Recent years have witnessed significant advancements in myopia control research through the application of diffuse optical technology(DOT)spectacle lenses. Myopia has emerged as a global public health challenge, affecting nearly half of the world's population, with childhood and adolescent myopia rates continuing to rise. DOT lenses represent an innovative myopia control intervention based on retinal contrast signal theory. These lenses incorporate micro-light scattering dots distributed across the lens surface to reduce retinal imaging contrast and modulate the influence of visual input on axial elongation, thereby slowing myopia progression. The core mechanism operates through refractive index differences between the lens substrate(1.53)and scattering dots(1.50), which generate optical scattering effects. This design maintains clear vision through a central 5 mm optical zone while effectively reducing contrast signal intensity in the peripheral retina. Large-scale randomized controlled trials, including the CYPRESS study, have demonstrated significant myopia control efficacy in children aged 6-10 years: 12-month follow-up data revealed a 74% reduction in myopia progression and a 50% reduction in axial elongation, with sustained safety and visual quality maintained over 4-year long-term follow-up. However, several aspects of DOT technology remain contentious and require further clinical validation, including its applicability across different age groups, optimal scattering dot density configurations, combined application effects with other myopia control methods, and long-term visual adaptation during extended use. This review systematically examines the theoretical foundations, design characteristics, clinical application progress, and future development directions of DOT technology, providing scientific evidence for clinical myopia prevention and control strategy formulation.

Vascular dementia (VaD) is the second commonest type of dementia which lacks of efficient treatments currently. Neuroinflammation as a prominent pathological feature of VaD, is highly involved in the development of VaD. In order to verify the therapeutic potential of PDE1 inhibitors against VaD, the anti-neuroinflammation, memory and cognitive improvement were evaluated in vitro and in vivo by a potent and selective PDE1 inhibitor 4a. Also, the mechanism of 4a in ameliorating neuroinflammation and VaD was systematically explored. Furthermore, to optimize the drug-like properties of 4a, especially for metabolic stability, 15 derivatives were designed and synthesized. As a result, candidate 5f, with a potent IC₅₀ value of 4.5 nmol/L against PDE1C, high selectivity over PDEs, and remarkable metabolic stability, efficiently ameliorated neuron degeneration, cognition and memory impairment in VaD mice model by suppressing NF-κB transcription regulation and activating cAMP/CREB axis. These results further identified PDE1 inhibition could serve as a new therapeutic strategy for treatment of VaD.

In skeletal system, the coupling effect between angiogenesis and osteogenesis can promote bone growth and maintain bone mass balance. Type H vessel is a special capillary subtype in bone with high expression of Endomucin (Emcn) and CD31. The essence of type H vessel is vascular endothelial cells, mainly distributed in the metaphysis, surrounded by bone progenitor cells, which mediates the coupling mechanism of angiogenesis and osteogenesis, involving a variety of cytokines and signaling pathways. Factors including platelet-derived growth factor type BB, slit guidance ligand 3, hypoxia-inducible factor 1-alpha, Notch, and vascular endothelial growth factor are involved in the coupling of angiogenesis and osteogenesis. Type H vessels transmit signals through a variety of cytokines to enhance the connection between angiogenesis and bone formation, thus regulating bone growth and bone homeostasis. In addition, this article discusses the research prospects of improving bone loss by using it as a target, so as to provide reference for clinical bone injury repair and anti-osteoporosis treatment.

