AIM: To investigate the change of myopic choroidal neovascularization treated by ranibizumab and evaluate their value in monitoring the effect of anti-vascular endothelial growth factor ( VEGF) therapy. ·METHODS: The study enrolled 30 patients ( 30 eyes ) diagnosed with myopic choroidal neovascularization. All affected eyes were treated with intravitreal ranibizumab 0. 05mL ( 10mg/mL ). Best corrected visual acuity ( BCVA ) , non-contact tonometer, ophthalmoscope, fundus fluorescein angiograph ( FFA ) and OCTA were evaluated monthly until 6mo. The changes of BCVA and central macular thickness ( CMT) were compared at 1, 3 and 6mo after treatment. ·RESULTS:All patients received an average of 1. 70±0. 65 injections. BCVA was 0. 96 ± 0. 17 ( LogMAR ) before therapy, and BCVA 1, 3 and 6mo after treatment respectively improved by 0. 23 ± 0. 09, 0. 34 ± 0. 07, 0. 38 ± 0. 11. The differences were significant ( t=5. 461, 8. 191, 8. 894; P<0. 05 ). Mean CMT decreased form 281. 07 ± 13. 72μm to 261. 33 ± 13. 13μm, 243. 47 ± 16. 65μm, 234. 73 ± 17. 52μm respectively 1, 3 and 6mo after treatment, showing significant differences (t=12. 007, 13. 360, 9. 531;P<0. 05). OCTA revealed a progressively smaller vascular lesion and reduction in capillary density. · CONCLUSION: Intravitreal ranibizumab for CNV secondary to pathologic myopia is effective and safe;OCTA is a noninvasive and time-saving new technology, and it also is a promising tool for clinicians to make preliminary diagnosis and assess treatment efficacy in the follow-up visits.

Objective To observe the effect of bronchial asthma combined with allergic rhinitis by azelastine hydrochloride nasal spray.Methods Eighty-seven cases of bronchial asthma combined with allergic rhinitis patients were divided into treatment group(45 cases)and control group (42 cases) by random number table method,both groups were given the treatment of bronchial asthma according to the guidelines for regulating,treatment group on the basis was combined with azelastine hydrochloride 1 spray per side,2times per day,for 3 months.Observe two groups of asthma symptoms within 3 months control situation,the number of antibiotics and hospitalization for acute exacerbation.Results Treatment group total effective rate,asthma control test score,number of antibiotics and due to the number of exacerbations hospitalization were superior to control group [93.33％(42/45) vs.76.19％(32/42),(23.80 ± 2.15)scores vs.(22.05 ±3.16) scores,13.3％ (6/45) vs.35.7％ (15/42),11.1％ (5/45) vs.33.3％ (14/42)] (P ＜ 0.05 or ＜ 0.01).Conclusion Combined by azelastine hydrochloride nasal spray may make a good control,reduce the use of antibiotics for acute attack and times of hospitalization,worthy of clinical application.

AIMTo investigate the antiarrhythmic effect of jumi (JM) extraction.

METHODSThe conventional antiarrhythmic methods were used.

RESULTSAdministration of JM extraction reduced the occurrence of ventricular fibrillation induced by chloroform in a dose-dependent manner in mice. Quinidine significantly decreased the number of ventricular premature beats and ventricular tachycardia, shortened the duration of arrhythmia in aconitine-treated rats. But JM extraction had no effect on aconitine-induced arrhythmia. Compared with control, arrhythmia score was lower in ischemia/reperfusion rats which pretreated with 2.0 g/kg of JM extraction.

CONCLUSIONJM extraction has obvious protection effects in chloroform- and ischemia-induced arrhythmia, but has no effect in aconitine-induced arrhythmia.

