A Study on the Persistent Trigeminal Artery and Its Classification Based on Magnetic Resonance Angiograph Images.

BACKGROUND: The persistent trigeminal artery (PTA) is the most common remnant of primitive circulation, communicating the developing carotid and vertebrobasilar junction. PURPOSE: This study aimed to evaluate the implementation of magnetic resonance angiography for the detection of PTA and to reclassify the variations based on Weon typing. Moreover, the correlation of various Weon types with the posterior cerebral artery (PCA), Willis ring, basilar artery (BA) dysplasia, and the relationship between PTA and arteriosclerosis were analyzed. METHODS: From November 2017 to October 2019, a total of 48,184 patients underwent magnetic resonance angiography examination in our hospital, and 79 patients were diagnosed with PTA. Of these, 70 patients with complete radiological and clinical information were included in this study. RESULTS: Among the 70 patients with complete data, 27 were classified as Weon type I (38.6%), 7 as type II (10%), 14 as type III (20%), 8 as type IV (11.4%), and 3 as type V (4.3%: type Va, 1 case; type Vb, 2 cases). The remaining 11 cases were PCA with mixed blood supply, so the new type VI was divided into 3 subtypes: type VIa, type VIb, and type VIc, and each subtype of type V was further refined into 4 subtypes. There were 32 cases of PTA with BA dysplasia, including 14 with type I (51.9%), 5 with type II (71.4%), 2 with type III (14.3%), 5 with type IV (62.5%), and 6 with type VI (54.5%). Cerebral infarction was found in 55 cases (78.6%) of PTA, among which 11 had a cerebral infarction in the posterior circulation blood supply area. There were 46 cases (65.7%) accompanied by intracranial arteriosclerosis, and in 6 cases, arteriosclerosis mainly occurred in the posterior circulation. CONCLUSIONS: We redefined the classification of PTA based on Weon typing for a better understanding of clinical symptoms and surgical risks. Moreover, PTA was correlated with the fetal origin of PCA, BA dysplasia, and posterior circulation arteriosclerosis. These factors may increase the incidence of cerebral infarction in the posterior circulation blood supply area.

Effect of physical exercise on weight loss and physical function following bariatric surgery: a meta-analysis of randomised controlled trials.

OBJECTIVES: We performed a meta-analysis of all of the available randomised controlled trials (RCTs) to investigate whether physical exercise contributes to weight loss or physical function improvement in adults receiving bariatric surgery. METHODS: We searched PubMed, Embase, the Cochrane Library, OVID and the CINAHL up through May 2018. RCTs that assigned adults with obesity to either an exercise training group or a no-exercise group after bariatric surgery were included. The primary outcomes were weight loss and physical function. Study bias was assessed using the Cochrane risk of bias tool, and the quality of evidence was assessed using GRADEpro. RESULTS: A total of eight studies met the inclusion criteria (n=347 participants). Most of the studies carried a low risk of bias due to randomisation and blinding. Compared with those without exercise intervention after surgery, patients engaging in physical exercise were associated with greater weight loss (weighted mean difference (WMD) -1.94 kg; 95% CI -3.18 to -0.69; n=8) and longer 6 min walk distance (6MWD; WMD29.67 m; 95% CI 25.97 to 33.37; n=2) during follow-up. By subgroup analyses, the additional weight loss in exercise group was related to the starting time and type of exercise: patients engaging in exercise 1 year or more after surgery and patients received aerobic-resistance exercise experienced more weight loss. Besides, patients in exercise training group also had lower systolic blood pressure and resting heart rate after surgery. The quality of evidence for these outcomes was moderate to very low. CONCLUSIONS: Physical exercise after bariatric surgery provides 1.94 kg additional weight loss and 29.67 m longer 6MWD compared with surgery alone. Moreover, engaging in exercise 1 year or more after surgery, and a combined aerobic and resistance training programme may result in greater weight loss.

Antiapoptotic role of the cellular repressor of E1A-stimulated genes (CREG) in retinal photoreceptor cells in a rat model of light-induced retinal injury.

OBJECTIVE: Light injury-induced apoptosis of retinal photoreceptor cells can lead to vision loss. The mechanism underlying such injury remains unclear, and there are no effective therapies at present. The aim of this study was to examine the potential antiapoptotic role of the cellular repressor of E1A-stimulated genes (CREG) in retinal cells in a rat model of light-induced retinal damage. METHODS: CREG proteins were injected into the vitreous space of rats in which light retinal injury was induced. An equal volume of PBS was injected into the vitreous space of a control group. Retinas were collected for H&E staining and Western blotting analysis 1, 3, and 7 days later. Inhibitors or agonist for P38, JNK, and AKT were injected into the vitreous space to verify CREG function. RESULTS: In rats with light-induced retinal injury, the CREG treatment inhibited the expression of apoptosis-related proteins caspase-3, caspase-8, and caspase-9 and signaling proteins phosphorylated ERK (P-ERK), phosphorylated JNK (P-JNK), phosphorylated P38 (P-P38), and phosphorylated AKT (P-AKT). An inhibitor of PI3K-AKT and an agonists of P38 and JNK abrogated the inhibitory effect of CREG on caspase-3 expression. CONCLUSION: CREG protected retinal cells against apoptosis by inhibiting P38/MAPK and JNK/MAPK signaling pathways and activating the PI3K-AKT signaling pathway.