Objective:To investigate the effect of dexmedetomidine combined with butorphanol on perioperative analgesia in patients subjected to cardiac surgery.Methods:Sixty-three patients who underwent elective cardiac surgery in Weihai Central Hospital from June 2019 to August 2020 were included in this study. They were divided into propofol + sufentanil group ( n = 21), dexmedetomidine + sufentanil group ( n = 23) and dexmedetomidine + butorphanol group ( n = 19) according to different analgesic methods. Postoperative analgesic satisfaction, Visual Analogue Scale score, hemodynamic changes (heart rate, respiratory rate, systolic blood pressure, diastolic blood pressure) and adverse reactions were compared among the three groups. Results:The satisfaction rate of postoperative analgesia in the dexmedetomidine + butorphanol group was 94.7% (18/19), which was significantly higher than 61.9% (13/21) in the propofol + sufentanil group and 60.8% (14/23) in the dexmedetomidine + sufentanil group ( χ2 = 6.16, 6.57, both P < 0.05). At 4, 12, 24 and 48 hours after tracheal extubation, Visual Analogue Scale score in the dexmedetomidine + butorphanol group were significantly lower than that in the propofol + sufentanil group and dexmedetomidine + sufentanil group (both P < 0.05). At the time of tracheal extubation and at 5 minutes after tracheal extubation, heart rate, respiratory rate, systolic blood pressure and diastolic blood pressure in the dexmedetomidine+butorphanol group were significantly lower than those in the propofol + sufentanil group and dexmedetomidine + sufentanil group (both P < 0.05). The incidence of adverse reactions in the dexmedetomidine + butorphanol group was 10.5% (2/19), which was significantly lower than 23.8% (5/21) in the propofol + sufentanil group and 30.43% (7/23) in the dexmedetomidine + sufentanil group [30.4% (7/23), χ2=21.94, P < 0.001]. Conclusion:Dexmedetomidine combined with butorphanol in cardiac surgery can not only stabilize postoperative blood pressure and heart rate, but also lower the degree of pain and is highly safe.

Detailed knowledge on tissue-specific metabolic reprogramming in diabetic nephropathy (DN) is vital for more accurate understanding the molecular pathological signature and developing novel therapeutic strategies. In the present study, a spatial-resolved metabolomics approach based on air flow-assisted desorption electrospray ionization (AFADESI) and matrix-assisted laser desorption ionization (MALDI) integrated mass spectrometry imaging (MSI) was proposed to investigate tissue-specific metabolic alterations in the kidneys of high-fat diet-fed and streptozotocin (STZ)-treated DN rats and the therapeutic effect of astragaloside IV, a potential anti-diabetic drug, against DN. As a result, a wide range of functional metabolites including sugars, amino acids, nucleotides and their derivatives, fatty acids, phospholipids, sphingolipids, glycerides, carnitine and its derivatives, vitamins, peptides, and metal ions associated with DN were identified and their unique distribution patterns in the rat kidney were visualized with high chemical specificity and high spatial resolution. These region-specific metabolic disturbances were ameliorated by repeated oral administration of astragaloside IV (100 mg/kg) for 12 weeks. This study provided more comprehensive and detailed information about the tissue-specific metabolic reprogramming and molecular pathological signature in the kidney of diabetic rats. These findings highlighted the promising potential of AFADESI and MALDI integrated MSI based metabolomics approach for application in metabolic kidney diseases.

Objective:To investigate the independent correlation between serum IL-6 level and delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) and to evaluate its predictive value for DCI.Methods:Consecutive patients with aSAH admitted to the Affiliated Hospital of Jining Medical University from June 2017 to June 2019 were enrolled retrospectively. They were divided into DCI group and non-DCI group according to the diagnostic criteria of DCI. Multivariate logistic regression analysis was used to determine the independent correlation between serum IL-6 and DCI. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value of serum IL-6 level for DCI. Results:A total of 160 patients with aSAH were enrolled. They aged 66.1±8.1 years, and 98 were males (61.3%); 76 patients (47.5%) had DCI. Multivariate logistic analysis showed that after adjusting for smoking, hypertension, systolic blood pressure, hyperlipidemia, and drug treatment, serum IL-6 (the first quartile as a reference, and the third quartile: odds ratio[ OR] 3.885, 95% confidence interval [ CI]1.361-7.189; the fourth quartile: OR 9.706, 95% CI 3.412-18.344), Glasgow Coma Scale score ( OR 2.174, 95% CI 1.325-4.538) and Fisher grade ( OR 3.267, 95% CI 1.638-6.725) were independently associated with DCI. The ROC curve showed that the area under the curve of serum IL-6 for predicting DCI was 0.777 (95% CI 0.706-0.849), and the optimal cut-off value was 13.01 ng/L. The sensitivity and specificity of predicting DCI were 72.4% and 71.4%, respectively. Conclusions:Serum IL-6 is an independent risk factor for DCI after aSAH, and has certain predictive value for DCI.

