Compared to other refractive surgeries, the implantable collamer lens(ICL)implantation procedure has become one of the most popular surgical options in refractive surgery. ICL surgery offers advantages such as reversibility, high-definition visual outcomes, and preservation of the corneal anatomical structure. The V4c model, which features a central port, is currently the most widely used in clinical practice and eliminates the need for peripheral iridotomy during the perioperative period. Although excellent uncorrected visual acuity can be achieved postoperatively, some patients may experience visual disturbances in the early postoperative period, such as halo and glare, which may affect visual comfort particularly under low-light conditions. This article reviews visual quality metrics after ICL V4c implantation, including higher-order aberrations(HOA), modulation transfer function(MTF), and contrast sensitivity(CS), along with influencing factors, and discusses potential relative deficits in postoperative visual quality and their underlying mechanisms.

The core pathological process of optic neuropathy caused by glaucoma is the progressive loss of retinal ganglion cells(RGCs). As the primary glial cells in the retina, Müller glial cells play a crucial and complex dual regulatory role in the pathological microenvironment of glaucoma. On one hand, Müller cells can exert endogenous protective effects by secreting neurotrophic factors, enhancing RGC viability through co-culture, and regulating glutamate metabolism. On the other hand, under sustained stress such as elevated intraocular pressure, Müller cells are activated by mechanosensitive channels(e.g., TRPV4), transforming into a reactive gliosis phenotype. This leads to the release of inflammatory cytokines that exacerbate RGC apoptosis, while their metabolic reprogramming and epigenetic alterations also contribute to the process of neuronal injury. This article systematically reviews the research progress on the dual roles of Müller cells in protecting and damaging the optic nerve in glaucoma, exploring new therapeutic strategies for neuroprotection by regulating their cellular states. It outlines the main controversies and unresolved issues in this field and, based on the latest research advances, analyzes the implications of targeting Müller cells for current clinical treatments and future development trends.

In recent years, the global prevalence of myopia has continued to rise. In China, myopia shows a trend toward widespread prevalence, earlier onset, and greater severity, and high myopia poses a serious threat to adolescent ocular health. Orthokeratology is currently one of the most effective clinical interventions for slowing myopia progression, yet its exact mechanisms of action have not been fully elucidated. Focusing on the various hypotheses proposed in the literature, this review summarizes the role of peripheral retinal defocus, choroidal thickness and blood flow, higher-order aberrations, accommodation, and biomechanics in myopia control with orthokeratology lenses. Specifically, the induction of peripheral myopic defocus through the reverse-geometry design of orthokeratology lenses constitutes the core mechanism by which axial elongation is slowed. After lens wear, choroidal thickening and increased blood perfusion improve the nutritional supply to the outer retina and inhibit scleral remodeling. Increases in higher-order aberrations, such as spherical aberration and coma, expand the depth of focus and reduce accommodative lag. Improvements in accommodative function and alterations in corneal biomechanics also act synergistically. These mechanisms are interrelated and act in a cascading manner to jointly inhibit axial elongation. This review aims to provide a theoretical basis for a deeper understanding of the mechanisms of orthokeratology lenses and to offer clinical references for individualized lens fitting, optimized lens design, and future research on myopia prevention and control.

Drug delivery system (DDS) holds promise in reducing off-target effects of antitumor drugs. The carriers of antitumor drug DDS mainly include nanoparticles, small molecules, nucleic acids, peptides, antibodies and cells, which carry antitumor drugs through linker to deliver the drugs to specific tumor tissues and cells. DDS will propel progress in the field of cancer precision medicine.

Tumor-related death is often associated with tumor metastasis. Metastasis process includes the acquisition of dissemination traits of tumor cells, dormancy awakening, and distant growth. Changing dissemination traits of cancer cells, maintaining and killing dormant tumor cells, editing pre-metastatic microenvironment, and reprogramming hallmarks of cancer will be key to block tumor metastasis. Bevacizumab, denosumab and cilengitide have been approved for clinical therapies. Tumor screening based on blood tests combined with artificial intelligence will provide new targeted metastasis strategies for clinical treatment.

Apparent accommodation originates from the residual accommodation function after the absence of classic lens accommodation, serving as a critical theoretical framework in the study of visual function after refractive cataract surgery. Different from Von Helmholtz's theory, which focuses on lens deformation, it evaluates the overall accommodation capability of the eye excluding the lens, with its mechanisms remaining debated. Apparent accommodation refers to the character that pseudophakic eyes retain a certain degree of refractive accommodation after natural lens removal or intraocular lens(IOL)implantation, despite the loss of physiological accommodation. This paper systematically reviews the historical development of apparent accommodation and the advances in assessment techniques, which have gradually contributed to the re-evaluation and expansion of classical theories of physiological accommodation. Recent studies attempt to decipher the synergistic effects between pupil, corneal, and central cognitive processing by integrating optical parameter measurements with neural adaptation. This reflects a shift in the field from a singular anatomical explanation to a more interdisciplinary and multi-dimensional model.

