As a common ophthalmic disease, floaters have a complex etiology. It involves changes in the structure and function of the vitreous body and is closely associated with factors like age and myopia. Vitreous liquefaction and posterior detachment play a crucial role in this regard. Clinically, patients usually experience the floating of dotted or linear black shadows in front of their eyes, and generally, floaters do not cause visual impairment. In the past, due to the limitations of traditional concepts and treatment methods, a conservative observation strategy was often adopted. However, an increasing number of patients have complained that floaters lead to difficulties in driving and reading, which seriously affects their visual quality and mental health. Consequently, the demand for treatment has been growing day by day. The existing treatment options each have their own advantages and disadvantages. The efficacy of drug treatment is limited and remains controversial. Vitrectomy has a definite curative effect, yet it comes with a high risk of complications. YAG laser vitreolysis is relatively safe, but its curative effect is restricted by factors such as the size and location of the opacities. Nanobubble-mediated vitreolysis is still in the research stage and is expected to offer patients safer and more effective treatment in the future. This article reviews the etiology of floaters and the latest progress in its treatment, aiming to deepen clinicians' understanding of floaters, provide a more comprehensive scientific basis for clinical diagnosis and treatment, and promote personalized and precise treatment.

As a common ophthalmic disease, floaters have a complex etiology. It involves changes in the structure and function of the vitreous body and is closely associated with factors like age and myopia. Vitreous liquefaction and posterior detachment play a crucial role in this regard. Clinically, patients usually experience the floating of dotted or linear black shadows in front of their eyes, and generally, floaters do not cause visual impairment. In the past, due to the limitations of traditional concepts and treatment methods, a conservative observation strategy was often adopted. However, an increasing number of patients have complained that floaters lead to difficulties in driving and reading, which seriously affects their visual quality and mental health. Consequently, the demand for treatment has been growing day by day. The existing treatment options each have their own advantages and disadvantages. The efficacy of drug treatment is limited and remains controversial. Vitrectomy has a definite curative effect, yet it comes with a high risk of complications. YAG laser vitreolysis is relatively safe, but its curative effect is restricted by factors such as the size and location of the opacities. Nanobubble-mediated vitreolysis is still in the research stage and is expected to offer patients safer and more effective treatment in the future. This article reviews the etiology of floaters and the latest progress in its treatment, aiming to deepen clinicians' understanding of floaters, provide a more comprehensive scientific basis for clinical diagnosis and treatment, and promote personalized and precise treatment.

AIM: To investigate the effects of hypobaric hypoxia in plateau on tear indexes and related anatomical structures in rabbits.METHODS: A total of 18 healthy New Zealand rabbits were selected and randomly divided into plateau group and control group, with 9 rabbits(18 eyes)in each group. The plateau group was housed in the Simulated Climate Cabin for Special Environment of Northwest of China, simulating hypobaric hypoxia at an altitude of 6 000 m. The control group was housed in a clean animal room with atmospheric pressure and oxygen. Changes in the tear meniscus height and non-invasive tear break-up time were detected by using RHCT-1 corneal topographer dry eye comprehensive analysis system, changes in tear secretion was measured by Schirmer Ⅰ test, before intervention and on the 3, 7 d, 2 and 4 wk. Meanwhile, the changes in tear composition before and after intervention in the plateau environment were analyzed using Raman Spectroscopy. The histopathological changes of the lower lid conjunctiva, cornea, lacrimal gland, and Hardarian gland were observed by hematoxylin-eosin(HE)staining after 4 wk of intervention, and the expression of mucin 5AC(MUC5AC)in conjunctiva was detected by immunohistochemistry.RESULTS: Compared with the control group, Schirmer Ⅰ test, tear meniscus height, first and average non-invasive tear break-up time in the plateau group decreased significantly since 3 d, and the difference was significant with the extension of observation time(P<0.05). The above indexes increased from 2 wk. After 4 wk of intervention, the protein and lipid content of the tear composition of rabbits in the plateau group increased, and the nucleic acid content decreased compared with the pre-intervention period. Compared with the control group, rabbits in the plateau group showed thickening of corneal stromal edema, an increase in the number of conjunctival cup cells, increase in the level of expression of MUC5AC, an increase in the level of expression of MUC5AC, an atrophy and flattening of cytoplasm in lacrimal epithelial cells, an enlargement of glandular lumen, and no obvious destructive changes in the Hardarian glands.CONCLUSION: Acute plateau environment can destroy the homeostasis of rabbit ocular surface, so that the tear secretion and the tear film stability decreases, but within a certain period of time, rabbits undergo compensation with the habituation to the hypobaric hypoxia environment, which can increase the tear secretion to a certain extent and restore the tear film stability.