Objective To investigate the roles of TrkA and TrkB in radiation-induced hippocampal neurogenesis impairment.Methods Fifty-six rats were randomized into radiation group and sham control group.Radiation group received whole brain irradiation at a single dose of 10 Gy.The hippocampus were separated from rats in day 1,day 3,day 14 and 1 month after irradiation.Western blot and RT-PCR were applied to detect the protein levels and mRNA levels.Golgi staining was used to observe the dendritic spine of hippocampus.Immunofluorescence was performed to detect neural precursor's proliferation.Results Compared with control group,the numbers of dendritic spine significantly decreased after irradiation and its shape change obviously.Immunofluorescence showed a significant decrease in neural precursor's proliferation comparing with control group (t =6.49,P ＜ 0.05).Protein level of TrkA expression increased (t =2.64,3.06,4.80,2.64,P ＜ 0.05),while the levels of TrkB protein expression decreased significantly (t =4.59,3.06,2.81,2.57,P ＜ 0.05).The mRNA level of TrkA expressions increased (t =4.57,3.06,5.39,5.86,P ＜ 0.05),while the mRNA level of TrkB decreased (t =14.87,11.69,4.98,P ＜ 0.05).Conclusions As a signaling pathways downstream of NGF and BDNF,TrkA and TrkB may play an important role in radiation-induced neurogenesis impairment.

Objective To establish a stable and reliable mouse model as an alternative to the traditional model of impaired glucose tolerance induced by calorie restriction and its effect on glucose homeostasis.Methods Forty 16-week-old SPF C57BL/6J mice (half male and half female) were randomly divided into four groups by sex and the way of feeding.The mice in the ad libitum (AL) group had free access to basic diet, while the mice in the intermittent fasting (IF) group had normal diet and fasting on alternate days, with free access to water on the fasting days.The changes of body weight and blood glucose concentration in each group were monitored, and intraperitoneal glucose tolerance test and insulin tolerance test in mice were performed before and after the 12-week IF treatment.Results At 12 weeks after IF treatment, the body weight and blood glucose concentration of mice did not show significant difference.After i.p.injection of glucose, the blood glucose concentration of IF mice was less increased than the AL group, and after the insulin injection, the blood glucose concentration was more decreased.Compared to the AL group, the areas under the curve of tolerance test in the IF group were significantly decreased (P < 0.05).Conclusions After IF treatment, the mice show an enhanced sensitivity to insulin and improved glucose tolerance.This establishment method of mouse model of intermittent fasting is easy and simple, therefore, can be used as an effective alternative to traditional calorie restriction model of impaired glucose tolerance.

Objective To explore the effects of various radiation doses on the NFAT3/c4 signaling pathway and the improvement effect of exogenous brain-derived neurotrophic factor(BDNF)on this pathway. Methods Four groups of one-month-old Sprague-Dawley rats received radiation doses of 0,2,10,and 20 Gy, respectively, in a single radiation. At three days after radiation, exogenous BDNF was injected stereotaxically into the bilateral hippocampus. Western blotting and RT-PCR were used to assess the levels of NFAT3/c4-related proteins in the hippocampus. Results The results of Western blotting and RT-PCR showed that the level of NFAT3/c4 was reduced in a dose-and time-dependent manner after ionizing radiation. Compared with the radiation alone group,the ionizing radiation plus BDNF group had significantly increased levels of NFAT3/c4 and CaN with increases in radiation dose and time. Conclusions Whole brain radiotherapy inhibits the CaN/NFAT3/c4 signaling pathway. Exogenous BDNF can promote the NFAT-dependent transcription and then improve the cognitive function.

Objective To investigate the effects of low dose radiation on dendritic growth of newborn neurons in the hippocampus of young rat.Methods One month-old male rats were randomized into radiation group aind sham control group.Radiation group received whole brain irradiation at a single dose of 2 Gy.Retrovirus expressing green fluorescent protein (GFP) was used to label newborn neurons in the hippocampus through stereotaxic intracranial infusion.Immunofluorescence assays were performed to detect dendritic architecture alterations induced by irradiation at different time points.Results Compared with control group,the lengths of total dendrite and the longest dendrite significantly decreased at 2 and 4 weeks after irradiation (t =3.10,2.07,2.94,4.02,P ＜ 0.05).The branching points of new born neurons were also decreased significantly at 2 weeks post irradiation (t =2.23,P ＜ 0.05).The number of new born neurons reduced at 4 weeks post irradiation (t =8.43,P ＜ 0.05).Conclusions Low dose radiation could inhibit newborn neuron growth in the hippocampus of young rat,which may be one of the most important mechanisms involved in radiation-induced cognitive impairment.