Purtscher retinopathy is an occlusive retinal microangiopathy typically associated with trauma. It is characterized by a series of retinal pathological manifestations, such as cotton wool spots, multiple gray plaques(Purtscher spots)in the posterior pole, and intraretinal hemorrhage. Notably, there is no history of direct ocular trauma, as this condition is commonly observed in cases of severe crush injuries to the head, chest, abdomen, limbs, and other regions. Purtscher-like retinopathy, on the other hand, describes extensive retinopathy occurring in the absence of trauma, often associated with conditions such as pancreatitis and connective tissue diseases. With advancements in imaging-assisted ultrastructure research, the understanding of the pathogenesis of this retinopathy has evolved. Initially, it was attributed to trauma-induced injury and the subsequent cascade of damage repair processes. However, current theories suggest that systemic lesions involving lipase, free fatty acids, or complement activation play a significant role in inducing endothelial damage to small retinal blood vessels, ultimately leading to vascular occlusion. The pathogenesis of Purtscher retinopathy is not isolated; it is now widely believed to involve anterior capillary arteriole embolism resulting from changes in retinal microvascular permeability. In addition to embolization, other mechanisms such as retinal vascular-lymphatic extravasation, vasospasm, endothelial injury, and complement activation are also considered crucial contributors to the development of this condition. This paper starts from the inflammation and vascular cascade reaction in the pathological process of trauma and non-trauma, and expounds the pathological mechanism of the disease so as to guide the clinical diagnosis and treatment, in order to find new ideas of diagnosis and treatment in the research of rare diseases.

There are differences in the images of the same visual object projected onto the retinas of the two eyes.Stereopsis is the perceptual ability of the brain to discern three-dimensional depth from these two-dimensional images with binocular disparities,enabling humans to accurately perceive the relative distance between objects and assess their relative depth in space.Panum's fusional area(PFA)encompasses the depth range,including the horopter where the visual object lies and the areas in front of and behind it,within which fused single vision can be achieved.Visual function within the PFA is closely related to the formation of depth perception.The monocular visual direction,the depth of the binocular horopter position,and the measurement methods and models for the theoretical horopter and empirical horopter are all closely asso-ciated with the characteristics of depth perception within the PFA range.This holds significant importance for studying the construction process of stereopsis.

Glaucoma is a blinding eye disease characterized by optic nerve damage and visual field defects,with a complex pathogenesis.Studies have shown that the abnormal activation of the cyclic GMP-AMP synthase-stimulator of in-terferon genes(cGAS-STING)signaling pathway may be closely related to the occurrence and development of glaucoma.New therapeutic strategies targeting this pathway,such as the cGAS small-molecule inhibitor RU.521 and the STING inhibi-tor H-151,have been shown to effectively alleviate pathological changes associated with glaucoma,and research into their mechanisms of action is becoming increasingly in-depth.This article aims to review the basic mechanisms of the cGAS-STING signaling pathway and its role in the pathogenesis of glaucoma,as well as the latest research progress of compounds targeting cGAS and STING in the treatment of glaucoma,in order to provide a new perspective for the immunotherapy of glaucoma.

Radiation-induced rectal injury (RRI) refers to inflammatory intestinal complications of patients with pelvic cavity, abdominal cavity and retroperitoneal tumor during or after radiotherapy, presenting symptoms such as diarrhea, abdominal pain, anal distension, bloody stool, etc. In severe cases, rectovaginal fistula, intestinal obstruction, canceration can occur, adversely affecting the quality of life of patients. The clinical factors of RRI involve total radiotherapy dose, tumor volume, radiotherapy mode and patient-related risk factors. The diagnosis mainly depends on imaging examinations (such as CT, MRI and ultrasound), endoscopy and laboratory examination. The mechanism of RRI is related to intestinal epithelial cell destruction, stem cell injury, microvascular changes and microbial flora imbalance. At present, there is no gold standard for RRI treatment, and the main measures include surgical treatment, internal medicine treatment, hyperbaric oxygen therapy and fecal microbiota transplantation, etc. In this article, the latest progress in the pathogenesis, diagnosis and treatment of RRI was reviewed.