreatment. In addition, SP600125 also decreased the Akt phosphorylation (n=6, P<0.05). These results demonstrate that insulin simultaneously activates both Akt and JNK, and the latter further increases the phosphorylation of Akt which attenuates MI/R injury and improves heart function; this cross-talk between Akt and JNK in the insulin signaling is involved in insulin-induced cardioprotective effect.
Animals ; Apoptosis ; Heart ; Insulin ; metabolism ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Myocardial Infarction ; Myocardial Ischemia ; Myocardial Reperfusion Injury ; Myocardium ; Myocytes, Cardiac ; Nitric Oxide Synthase Type III ; Phosphatidylinositol 3-Kinase ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; Signal Transduction

Anemia, Hemolytic, Autoimmune ; etiology ; Child, Preschool ; Humans ; Macrophage Activation Syndrome ; etiology ; Male ; Mucocutaneous Lymph Node Syndrome ; complications