Objective    To analyze a new classification of the left apicoposterior segmental bronchus and summarize its clinical significance. Methods     We accessed the computed tomography imaging data of the inpatients treated in the Department of Thoracic Surgery, Henan Provincial People's Hospital between January and November 2021. We observed and classified the branching pattern of the left apicoposterior segmental bronchus (B1+2) using three-dimensional computed tomography bronchography and angiography (3D-CTBA) technique. And we filtered out the patients who underwent thoracoscopic left apicoposterior segmentectomy and analyzed their clinical data retrospectively to summarize the instructing significance of different bronchial classification in the accurate and safe operation of left apicoposterior segmentectomy. Results     Finally 240 patients were collected, including 131 males and 109 females with a median age of 51.0 (19.0-77.0) years. The anatomical pattern of the left apicoposterior segmental bronchus was divided into four main types based on the branching pattern of the outer subsegmental bronchi (B1+2c): type Ⅰ 10% (24 patients), type Ⅱ 54% (130 patients) , type Ⅲ 17% (40 patients) , type Ⅳ 18% (43 patients) and other variations 1% (3 patients). Thirty-two patients smoothly underwent thoracoscopic left apicoposterior segmentectomy, including 23 patients of type Ⅰ and type Ⅱ receiving LS1+2 resection, the other 9 patients of type Ⅲ and type Ⅳ receiving LS1+2 resection (3 patients), LS1+2c resection (4 patients) and LS1+2(a+b) resection (2 patients). Conclusion     This new classification systematically and concisely elucidates the branching characteristics of the left apicoposterior bronchus. Different branching types are instructive to the left apicoposterior segmentectomy.

Background Lipid metabolism in liver shows circadian-dependent profiles. The hepatotoxicity of environmental chemicals is dependent on circadian time. Objective To observe the effects of bisphenol A (BPA) exposure at different zeitgeber time (ZT) on hepatic and blood lipid metabolism and decipher the underlying mechanisms related to circadian rhythm in mice. Methods Thirty-five female C57BL/6J mice were sacrificed every 4 h in a light-dark cycle (12 h/12 h). The liver tissues were collected to describe the circadian profiles of hepatic Rev-erba, Bmal1, Clock, Srebp1c, and Chrebp mRNA expression levels within 24 h. Thirty female mice were divided into 6 groups by the timing (ZT3 represents the 3 h after light on, ZT15 represents the 3 h after light off) and dose (50 or 500 μg·kg⁻¹·d⁻¹) of BPA exposure to observe hepatotoxicity. Mice were gavaged with designed doses of BPA once per day for 4 weeks. Mice were maintained with ad libitum access to food and water and measured body weight weekly. After the experiment, mice were euthanatized and liver tissues were separated to determine the biochemical indicators of lipid metabolism and lipid metabolism- and circadian-related gene mRNA expressions. Results Hepatic Rev-erba, Bmal1, Clock, Srebp1c, and Chrebp mRNA expression levels were rhythmic during a 24 h period in mice. At ZT3 and ZT15, BPA did not alter body weight, plasma glucose, plasma total cholesterol, plasma low density lipoprotein cholesterol, and plasma triglycerides (P>0.05). The plasma high density lipoprotein cholesterol decreased in the 50 μg·kg⁻¹·d⁻¹ BPA group at ZT3 by 14.56% compared with the control group (P<0.05). The liver triglycerides increased in the 50 μg·kg⁻¹·d⁻¹ BPA group at ZT15 by 115.20% compared with the control group (P<0.05). BPA decreased Srebp1c mRNA expression level when dosing at ZT3 and increased Chrebp, Srebp1c, and Acc1 mRNA expression levels when dosing at ZT15 compared with the control group (P<0.05). BPA increased Bmal1 mRNA expression level and decreased Rev-erbα mRNA expression level at ZT3 exposure and decreased Bmal1 and increased Rev-erbα mRNA expression level at ZT15 exposure (P<0.05). Conclusion BPA exposure at light or dark period has different effects on hepatic lipid metabolism in mice. Hepatic lipid deposit appears when BPA is dosed at dark period. Rev-erbα-Bmal1 regulation circuits and the subsequent upregulation of Srebp1c and Chrebp and the target gene Acc1 may be involved.

