AIM: To investigate the effect of microRNA-96-5p(miR-96-5p)on proliferation and apoptosis of rat retinal vascular endothelial cells induced by high glucose and to explore its mechanism.

METHODS: SD rat retinal vascular endothelial cells(RRVEC)were cultured and the RRVEC was divided into control group(NG)and high glucose group(HG). The high glucose-induced RRVECs were harvested separately or co-transfected with miR-96-5p mimic, miR-NC, si-FOXO4, si-NC. The expression of miR-96-5p and FOXO4 was detected by qRT-PCR and Western blotting, respectively. MTT assay was used to detect the proliferation activity. Flow cytometry was used to detect the apoptosis rate. The dual luciferase reporter assay validated the target gene of miR-96-5p. Western blotting was used to detect the expression of CyclinD1, p21, p27, Bcl-2, Bax and cleaved-caspased-3.

RESULTS:The expression levels of miR-96-5p, CyclinD1 and Bcl-2 in RRVEC were significantly decreased after high glucose treatment, and the expression levels of FOXO4, p21, p27, Bax and cleaved-caspased-3 were significantly increased, inhibiting cell proliferation activity, but promoting apoptosis. Overexpression of miR-96-5p and inhibition of FOXO4 expression increased the expression levels of CyclinD1 and Bcl-2, inhibited the expression of p21, p27, Bax, cleaved-caspased-3, enhanced cell proliferation and inhibited apoptosis. Dual luciferase reporter assay demonstrated that FOXO4 was a target gene for miR-96-5p. Overexpression of FOXO4 reversed the effect of miR-96-5p overexpression on high glucose-induced proliferation and apoptosis of RRVEC.

CONCLUSION:miR-96-5p inhibits high glucose-induced apoptosis of rat retinal vascular endothelial cells and promotes cell proliferation by targeting FOXO4.

A systematic review of visual snow syndrome(VSS)was introduced in this article. Scientists don't know what caused visual snow syndrome for sure, but studies have shown that patients with VSS experience continuous television-static-like tiny flickering dots in the entire visual field and additional visual symptoms such as palinopsia, entoptic phenomena or photophobia or nyctalopia. Literature in recent years on the clinical and pathophysiological researches of VSS was reported, and in the latest literature, the VSS was more inclined to be seen as a visual processing disorder. It should be distinguished from the migraine and other diseases. In terms of treatment, current studies focused on experimental studies. Some case reports showed that anti-Seizure medications, antidepressants, or acetazolamide and colored filter-sheet may be effective in eliminating symptoms.

SGLT2 inhibitors currently have clear benefits in the treatment of heart failure whether combined with diabetes or not. Ventricular remodeling after myocardial infarction leads to the occurrence and development of heart failure, and eventually leads to death. There are relatively few studies on SGLT2 inhibitors in patients with myocardial infarction. The purpose of this article is to review the research progress of SGLT2 inhibitors application before and after myocardial infarction.

Since the first intraocular lens(IOL)was implanted by Harold Ridley in 1949 and the widespread use of depth-of-focus extended intraocular lens(EDOF IOL)clinically, the IOL has been constantly updated and developed, aiming to provide patients with good postoperative visual quality. The residual astigmatism is one of the important factors affecting the postoperative visual quality of cataract patients, 35%-40% of cataract patients have astigmatism of 1.00 D, and 19%-22% have astigmatism of 1.50 D. Therefore, it is important to understand the inclusiveness of EDOF IOL for astigmatism, so that the right IOL can be selected for the patient. This article summarizes the inclusiveness of different types of EDOF IOL for astigmatism and their advantages and disadvantages, with the expectation that it will provide a reference in selecting EDOF IOL for patients with different residual astigmatism.

Retinopathy of prematurity(ROP), an abnormal vascular proliferative retinopathy of prematurity, is a serious condition that can lead to retinal detachment or blindness. With the development of neonatal medicine, the survival rate of low birth weight and low gestational age infants has been increasing, as well as the incidence of ROP. Therefore, studying ROP's pathogenesis and influencing factors is of great clinical importance. Numerous studies have been conducted on the risk factors for ROP, including gestational age, oxygen intake, mode of delivery, neonatal bronchopulmonary dysplasia, and the use of surfactants. At present, it is widely accepted both at home and abroad that preterm birth, low birth weight, and high oxygen concentration after birth are independent risk factors for ROP. In recent years, more and more scholars have found that abnormalities in blood indicators in preterm infants may be associated with the development of ROP. This article reviews the effects of platelets, haemoglobin, blood glucose, inflammatory cells, and lipids on ROP, providing a reference for identifying and preventing risk factors for ROP.

Meibomian gland dysfunction is a chronic and diffuse disease of the meibomian glands, characterized by obstruction and(or)abnormal secretion of the terminal ducts. Clinically, it can lead to tear film abnormalities and inflammation of the ocular surface, resulting in symptoms of ocular irritation and potential corneal damage that may impact visual function. Meibomian gland dysfunction can be classified into two types based on meibomian gland secretion: low secretion type and high secretion type. The low secretion type further includes acinar atrophy type and obstruction type. In recent years, research has revealed that patients with diabetes experience chronic damage to their meibomian gland tissue in the early stages of the disease, leading to structural and functional changes. The incidence and severity of meibomian gland dysfunction are higher in diabetic patients. However, there are numerous complex factors contributing to this condition in diabetes patients, and mechanisms remain unclear at present. This article reviews both domestic and international research progress on the pathological mechanism underlying meibomian gland dysfunction in diabetes.

ObjectiveAlzheimer's disease and vascular dementia are responsible for more than 80% of dementia cases. These two conditions share common risk factors including hypertension. Cerebral small vessel disease (CSVD) is strongly associated with both hypertension and cognitive impairment. In this review, we identify the pathophysiological changes in CSVD that are caused by hypertension and further explore the relationship between CSVD and cognitive impairment.

