Mechanism underlying spatial vision deficit of monocular amblyopia based on the theory of Magnocellular and Parvocellular (M-P) pathways / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the relationship between the characteristics of spatial vision deficit and the degree of amblyopia in monocular amblyopes, and to analyze its mechanism with the theory of Magnocellular and Parvocellular pathways.</p><p><b>METHODS</b>One hundred and eleven patients with monocular amblyopes aged 7-34 were included in this study. Distance best corrected visual acuity (BCVA) in logMAR units and contrast sensitivity function test were performed on both eyes in all patients with ETDRS digital visual chart and functional test system OPTECR 6500. The spatial vision of amblyopic and non-amblyopic eyes was evaluated by the AULCSF, Smax, Frmax and cutSF derived from the curve of contrast sensitivity function.</p><p><b>RESULTS</b>The degree of amblyopia was significantly correlated with the difference of AULCSF between the amblyopic and non-amblyopia eyes (r=-0.83, P<0.01). BCVA of amblyopic eyes was significantly correlated with AULCSF, CutSF, Smax, Frmax(r=-0.68, -0.80, -0.73, -0.56, respectively; P<0.01). In amblyopic eyes, significant difference in BCVA, AULCSF, Smax, Frmax and CutSF was seen among different amblyopic groups (P<0.01), which was defined by the degree of amblyopia. In non-amblyopic eyes,no significant difference in BCVA, AULCSF, Smax, Frmax and CutSF was noted among different amblyopic groups (P>0.05). In mild amblyopes, no significant difference in AULCSF and Frmax was found between the amblyopic eyes and non-amblyopic eyes (P>0.05), while Smax and CutSF were significantly different. However, in moderate and severe amblyopes, significant differences in BCVA, AULCSF, Smax, Frmax and CutSF was seen between the amblyopic and non-amblyopic eyes (P<0.01). In amblyopic eyes, significant difference in contrast sensitivity was noted in all kinds of spatial frequencies among different amblyopic groups (P<0.01), and in non-amblyopic eyes, significant differences in contrast sensitivity was not seen in all kinds of spatial frequencies among different amblyopic groups.</p><p><b>CONCLUSIONS</b>The AULCSF, CutSF, Smax and Frmax are accorded with visual acuity for evaluation of the spatial vision of amblyopia. As the severity of amblyopia increases, the overall function of spatial vision in amblyopic eyes gradually decreases, the resolution ability of high spatial frequency is gradually weaken, the peak of contrast detection function gradually descends, and the optimal spatial frequency for contrast detection offsets toward low level of spatial frequency. Mild monocular amblyopia produces spatial contrast sensitivity loss in high spatial vision, suggesting there may be decreased sensitivity of the Parvocellular pathway, and no significant anomalous processing of Magnocellular Pathway. Whereas, in moderate and severe amblyopes, a generalized loss of sensitivity is observed at each spatial frequency. This result shows that both Magnocellular and Parvocellular pathways are damaged in different degrees, especially in Parvocellular pathway.</p>

Synergism between carnosic acid and arsenic trioxide on induction of acute myeloid leukemia cell apoptosis is associated with modulation of PTEN/Akt signaling pathway / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the synergistic effects of carnosic acid (CA) with arsenic trioxide (As₂O₃) on proliferation and apoptosis in HL-60 human myeloid leukemia cells, and the major cellular signaling pathway involved in these effects.</p><p><b>METHODS</b>HL-60 cellular proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) analysis. Cell cycle distribution and apoptosis were monitored by flow cytometry. The activation of casepase-9, Bcl-2-associated agonist of cell death (BAD), p-BAD, p27, phosphatase and tensin homolog deleted on chromosome ten (PTEN), Akt, p-Akt was assessed by Western blot analysis. The expression of PTEN mRNA was tested by reverse transcription polymerase chain reaction (RT-PCR) analysis.</p><p><b>RESULTS</b>CA reduced HL-60 cell viability in a dose- and time-dependent manner, and induced G1 arrest and apoptosis. Moreover, CA upregulated PTEN expression, blocked the Akt signaling pathway, subsequently inhibited phosphorylation of BAD, reactivated caspase-9, and elevated levels of p27. CA also augmented these effects of As₂O₃.</p><p><b>CONCLUSION</b>CA might be a novel candidate of the combination therapy for leukemia treatment; these effects were apparently associated with the modulation of PTEN/Akt signaling pathway.</p>

Study on reversing mechanism of multidrug resistance of K562/A02 cell line by carnosic acid / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the effects of carnosic acid (CA) on reversal of the multidrug resistance (MDR) of human leukemia cell line K562/A02 and its mechanism.</p><p><b>METHODS</b>MTT assay was used to determine the sensitivity of K562/A02 cells to adriamycin (ADM) pre-and post-treated with CA. Flow cytometry (FCM) and laser scanning confocal microscopy (LSCM) were used to measure intracellular fluorescence intensity and concentration of ADM respectively. The expression level of mdr1 was detected by semi-quantitative RT-PCR. P-glycoprotein (P-gp) expression was detected by FCM and Western blot.</p><p><b>RESULTS</b>CA decreased IC(50) of ADM in K562/A02 cells from 16.31 µg/mL to 1.35 µg/mL, being a 12.08-fold decrease. The intracellular ADM fluorescence intensity of K562/A02 was increased from 17.05 to 60.53 after treated with CA (P < 0.01). In living K562/A02 cells, after treated with CA, the diffuse distribution of intracellular ADM was recovered in both nuclear and cytoplasm, and the concentration of intracellular ADM increased from 4.93µg/mL to 15.43µg/mL. RT-PCR assay showed that CA inhibited the expressions of mdr1 mRNA in K562/A02 cells (P < 0.01). Mean fluorescence intensity of P-gp detected by FCM in CA-treated K562/A02 was decreased to 22.80 as compared with that in untreated K562/A02 cells (44.40, P < 0.05).</p><p><b>CONCLUSION</b>CA can reverse the MDR of K562/A02 cells in vitro. The mechanism may be associated with down-regulation of mdr1 and inhibition of P-gp function.</p>