Animals ; Anti-Arrhythmia Agents ; therapeutic use ; Arrhythmias, Cardiac ; chemically induced ; drug therapy ; Female ; Male ; Mice ; Plant Extracts ; therapeutic use ; Rats ; Rats, Sprague-Dawley

BACKGROUNDManagements of optic neuritis (ON) included high-dose corticosteroids or combined with systemic immunomodulatory agents. It was important to make a correct diagnosis of ON before initiation of treatment. The purpose of the study was to report and analyze the clinical features of retinal diseases in patients who were misdiagnosed as having retrobulbar ON.

METHODSRetrospective review of 26 patients (38 eyes) initially diagnosed with retrobulbar ON but were ultimately diagnosed with retinal or macular diseases. Data obtained from fundus examination, fluorescence fundus angiography (FFA), automated static perimetry, full-field electroretinogram (ffERG), multifocal electroretinogram (mfERG), and optical coherence tomography (OCT) were evaluated.

RESULTSThirty-eight eyes of 26 patients were found to have misdiagnosis of retrobulbar ON, based on normal or slight abnormal fundus findings and abnormal visual evoked potentials (VEP). The mean age of the patients was 34 years and the correct diagnosis of the patients included acute zonal occult outer retinopathy (AZOOR, 15 eyes, 14 patients), occult macular dystrophy (OMD, 8 eyes, 4 patients), cone or cone-rod dystrophy (10 eyes, 5 patients), acute macular neuroretinopathy (AMNR, 3 eyes, 2 patients), and cancer-associated retinopathy (CAR, 2 eyes, 1 patient).

CONCLUSIONWhen attempting to diagnose retrobulbar ON in clinical practice, it is crucial to carry out necessary examinations of the retinal function and morphology to decrease misdiagnosis.

Adult ; Aged ; Electroretinography ; Female ; Humans ; Male ; Middle Aged ; Optic Neuritis ; diagnosis ; Retinal Diseases ; diagnosis ; Retrospective Studies ; Tomography, Optical Coherence

BACKGROUNDCompound anisodine (CA) is a compound preparation made from hydrobromide anisodine and procaine hydrochloride. The former is an M-choline receptor blocker with the function of regulating the vegetative nervous system, improving microcirculation, and so on. The latter is an antioxidant with the activities of neuroprotection. This study aimed to investigate the potential neuroprotection of CA, which affects the degeneration of the retinal ganglion cells (RGCs) in an animal model with chronic ocular hypertension.

METHODSFemale C57BL/6J mice (n = 24) were divided randomly into four groups: normal control group without any treatment (Group A, n = 6); CA control group with feeding the CA solution (Group B, n = 6); microbeads (MBs) control group with injecting MB into the anterior chamber (Group C, n = 6); CA study group with MB injection and with feeding the CA solution (Group D, n = 6). Intraocular pressure (IOP) was measured every 3 days after MB injection. At the 21st day, neurons were retrograde-labeled by Fluoro-Gold (FG). Animals were sacrificed on the 27th day. Retinal flat mounts were stained immunohistologically by α2-III-tubulin. FG-retrograde-labeled RGCs, α2-III-tubulin-positive RGCs, and α2-III-tubulin-positive nerve fibers were quantified.

RESULTSMice of Groups C and D expressed the incidence of consistent IOP elevation, which is above the IOP level of Group A with the normal one. There is no significant difference in IOP between Groups A and B (P > 0.05). On the 27th day, there were distinct loss in stained RGCs and nerve fibers from Groups C and D compared with Group A (allP < 0.001). The quantity was significantly higher in Group D as compared to Group C (allP < 0.001) but lower than Group A (allP > 0.001). There was no significant difference in the quantity of RGCs and nerve fibers between Groups A and B (allP > 0.05).

CONCLUSIONSThese findings suggest that CA plays an importantly neuroprotective role on RGCs in a mouse model with chronic ocular hypertension.

Animals ; Cell Survival ; drug effects ; Female ; Immunohistochemistry ; Intraocular Pressure ; drug effects ; Mice ; Mice, Inbred C57BL ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Ocular Hypertension ; drug therapy ; Random Allocation ; Retinal Ganglion Cells ; drug effects ; Scopolamine Derivatives ; pharmacology ; therapeutic use