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Objective:To investigate the effects of bandaging methods on breast cancer associated lymphoedema.Methods:By simple random sampling method, a total of 90 cases of breast cancer associated lymphoedema patients who received complex decongestion therapy in Hubei Cancer Hospital from May 2020 to My 2021 were randomly assigned to experimental group and control group, with 45 cases in each group. All patients received complex decongestion therapy. At the pressure bandage stage, the control group received figure-of-eight shape bandaging methods, the experimental group implemented modified bandaging methods: the figure-of-eight shape bandaging methods was used below the elbow joint, the spiral bandaging methods was used above the elbow joint. The arm circumference of affected limb, extracellular water/total body water ratio, general comfort questionnaire, bandage loosening rate as well as bandage loss was compared between two groups.Results:At 20 days after treatment, the arm circumference of affected limb in L 3, L 4 were (20.69 ± 2.06) cm, (25.76 ± 3.79) cm and extracellular water/total body water ratio was (10.15 ± 2.49)% in the experimental group, which were lower than those in the control group (21.97 ± 3.45) cm, (27.33 ± 3.25) cm and (11.67 ± 3.12)%, the differences were significant ( t=2.13, 2.11 and 2.56, all P<0.05); the physiological demension scores and total general comfort questionnaire scores were (11.07 ± 2.09) points and (81.71 ± 5.65) points in the experimental group, which were higher than those in the control group (8.36 ± 2.28) points and (77.29 ± 7.52) points, the difference were statically significant ( t=5.88 and 3.16, P<0.05). The bandage loosening rate was 2.2% in the experimental group, 6.7% in the control group, there was no significant difference between two groups ( χ2=1.05, P>0.05). The average bandage loss was (3.47 ± 0.53) rolls in the experimental group, which was lower than that in the control group (3.79 ± 0.40) rolls, the difference was statically significant ( t=3.28, P<0.01). Conclusions:Modified bandaging methods can decrease breast cancer associated lymphoedema, improve the degree of patient comfort and reduce bandage usage.
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Objective To investigate ASPS induced G_2/M arrest in lung cancer cell line H446 and its effect on ERK MAP kinase signal transduction pathways. Methods Cell cycle phases were inspected by flow cytometery (FCM) ; Western blot analysis was used to inspect the proteins of ERK, p-ERK. Results Compared with control group, G_2/M phase cells increased with concentration significantly, G_0/G_1 phase cells were not different, G_2/M phase cells and G_0/G_1 phase cells were not different when pre-incubated with PD98059 prior to exposure to ASPS of different concentrations, protein of p-ERK was significantly increased, expression of ERK was no different. Conclusion ASPS may induce G_2/M arrest of H446 cells possibly by activation ERK MAP kinase pathways.
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Objective The present study is to investigate IL-24 gene(Ad5F35-hIL-24) effect on the topoisommeraseⅡα(topoⅡα) and Caspase-3 expression in glioma cell line U251. Methods After transfected the U251 glioma cells with the Ad5F35-hIL-24, the methyl thiazolyl tetrazolium (MTT) was used to analyse the inhibition rate of Ad5F35-hIL-24 on the cells. Hoechst 33258 fluorescent staining and flow cytometric assay were used to detect apoptosis. The immunohistochemistry assay was used to detect topoⅡα expression, and Western blotting was applied to detect the protein expression of topoⅡα and caspase-3. Transwell experiment was used to test the invasiveness of the cells. Results It was found that the Ad5F35-hIL-24 could inhibit U251 cell proliferation and induce apoptosis in a dose dependent manner compared with the control groups. It showed that Ad5F35-hIL-24 could inhibit topoⅡα expression reveled by immunohistochemistry and Westeren blotting, while it increased caspase-3 protein expression. The Transwell experiment showed that the Ad5F35-hIL-24 could reduce the invasiveness of the U251 glioma cells.Conclusion The exogenous IL-24 gene can inhibit the cell proliferation and induce apoptosis of U251 glioma cells. The topoⅡα and Caspase-3 are the important molecular targets of the IL-24 gene. These results may give support for the IL-24 gene usage in clinical treatment for glioma patients.