Objective: Viscoelasticity is an essential feature of nerves, although little is known about their viscous properties. The discovery of shear wave dispersion (SWD) imaging has presented a new approach for the non-invasive evaluation of tissue viscosity.The present study investigated the feasibility of using SWD imaging to evaluate diabetic neuropathy using the sciatic nerve in a diabetic rat model. Materials and Methods: This study included 11 diabetic rats in the diabetic group and 12 healthy rats in the control group.Bilateral sciatic nerves were evaluated 3 months after treatment with streptozotocin. We measured the nerve cross-sectional area (CSA), nerve stiffness using shear wave elastography (SWE), and nerve viscosity using SWD imaging. The motor nerve conduction velocity (MNCV) was also measured. These four indicators and the histology of the sciatic nerves were then compared between the two groups. The performance of CSA, SWE, and SWD imaging in distinguishing the two groups was assessed using receiver operating characteristic (ROC) analysis. Results: Nerve CSA, stiffness, and viscosity in the diabetic group was significantly higher than those in the control group (all p < 0.05). The results also revealed a significantly lower MNCV in the diabetic group (p = 0.005). Additionally, the density of myelinated fibers was significantly lower in the diabetic group (p = 0.004). The average thickness of the myelin sheath was also lower in the diabetic group (p = 0.012). The area under the ROC curve for distinguishing the diabetic neuropathy group from the control group was 0.876 for SWD imaging, which was significantly greater than 0.677 for CSA (p = 0.030) and 0.705 for SWE (p = 0.035). Conclusion Sciatic nerve viscosity measured using SWD imaging was significantly higher in diabetic rats. The viscosity measured using SWD imaging performed well in distinguishing the diabetic neuropathy group from the control group.Therefore, SWD imaging may be a promising method for the evaluation of diabetic neuropathy.

OBJECTIVE：To study the regulatory effects of stilbene glucosid e（TSG）on c-Jun N-terminal kinase （JNK）and protein phosphortase 2B（PP2B）in APP/PS1/Tau transgenic dementia （3×Tg-AD）mice，and to explore its potential mechanism of anti-Alzheimer’s disease （AD）. METHODS ：Totally 45 male 3×Tg-AD mice were randomly divided into model group ，positive control group （huperzine A ，0.15 mg/kg），TSG low-dose ，medium-dose and high-dose groups （0.033，0.1，0.3 g/kg），with 9 mice in each group. Another 9 normal male C 57BL/6J mice were included into normal control group. Administration groups were given relevant medicine intragastrically ，once a day ，for consecutive 60 d. Normal control group and model group were given constant volume of normal saline intragastrically. After medication ，Morris water maze experiment was used to test the spatial learning and memory ability of mice in each group ；Nissl staining was used to observe the changes of Nissl bodies in cerebral cortex and hippocampus ；mRNA and protein expressions of JNK and PP 2B were detected by qRT-PCR and Western blotting assay. RESULTS：Compared with normal control group ，the escape latency was significantly prolonged （P＜0.01），the retention time of the original platform quadrant was significantly shortened （P＜ and the times of crossing the platform was significantly reduced in model group （P＜0.01）；the number of Nissl bodies in cerebral cortex and hippocampus was significantly 729011126@qq.com reduced，the staining was slight ；the relative expressions of JNK mRNA and protein were significantly increased （P＜ 0.01），and the relative expressi ons of PP 2B mRNA and protein were significantly decreased （P＜0.01）. Compared with model group ，the escape latency was significantly shortened in positive control group and TSG groups （P＜0.01）；the retention time of the original platform quadrant was significantly prolonged （P＜0.01）；the times of crossing the platform was significantly increased （P＜0.01）；the number of Nissl bodies in cerebral cortex and hippocampus was increased significantly ，the staining was heavy ；the relative expression of JNK protein was significantly decreased（P＜0.05 or P＜0.01），the relative expressions of PP 2B mRNA and protein were significantly increased （P＜0.01）， while the relative expression of JNK mRNA was significantly decreased in TSG high-dose group （P＜0.05）. CONCLUSIONS ：TSG can improve the learning and memory ability and neuronal damage of 3 × Tg-AD mice. The mechanism may be related to down-regulating the transcription and expression of protein kinase JNK ，up-regulating the transcription and expression of protein phosphatase PP 2B.

