Fatty acid composition of Drosophila photoreceptor light-sensitive microvilli

Phototransduction, the mechanism underlying the electrical response to light in photoreceptor cells, has been thoroughly investigated in Drosophila melanogaster, an essential model in signal transduction research. These cells present a highly specialized photosensitive membrane consisting of thousands of microvilli forming a prominent structure termed a rhabdomere. These microvilli encompass the phototransduction proteins, most of which are transmembrane and exclusively rhabdomeric. Rhabdomere membrane lipids play a crucial role in the activation of the transient receptor potential ionic channels (TRP and TRPL) responsible for initiating the photoresponse. Despite its importance, rhabdomere lipid composition has not been established. We developed a novel preparation enriched in rhabdomere membranes to perform a thorough characterization of the lipidomics of Drosophila rhabdomeres. Isolated eyes (500) were homogenized and subjected to a differential centrifugation protocol that generates a fraction enriched in rhabdomere membrane. Lipids extracted from this preparation were identified and quantified by gas chromatography coupled to mass spectrometry. We found an abundance of low sterol esters (C16:0, C18:0), highly abundant and diverse triglycerides, free fatty acids, a moderate variety of mono and diacyglycerols (C:16:0, 18:0, C18:1) and abundant phospholipids (principally C18:2). This preparation opens a new avenue for investigating essential aspects of phototransduction.

Magnetic resonance diffusion tensor imaging for optic nerves and optic radiation in blind patients / 中华眼底病杂志

Objective To observe the characteristics of magnetic resonance diffusion tensor imaging (MR-DTI)for optic nerves and optic radiation in blind patients. Methods The optic nerves and optic radiation of 20 blind patients (blind group) and 20 controls (control group) were scanned by MR-DTI.Fractional anisotropy (FA) and directional encoded color (DEC) maps were acquired through postprocessing with the aid of volume-one 1. 72 software. The signal intensity of optic nerves and optic radiation were then observed. The FA, mean diffusivity (MD), λ∥ and λ⊥ value of bilateral optic nerves and optic radiation in two groups were measured in the DEC maps. Results While the high signal intensity was found in bilateral optic nerves in FA and DEC maps in control group, the signal decreased markedly in the blind group. The FA and λ∥ value of optic nerves in the blind group were declined obviously compared to that in the control group. The difference was statistically significant (t= 16. 294, 14. 660;P=0. 000). The MD and λ⊥ value of optic nerves in the blind group were increased obviously compared to that in the control group, the difference was also statistically significant (t=8. 096, 8. 538;P = 0. 000). The high signal intensity was found in bilateral optic radiation in FA and DEC maps in both the blind and control groups. There were no statistic differences in FA and MD value in bilateral optic radiation between the blind and control groups (Left:t=1.456,1.811;P = 0. 152,0.076. Right:t = 0. 779,0. 073;P = 0. 440,0. 942). Conclusion A low signal intensity of bilateral optic nerves and a high signal intensity of bilateral optic radiation were found in blind patients.

Early Reversible Changes on ERG in Pharmaceutically Induced Retinal Degeneration in Rats

PURPOSE: To evaluate the early ERG (electroretinogram) changes in N-methyl-N-nitrosourea (MNU)-induced retinal degeneration in rats. METHODS: Thirty-six 6-week-old male rats were injected intraperitoneally with 60mg/kg MNU and divided into 6 groups. Histology and ERG were recorded for the rats of each group before treatment and at 3, 6, 12, 18, and 24 hours after MNU injection. Promptly after the ERG recording, rats were sacrificed and the eyeballs prepared for histologic sectioning. The Tdt-mediated dUTP-digoxigenin nick end labeling (TUNEL) method was used to detect photoreceptor cell death. RESULTS: The first decreases of ERG responses were noticed maximally at 3 hours after the treatment. Thereafter, the amplitude of the responses was partially recovered at 12 hours post-treatment. The second decrease of ERG amplitudes was observed in the 18-hour recordings, and those changes progressed to 24 hours after the treatment. In the histologic findings, TUNEL (+) cells in the Outer Nuclear Layer (ONL) were not detected at 3 hours after MNU injection, but were initially noticed at 6 hours post-injection. CONCLUSIONS: The first decreases of ERG amplitudes proceeded the appearance of TUNEL (+) cells in ONL, and these electrophysiological changes seemed to not be related to photoreceptor cell death. We propose that electrophysiological changes observed might be related to the MNU-induced activity enhancement of guanylate cyclase in the phototransduction pathway. We also show that photoreceptor cell death in the MNU-induced retinal degeneration model occurs at 6 hours after the treatment, which is earlier than the results of previous reports.

The role of signal transduction molecule PLC in streptococcus pneumoniae inducing filamentous actin rearrangement in type n pneumocytes in vitro / 中华检验医学杂志

Objective To investigate whether S. pn can provoke filamentous actin (F-actin) rearrangements in vitro , which will further lead to S. pn invasion of A549 and the relationship between PLC signaling molecule and. the invasion events. Methods Labelled F-actin with FITC-phalloidin, we observed F-actin rearrangements by S. pn adhesion of type Ⅱ pneumocytes ( A549). S. pn invasion of A549 cells was determined by pretreating A549 cells with Cytochalasin D . To investigate whether F-actin rearrangements can be blocked by PLC inhibitor, A549 cells were pretreated with PLC inhibitors U73122. Results Intact S. pn can promote F-actin rearrangements. Cytochalasin D is able to prevent S. pn invasion of A549 cells. Inhibitors of PLC signal transduction molecules block F-actin rearrangements dose dependently. Conclusion S. pn can provoke F-actin rearrangements through PLC signaling pathways, which will further lead to S. pn invasion of A549 cells.