The cerebellum is sensitive to ethanol (EtOH) consumption. Chronic EtOH consumption impairs motor learning by modulating the cerebellar circuitry synaptic transmission and long-term plasticity. Under in vitro conditions, acute EtOH inhibits both parallel fiber (PF) and climbing fiber (CF) long-term depression (LTD). However, thus far it has not been investigated how chronic EtOH consumption affects sensory stimulation-evoked LTD at the molecular layer interneurons (MLIs) to the Purkinje cell (PC) synapses (MLI-PC LTD) in the cerebellar cortex of living animals. In this study, we investigated the effect of chronic EtOH consumption on facial stimulation-evoked MLI-PC LTD, using an electrophysiological technique as well as pharmacological methods, in urethane-anesthetized mice. Our results showed that facial stimulation induced MLI–PC LTD in the control mice, but it could not be induced in mice with chronic EtOH consumption (0.8 g/kg; 28 days). Blocking the cannabinoid type 1 (CB1) receptor activity with AM-251, prevented MLI-PC LTD in the control mice, but revealed a nitric oxide (NO)-dependent long-term potentiation (LTP) of MLI–PC synaptic transmission (MLI-PC LTP) in the EtOH consumption mice. Notably, with the application of a NO donor, S-nitroso-N-Acetyl-D, L-penicillamine (SNAP) alone prevented the induction of MLI–PC LTD, but a mixture of SNAP and AM-251 revealed an MLI-PC LTP in control mice. In contrast, inhibiting NO synthase (NOS) revealed the facial stimulation-induced MLI-PC LTD in EtOH consumption mice. These results indicate that long-term EtOH consumption can impair the sensory stimulation-induced MLI–PC LTD via the activation of a NO signaling pathway in the cerebellar cortex in vivo in mice. Our results suggest that the chronic EtOH exposure causes a deficit in the cerebellar motor learning function and may be involved in the impaired MLI–PC GABAergic synaptic plasticity.

To investigate wavefront aberrations in the entire eye and in the internal optics (lens) and retinal image qualities according to different lenticular opacity types and densities. Forty-one eyes with nuclear cataract, 33 eyes with cortical cataract, and 29 eyes with posterior subcapsular cataract were examined. In each group, wavefront aberrations in the entire eye and in the internal optics and retinal image quality were measured using a raytracing aberrometer. Eyes with cortical cataracts showed significantly higher coma-like aberrations compared to the other two groups in both entire eye and internal optic aberrations (P = 0.012 and P = 0.007, respectively). Eyes with nuclear cataract had lower spherical-like aberrations than the other two groups in both entire eye and internal optics aberrations (P < 0.001 and P < 0.001, respectively). In the nuclear cataract group, nuclear lens density was negatively correlated with internal spherical aberrations (r = −0.527, P = 0.005). Wavefront technology is useful for objective and quantitative analysis of retinal image quality deterioration in eyes with different early lenticular opacity types and densities. Understanding the wavefront optical properties of different crystalline lens opacities may help ophthalmic surgeons determine the optimal time to perform cataract surgery.

Background: Individualized corneal refractive surgery requires an understanding of the basis of higher-order aberrations before surgery. To investigate the characteristics and distribution of anterior surface wavefront aberrations in patients suitable for corneal refractive surgery. Methods: A total of 121 myopic patients (121 eyes, 18-45 years old) who underwent corneal refractive surgery were recruited from January to May 2016 at Affiliated Hospital, Yanbian University. Patients were randomly selected by the Pentacam anterior segment analysis system with a spherical equivalent (SE) of −0.25 to −10.00 D. The corneal anterior aberrations (total higher-order aberration; spherical aberration; Coma; Trefoil) and Q and K values were detected, and a correlation analysis of the relevant parameters was carried out. Results: The root-mean-square (RMS) of the third to sixth order aberrations of the corneal anterior wavefront aberrations at a 6 mm analysis diameter showed a decreasing trend in patients suitable for the corneal refractive surgery, and the RMS of the third order aberrations accounted for 62.92% of the total HOAs. The coma ratio (coma/total cornea higher-order aberrations) was increased with the increasing diopters, while the spherical aberration ratio (spherical aberration/total cornea higher-order aberrations) was not changed. In addition, the spherical aberration was 0.203 ± 0.082 μm (range: 0.061 to 0.503 μm), and the Q 30 was −0.19 ± 0.03 (range: −0.58 to 0.31). There were significant differences in the coma aberrations of preoperative corneal anterior surface (3, 1) between the low, middle and high myopia groups (P = 0.013). The spherical equivalent was positively correlated with the corneal coma of the anterior corneal surfaces (R = −0.241, P = 0.009), and the Q value was positively *Chengzhe Wu and Xun Cui contributed equally to this research.

Background Genistein, an isoflavonoid that can inhibit protein tyrosine kinase (PTK) phosphorylation, was proved to play pivotal roles in the signal transduction pathways of hypoxic disorders. Aim of the stud y: In this study, we established a rat model of isolated beating atrium and investigated the regulator role of genistein and its downstream signaling pathways in acute hypoxia-induced ANP secretion. Methods Radio-immunoassay was used to detect the ANP content in the atrial perfusates. Western blot analysis was used to determine the protein level of hypoxia-inducible factor-1α (HIF-1α), and GATA4 in the atrial tissue. Results The results showed that acute hypoxia substantially promoted ANP secretion, whereas this effect was partly attenuated by the PTKs inhibitor genistein (3 µM). By western blotting analysis, we found that hypoxia-induced the increase in phosphorylation of Akt and transcriptional factors, including HIF-1α, were also reversed by genistein. The perfused HIF-1α inhibitors rotenone (0.5 µM) or CAY10585 (10 µM) plus genistein significantly abolished the enhanced ANP section induced by hypoxia. Additionally, the perfused PI3K/Akt agonist IGF-1 (30 µM) also abolished ANP secretion induced by genistein as well as inhibited expression of HIF-1α. Conclusions In summary, our data suggested that acute hypoxia markedly increased ANP secretion by PTKs through the PI3K/HIF-1α depended pathway.