Chloroplasts are the sites for photosynthesis, and two Golden2-like factors act as transcriptional activators of chloroplast development in rice (Oryza sativa L.) and maize (Zea mays L.). Rice OsGLK1 and OsGLK2 are orthologous to maize ZmGLK1 (ZmG1) and ZmGLK2 (ZmG2), respectively. However, while rice OsGLK1 and OsGLK2 act redundantly to regulate chloroplast development in mesophyll cells, maize ZmG1 and ZmG2 are functionally specialized and expressed in different cell-specific manners. To boost rice chloroplast development and photosynthesis, we generated transgenic rice plants overexpressing ZmG1 and ZmG2, individually or simultaneously, with constitutive promoters (pZmUbi::ZmG1 and p35S::ZmG2) or maize promoters (pZmG1::ZmG1, pZmG2::ZmG2, and pZmG1::ZmG1/pZmG2::ZmG2). Both ZmG1 and ZmG2 genes were highly expressed in transgenic rice leaves. Moreover, ZmG1 and ZmG2 showed coordinated expression in pZmG1::ZmG1/pZmG2::ZmG2 plants. All Golden2-like (GLK) transgenic plants had higher chlorophyll and protein contents, Rubisco activities and photosynthetic rates per unit leaf area in flag leaves. However, the highest grain yields occurred when maize promoters were used; pZmG1::ZmG1, pZmG2::ZmG2, and pZmG1::ZmG1/pZmG2::ZmG2 transgenic plants showed increases in grain yield by 51%, 47%, and 70%, respectively. In contrast, the pZmUbi::ZmG1 plant produced smaller seeds without yield increases. Transcriptome analysis indicated that maize GLKs act as master regulators promoting the expression of both photosynthesis-related and stress-responsive regulatory genes in both rice shoot and root. Thus, by promoting these important functions under the control of their own promoters, maize GLK1 and GLK2 genes together dramatically improved rice photosynthetic performance and productivity. A similar approach can potentially improve the productivity of many other crops.

Purpose To report the incidence and associated factors for the development of vitreomacular interface abnormality (VMIA) in patients with diabetic macular edema (DME) who received intravitreal injection (IVI) of anti-VEGF (Bevacizumab and Ranibizumab) treatment. Methods A retrospective observational study. Patients with DME followed at least 6 months were reviewed. Baseline bestcorrected visual acuity (BCVA), central retinal thickness (CRT) and final BCVA, CRT in eyes with and without VMIA were compared. Multiple logistic regression was also used to investigate the risk factors of VMIA formation in patients with DME treated by anti-VEGF. Results A total of 201 eyes in 142 patients met the inclusion criteria of the study. VMIA developed in 44 eyes (21.89%) of patients during a mean follow-up period of 40.84 months. The estimated mean incidence of VMIA formation was 6.43% per year. Poor baseline BCVA was found to be a risk factor for VMIA development (P = 0.001, odds ratio = 5.299, 95% confidence interval: 1.972 to 14.238). There was no difference between eyes with and without VMIA formation in improving BCVA (P = 0.557) and lowering the macular edema (eyes without VMIA formation: − 107.72 ± 171.91 μm; eyes with VMIA formation: − 155.02 ± 212.27 μm, P = 0.133). Conclusions This study revealed the incidence of VMIA formation in IVI anti-VEGF treated DME eyes was 6.43%.Poor baseline BCVA was found to be a risk factor for VMIA formation. Both eyes with and without VMIA development had favorable response to anti-VEGF treatment.

Background and purpose:The expression of multiple pharmacological phenotypes including a1L-adrenoceptor has recently been reported for a1-adrenoceptors. The purpose of the present study was to identify a1-adrenoceptor phenotypes in the irises of pigmented and albino rabbits. and 5-methylurapidil, while two components with high and low affinities for prazosin, RS-17053 and 5-methylurapidil were identified in irises from albino rabbits. In contrast, specific binding sites for [ 3 H]-prazosin were not clearly detected because a high proportion of non-specific binding and/or low affinity for prazosin occurred. Contractile responses of iris dilator muscle to noradrenaline were antagonized by the above ligands, and their antagonist affinities were consistent with the binding estimates at low-affinity sites identified in both strains of rabbits. Conclusions and implications:A typical a1L phenotype with extremely low affinity for prazosin is exclusively expressed in the iris of pigmented rabbits, while two distinct phenotypes (a1A and a1L) with high and moderate affinities for prazosin are co-expressed in the iris of albino rabbits. This suggests that a significant difference in the expression of phenotypes of the a1-adrenoceptor occurs in the irises between the two strains of rabbits.

The aim of the present study was to investigate whether picrotoxin-induced locomotor hyperactivity and hypertension can be inhibited by dopaminergic inhibition in rat amygdala. Locomotor activity was detected using a modularized infrared light matrix system in freely moving rats. In anaesthetized rats, blood pressure was measured while dopamine release was detected using in vivo voltammetry with carbon fibre electrodes. Systemic administration of picrotoxin (1-4 mg/kg) increased both locomotor activity (including horizontal motion, vertical motion and total distance travelled) and the number of turnings (both clockwise and anticlockwise), but inhibited postural freezing. The locomotor hyperactivity induced by systemic administration of picrotoxin was mimicked by direct injection of a small dose (1-3 micro g in 1.0 micro L) of picrotoxin into the amygdala. In vivo voltammetry data revealed that systemic administration of picrotoxin increased the release of dopamine in the amygdala of rat brain accompanied by hypertension. Local injection of kainic acid into the paramedian reticular nucleus (PRN) of the medulla oblongata decreased both the spontaneous release of dopamine in the amygdala and spontaneous levels of locomotor activity in rats. Furthermore, the picrotoxin-induced locomotor hyperactivity, hypertension and increased amygdaloid dopamine release were all suppressed following chemical stimulation of the PRN with kainic acid. Blockade of dopamine receptors with systemic or intra-amygdaloid injection of haloperidol (a dopamine receptor antagonist) significantly attenuated the picrotoxin-induced locomotor hyperactivity and hypertension. These results demonstrate that picrotoxin-induced hyperactivity and hypertension involve an increase in amygdaloid dopamine transmission that can be modulated by ascending projections from the PRN in the medulla oblongata.