GRGM-13 comprising 13 plant and animal products, inhibited oxidative stress induced apoptosis in retinal ganglion cells by inhibiting P2RX7/p38 MAPK signaling pathway.

OBJECTIVE: To determine the effectiveness of GRGM-13 on oxidative stress induced apoptosis of retinal ganglion cells (RGCs) and revealed its possible mechanism. MATERIALS AND METHODS: Caspase-3 activity, MDA level, and glutathione peroxidase level were detected by Caspase-3 assay kit, Lipid Peroxidation MDA Assay Kit, and Total Glutathione Peroxidase Assay Kit, respectively. Protein levels of Bax, Bcl-2, p-p38 and p38 were observed by Western Blot. Reactive oxygen species assay kit was used to determine intracellular ROS level. Apoptotic cells were measured by flow cytometry. RESULTS: GRGM-13 inhibited apoptosis of RGCs and ROS level in rat retinal tissue and RGC-5 cells, and the decrease degree strengthened with the increase of GRGM-13 concentration. In addition, ROS upregulated p-p38 expression, while GRGM-13 reversed this effect. We also found that p38 inhibitor SB202190 did not change L-glutamate (Glu) or H2O2-induced ROS level, while SB202190 inhibited apoptosis of RGC-5 cells. Finally, we observed that P2 × 7R agonist BzATP reversed the inhibition effect of GRGM-13 on RGC-5 cell apoptosis, ROS level and p-p38 expression, while si-P2 × 7R inhibited oxidative stress-induced phosphorylation of p38. CONCLUSION: GRGM-13 could inhibit oxidative stress-induced RGCs apoptosis via inhibiting P2RX7/p38 MAPK pathway, which revealed the possible mechanism of GRGM-13 on stress-induced RGCs apoptosis and provided new Chinese medicine for the treatment of glaucoma.

Down-regulation of microRNA-155 attenuates retinal neovascularization via the PI3K/Akt pathway.

PURPOSE: We aimed to investigate the anti-angiogenic properties of miR-155 via in vitro and in vivo studies. METHODS: miR-155 was knocked down using lentivirus-mediated RNA interference. The proliferation, migration, and tube formation of human retinal microvascular endothelial cells (HRMECs) were measured using BrdU, Transwell, and Matrigel assays, respectively. An oxygen-induced retinopathy (OIR) model was induced using neonatal C57BL/6J pups. Anti-miR-155 was intravitreally injected on postnatal day 12, and the retinal non-perfused areas and extent of neovascularization were measured on postnatal day 18 using transcardiovascular fluorescein isothiocyanate (FITC)-dextran perfusion and retina sections. A laser-induced choroidal neovascularization (CNV) model was induced in adult C57BL/6J mice. To evaluate the leakage areas, fundus fluorescein angiography was performed on day 14 after anti-miR-155 intravitreal injection. The neovascularization area of the CNV model was also examined in confocal and retina section studies. The expression levels of SHIP1 and p-Akt (Thr308, Ser473, and Thr450) were evaluated both in vitro and in vivo. RESULTS: The expression of miR-155 was elevated in HRMECs after treatment with vascular endothelial growth factor (VEGF) and in neovascularized mouse model retinas. Anti-miR-155 lentivirus reduced the VEGF-induced proliferation, migration, and tube formation abilities of HRMECs. Anti-miR-155 attenuated retinal neovascularization in in vivo CNV and OIR models. In VEGF-treated HRMECs and retina neovascularization models, p-Akt (Ser473) was significantly upregulated, while SHIP1 was downregulated. Conversely, the inhibition of miR-155 restored the expression of SHIP1 and reduced the phosphorylation of effectors in the Akt (Ser473) signaling pathway. CONCLUSIONS: The results revealed that the downregulation of miR-155 attenuated retinal neovascularization via the phosphatidylinositol 3-kinase (PI3K)/Akt pathway.

Suppressing autophagy protects photoreceptor cells from light-induced injury.

Autophagy, a conserved cellular self-degradation process, not only serves to protect cells at critical times during development and nutrient stress, but also contributes to cell death. Photoreceptor cells are unique neurons which when directly exposed to the light, transduces light stimuli into visual signal. However, intense light exposure can be cytotoxic to the retina. So far, the precise mechanism underlying retina light injury remains unknown, and the effective therapy is still unavailable. Here, we found that visible light exposure activated the mitogen-activated protein kinases (MAPK) pathway and led to remarkable autophagy in photoreceptor cells (661W cells). Directly blocking autophagy with 3MA or LY294002 markedly attenuated light-induced death in 661W cells. Among the activated downstream factors of MAPK pathway, ERK, not JNK or p-38, played a critical role in light-induced death mechanism. Inhibiting the activation of ERK with its specific inhibitor PD98059 significantly suppressed light-induced autophagy and protected 661W cells from light injury. These results indicate that autophagy is an essential event in light-induced photoreceptor death and that directly blocking autophagy or suppressing autophagy by inhibiting the ERK pathway could effectively attenuates light-induced damage. These observations may have a potential application in the treatment of retinal light injury.