OBJECTIVE：To study the e ffects of stilbene glycoside c（TSG）on phosphorylation of Thr 205，Ser404 sites of Tau protein in Aizheimer ’s disease （AD）model mice ，and to investigate the potential anti-AD mechanism of TSG. METHODS ：APP/ PS1/Tau three transgenes （3×Tg-AD）mice were randomly divided into model group ，positive control group （huperzine，0.15 mg/kg），TSG low-dose ，medium-dose and high-dose groups （0.033，0.1，0.3 g/kg），with 6 mice in each group. In addition ，6 C57BL/6J mice were chosen as normal control group. Administration groups were given relevant medicine intragastrically. Model group and normal control group were given equal volume of normal saline intragastrically ，once a day ，for consecutive 60 days. After last medication ，immunofluorescence staining was used to detect Tau protein and phosphorylated Tau protein （Thr205， Ser404 sites） distribution and expression in brain tissue of mice in each group. Western blotting assay was used to detect phosphorylated Tau protein （Thr205，Ser404 sites）expression level in brain tissue of mice in each group. RESULTS ：Compared with normal control group ，the expression of Tau protein，phosphorylated Tau protein （Thr205，Ser404 sites）in 729011126@qq.com the brain tissue of mice were increased in model group ，which were easy to aggregate and distributed more widely ；theirrelative expression were increased significantly （P＜0.01）. Results of Western blotting assay showed that the expression levels of phosphorylat ed Tau protein （Thr205，Ser404 sites）were increased significantly （P＜0.01）. Compared with model group ，the expression of Tau protein ，phosphorylated Tau protein （Thr205，Ser404 sites） in the brain tissue of mice were decreased in positive control group and TSG groups ；aggregation decreased，distribution narrowed and their relative expression were decreased significantly （P＜0.01）. Results of Western blotting assay showed that the expression levels of phosphorylated Tau protein （Thr205，Ser404 sites）were decreased significantly （P＜ 0.01）. Compared with positive control group ，There was no significant difference in the distribution of Tau protein ，phosphorylated Tau protein （Thr205，Ser404 sites）in the brain tissue of mice in TSG groups ；the relative expression were not statistically significant（P＞0.05）；but Western blotting assay showed the expression levels of phosphorylated Tau protein （Thr205 site）in TSG medium-dose and high-dose groups as well as the expression levels of phosphorylated Tau protein （Ser404 site）in TSG groups were decreased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS ：TSG can play an anti-AD effect on AD model mice by down-regulating the expression of phosphorylated Tau protein （Thr205，Ser404 sites）in brain tissue.

Objective: To investigate the frequency of KRAS mutation in mucinous epithelial lesions of the endometrium, and analyze the correlation between KRAS mutation and the clinicopathologic features. Methods: The cohort included forty-three cases of mucinous epithelial lesions of the endometrium selected from July 2015 to October 2017 from Beijing Obstetrics and Gynecology Hospital, and 22 control cases. Genomic DNA was extracted from formalin-fixed paraffin-embedded tissue sections. Polymerase chain reaction amplification for KRAS exons 2 and 3 was performed, followed by sequencing using capillary electrophoresis. The Fisher exact test was used to compare the prevalence of KRAS mutation among the different groups. Results: The patients′age ranged from 33 to 77 years [mean (55.12±9.34) years, median 55 years]. None of the eight cases of endometrial hyperplasia with mucinous differentiation without atypia showed KRAS mutation. The frequency of KRAS mutations was 1/10 in endometrial atypical hyperplasia, 1/12 in endometrioid carcinoma, 4/11 in endometrial atypical hyperplasia with mucinous differentiation (EAHMD), 6/15 in endometrioid carcinoma with mucinous differentiation (ECMD) and 8/9 in mucinous carcinoma (MC), respectively. The differences were statistically significant between MC versus EC (P<0.01) and MC versus ECMD (P<0.05). Conclusion The high frequency of KRAS mutation in EAHMD, ECMD and MC indicates that KRAS mutational activation is implicated in the pathogenesis of endometrial mucinous carcinoma.

Objective Recent studies have indicated that early brain injury is the leading cause of death in patients with subarachnoid hemorrhage ( SAH) .Our study investigated the role of aminoguanidine ( AG) in early brain injury after SAH . Methods Sixty-eight male SD rats were equally randomized into four groups of equal number :control, sham, SAH, and AG.The animals in the sham group were injected with isotonic saline solution , while those of the latter two groups with femoral artery blood ( FAB) and FAB+AG, respectively, into the pre-chiasmatic cistern to induce SAH. At 24 hours after modeling , all the rats were killed for HE staining , obtainment of behavioral neurological assessment ( BNA ) scores by Garcia, measurement of the apoptosis of neurons by TUNEL , and de-termination of the expressions of the iNOS and NSE proteins by West-ern blot. Results The results of HE staining showed the presence of more red blood cells in the subarachnoid cavity of the rats in the SAH group, with a significantly decreased BNA score ( 14.47 ± 0.62) as compared with those in the control (17.94 ±0.24), sham (17.59 ±0.51), and AG group (15.71 ±0.47) (P<0.05). The rate of positive cells was remarkably higher in the SAH group ([42.38 ±2.38]%) than in the control ([6.35 ±0.94]%), sham ([6.85 ±0.69]%), and AG group ([30.48 ±2.89]%) ( P<0.01), with significant differences among the latter three groups (P<0.05).The expressions of iNOS and NSE were markedly higher in the SAH group ([3.86 ±0.07] and [1.59 ±0.06]) than in the control (0 and[0.35 ±0.09]), sham ([2.96 ±0.34] and [0.38 ±0.08]), and AG group ([3.41 ±0.04] and [0.70 ±0.12]) ( P<0.05).Both the expression levels of iNOS and NSE were positively correlated with the rate of positive cells (r=0 .879 and 0.935, P<0.01). Conclusion AG can alleviate early brain injury after SAH in SD rats by improving the neuro-ethologic function , suppressing the apoptosis of neurons , and reducing the expressions of iNOS and NSE .