Data SourcesWe searched and scanned the PubMed database for recently published literatures up to December 2017. We used the keywords of "hypertension", "cerebral small vessel disease", "white matter lesions", "enlarged perivascular spaces", "lacunar infarcts", "cerebral microbleeds", and "cognitive impairment" in the database of PubMed.

Study SelectionArticles were obtained and reviewed to analyze the hypertension-induced pathophysiological changes that occur in CSVD and the correlation between CSVD and cognitive impairment.

ResultsIn recent years, studies have demonstrated that hypertension-related changes (e.g., small vascular lesions, inflammatory reactions, hypoperfusion, oxidative stress, damage to autoregulatory processes and the blood-brain barrier, and cerebral amyloid angiopathy) can occur over time in cerebral small vessels, potentially leading to lower cognitive function when blood pressure (BP) control is poor or lacking. Both isolated and co-occurrent CSVD can lead to cognitive deterioration, and this effect may be attributable to a dysfunction in either the cholinergic system or the functionality of cortical and subcortical tracts.

ConclusionsWe explore the currently available evidence about the hypertensive vasculopathy and inflammatory changes that occur in CSVD. Both are vital prognostic indicators of the development of cognitive impairment. Future studies should be performed to validate the relationship between BP levels and CSVD progression and between the numbers, volumes, and anatomical locations of CSVD and cognitive impairment.

As our country steps into the aging society gradually, the number of cognitive impairments and the prevalence rate are increasing yearly. The family and society bear a heavy burden. It is more important to explore the more direct and Objective morphological changes of cognitive impairment through neural structural imaging , which is better for early diagnosis, intervention and delay or even prevent its progress. Here we present a review of this topic focusing on neural structural imaging in the assessment of cognitive impairment.

Objective: To investigate the effects of fecal microbiota transplantation on septic gut flora and the cortex cholinergic anti-inflammatory pathway in rats. Methods: Sixty clean grade male Sprague-Dawley (SD) rats were divided into normal saline (NS) control group, sepsis model group and fecal microbiota transplantation group by random number table, with 20 rats in each group. The rat model of sepsis was reproduced by injection of 10 mg/kg lipopolysaccharide (LPS) via tail vein, the rats in the NS control group was given the same amount of NS. The rats in the fecal microbiota transplantation group received nasogastric infusion of feces from healthy donor on the 1st day, 2 mL each time, for 3 times a day, the other two groups were given equal dose of NS by gavage. Fecal samples were collected on the 7th day after modeling, the levels of intestinal microbiota composition was determined using the 16SrDNA gene sequencing technology. The brain function was evaluated by electroencephalogram (EEG), and the proportion of each waveform in EEG was calculated. After sacrifice of rats, the brain tissues were harvested, the levels of protein expression of α7 nicotinic acetylcholine receptor (α7nAChR) were determined by Western Blot, and positive cells of Iba-1 in brain tissue were detected by immunohistochemistry method. The levels of interleukins (IL-6 and IL-1β) and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). Results: Seven days after the reproduction of the model, all rats in the NS control group survived, while 10 rats and 8 rats died in the sepsis model group and fecal microbiota transplantation group, respectively, with mortality rates of 50% and 40% respectively. Finally, there were 20 rats in the NS control group, 10 in the sepsis model group and 12 in the fecal microbiota transplantation group. Compared with the NS control group, the diversity and composition of intestinal flora were changed, the incidence of abnormal EEG increased significantly, the expression of α7nAchR in the cortex decreased significantly, and the levels of Iba-1, TNF-α, IL-6 and IL-1β were significantly increased in the model group, suggested that the intestinal flora was dysbiosis, and severe inflammatory reaction occurred in the cerebral cortex, and brain function was impaired. Compared with the model group, the diversity of intestinal flora in the fecal microbiota transplantation group was significantly increased (species index: 510.24±58.76 vs. 282.50±47.42, Chao1 index: 852.75±25.24 vs. 705.50±46.50, both P < 0.05), the dysbiosis of intestinal flora at phylum, family, genus level induced by LPS were also significantly reversed, and with the improvement of intestinal flora, the incidence of abnormal EEG waveforms was lower in the fecal microbiota transplantation group compared with that in the model group [25.0% (3/12) vs. 80.0% (8/10), P < 0.05], and the expression of α7nAChR protein in the cerebral cortex was significantly increased (α7nAChR/β-actin: 1.56±0.05 vs. 0.82±0.07, P < 0.05), immunohistochemistry analysis showed that Iba-1 positive expression of microglia decreased significantly, and cerebral cortex TNF-α, IL-6, IL-1β levels were significantly decreased [TNF-α (ng/L): 6.28±0.61 vs. 12.02±0.54, IL-6 (ng/L): 28.26±3.15 vs. 60.58±4.62, IL-1β (ng/L): 33.63±3.48 vs. 72.56±2.25, all P < 0.05]. Conclusion The results reveal that fecal microbiota transplantation has remarkably modulated the dysbiosis of intestinal microbiota and activated cholinergic anti-inflammatory pathway, and ameliorate the brain dysfunction in septic rats.

Neurosteroids are synthesized from cholesterol within the microglia of the central nervous system. They are classified as dehydroepiandrosterone,progesterone, pregnenolone,allopregnanolone and other peripheral steroids. Neurosteroids such as allopregnanolone are positive allosteric modulators of GABAA receptors and exert anxiolytic and antidepressant-like behavior. Neuroactive steroids play a significant role in neurodevelopment in terms of internal environment homeostasis. This paper reviews the biosynthesis, metabolism regulatory effect on the response to stress and therapeutic potentials of neurosteroids.