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Objective To introduce a reliable method to induce neural stem cells directed differentiating into neurons in vitro. Methods The rat neural stem cells were cultured in selected serum-free medium. After cultured for 2, 3 passages,the neurospheres or single-cells isolated from neurospheres were cultured in conditioned medium to induce directed differentiating into neurons. Besides morphological observation of those cells under inverted microscope, NSE immunocytochemistry was carried out to detect the differentiating ratio of those cells from neural stem cells into neurons. Results It was shown that the conditioned medium could induce neural stem cells differentiating into neurons effectively in both neurospheres culture mode or single-cells culture mode. Furthermore, compared with the neurospheres culture mode, the single-cells culture mode showed more synchronous in the differentiation process and higher in the percentage of NSE-positive cells. Conclusion This method can induce neural stem cells directed differentiating into neurons effectively and stablely.
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Objective To investigate the mechanism of cisplatin enhanceing the effect of tineposide killing small cell lung cancer cell line by combination of the two drug.Methods The microculture tetrazolium(MTT) assay was used to determine the inhibition rates of CDDP combined with VM-26.Acridine orange/ethidium bromide(AO/EB) fluorescent staining was used to show the cell vitality rates,DNA disruption ladder were applied to reveal cell apoptosis.The mRNA and protein level of topoisomerase Ⅱ(Topo Ⅱ) and transcript factor SP1 were measured by semi-quantitative RT-PCR and western blot.Results There is synergistic effect between the two drug.The cell vitality rates were decreased in combination group than that of CDDP or VM-26 used alone.the combination treatment group resulted in more serious DNA strand breakage.The expression of Topo Ⅱ?,? and SP1 mRNA and protein both increased in CDDP treatment group,while the Topo Ⅱ?,? expression decreased and(the SP1 expression) has no obviously change in VM-26 treatment group.In combination group,Topo Ⅱ? expressionwere decreased comparing with CDDP used alone,SP1 expression increased comparing with VM-26 used alone,but has no obviously change as comparing with CDDP used alone.Conclusion CDDP could enhance Topo Ⅱ expression through up-regulating SP1 expression,which offer more target for Topo Ⅱ inhibitor VM-26 to act on killing small cell lung cancer cell.
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<p><b>OBJECTIVE</b>To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro.</p><p><b>METHODS</b>PIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA.</p><p><b>RESULTS</b>CCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide.</p><p><b>CONCLUSION</b>CCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.</p>
Subject(s)
Animals , Female , Rats , Cells, Cultured , Culture Media, Conditioned , Chemistry , Lipopolysaccharide Receptors , Lipopolysaccharides , Pharmacology , Macrophages, Alveolar , Cell Biology , Metabolism , Rats, Sprague-Dawley , Sincalide , Pharmacology , Specific Pathogen-Free Organisms , Tumor Necrosis Factor-alpha , Bodily SecretionsABSTRACT
AIM:To look for a better method to deal with interstitial lung disease,interferon-gamma(IFN-?)combined with methylprednisolone(M-pred)to influence human embryonic lung fibroblast on proliferation,collagen synthesis and the expression of transforming growth factor-?1(TGF-?1)protein and mRNA were investigated.METHODS:Exponentially growing cells were preincubated for 48 h before harvested.The microculture tetrazolium(MTT)assay was used to measure the inhibition ratios of M-pred combined with different concentrations of IFN-?.The expression of proliferation cell nuclear antigen(PCNA)was detected by immunocytochemical analysis.Hydroxyproline kit was adopted to detect collagen synthesis.The expressions of TGF-?1 mRNA and protein were detected respectively by RT-PCR and Western blotting.RESULTS:Methylprednisolone,IFN-? as well as the combination of methylprednisolone and IFN-? inhibited the proliferation of HELF and the expression of PCNA in comparison with control group(P
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Objective To observe the connections between enkephalin immunoreactive(ENK-ir) terminals and ?-aminobutyric acid immunoreactive(GABA-ir) neurons in the rostral portion of the nucleus tractus solitarious(rNTS) of the rat. Methods Double-immunofluorescent labeling method and the pre-embedding immunohistochemical staining combined with immuno-gold particles labeling technique for electron microscopic detection were used in the present study. Results Under the laser scanning confocal microscope,dense ENK-ir fibers and terminals and some GABA-ir neurons were observed in the rNTS.Close contacts between ENK-ir terminals and GABA-ir cell bodies were also detected.By using the electron microscopic technique,ENK-ir reaction products were found to be mainly localized on the surface of round clear vesicles and dense-cored vesicles in the axon terminals.ENK-ir terminals formed symmetric,which was a dominant pattern,and asymmetric synaptic connections with GABA-ir and immunonegative cell bodies and dendrites.Conclusion The ENK-ir terminals might take part in the transmission and regulation of the taste information in the rNTS through inhibiting,exciting the GABAergic neurons or inhibiting directly the activity of neurons within the rNTS.