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.

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.

As one of the typical bioorthogonal chemistry reactions, click chemistry joins molecules similar to “Lego”. Bioorthogonal click chemistry is used to modify cancer cells, design antitumor drugs, delivery drugs, manipulate immune cells, and help preclinical evaluation. Click chemistry provides a promising approach for discovering molecules and targeting cancer in cancer research.

Optical tweezers are a means to manipulate objects with light. Optical tweezers can obtain a nanometer space, piconewton force, and a millisecond resolution; thus, they are excellently suited for studying biological processes from the single-cell to the single-molecule level. Optical tweezers can screen and manipulate tumor cells, study single molecule, and monitor cancer treatments. Thus, optical tweezers will promote the progress of cancer research and treatments.

Cancer phenotypic plasticity includes dedifferentiation, blocked differentiation and trans- differentiation, and differentiation therapy targeting tumor cell plasticity is becoming a new therapeutic model for human cancers. The application of inducing differentiation, initiating differentiation and regulating differentiation in tumor differentiation therapy will promote the directed differentiation of tumor cells into mature cells and the remodeling of phenotypes, thus to achieve the purpose of cancer treatment.

Objective In this study,we analyzed the transcriptome sequences of Kupffer cells exposed to simulated microgravity for 3 d and conducted biological experiments to determine how microgravity initiates apoptosis in Kupffer cells. Methods Rotary cell culture system was used to construct a simulated microgravity model.GO and KEGG analyses were conducted using the DAVID database.GSEA was performed using the R language.The STRING database was used to conduct PPI analysis.qPCR was used to measure the IL1B,TNFA,CASP3,CASP9,and BCL2L11 mRNA expressions.Western Blotting was performed to detect the level of proteins CASP3 and CASP 9.Flow cytometry was used to detect apoptosis and mitochondrial membrane cells.Transmission electron microscopy was used to detect changes in the ultrastructure of Kupffer cells. Results Transcriptome Sequencing indicated that simulated microgravity affected apoptosis and the inflammatory state of Kupffer cells.Simulated microgravity improved the CASP3,CASP9,and BCL2L11 expressions in Kupffer cells.Annexin-V/PI and JC-1 assays showed that simulated microgravity promoted apoptosis in Kupffer cells.Simulated microgravity causes M1 polarization in Kupffer cells. Conclusion Our study found that simulated microgravity facilitated the apoptosis of Kupffer cells through the mitochondrial pathway and activated Kupffer cells into M1 polarization,which can secrete TNFA to promote apoptosis.

Cytotoxic agents, molecular targeted agents and immune checkpoint inhibitors consist of the fundamental model of cancer systematic treatments. Anti-tumor drugs with new mechanisms of action, including kinase inhibitors, therapeutic antibodies, nucleic acid blocks, therapeutic vaccines, gene-edited immune cells, living microrobots and digital drugs, will change this existing model. Drugs targrting nerves, polysaccharides, lipids and microflora may gradually enter clinical applications.

Objective The aim of this study was to explore the correlation between the methylation status of microRNA let-7a-3 in esophageal squamous cell carcinoma(ESCC)and the expression of insulin-like growth factor 2(IGF-Ⅱ).Methods The methylation specific PCR(qMSP)was used to detect the methylation status of let-7a-3 in 83 cases of esophageal cancer and corre-sponding adjacent normal tissues.The enzyme linked immunosorbent assay(ELISA)was used to detect the expression of IGF-Ⅱ in plasma.Results The degree of let-7a-3 methylation in cancer tissues of 83 patients with ESCC was significantly higher than that in normal tissues adjacent to cancer(P<0.001).The expression of IGF-Ⅱ in the plasma of 83 patients with ESCC was positively corre-lated with the methylation degree of let-7a-3,which was statistically significant(r=0.600,P<0.001).Conclusion microRNAlet-7a-3 may participate in the occurrence and progression of ESCC by regulating the methylation of downstream molecules,which is of great significance for understanding the mechanisms of ESCC development and providing a basis for the diagnosis and prognosis of ESCC.

Immune checkpoint consists of inhibitory and stimulatory molecules. Drugs blocking inhibitory checkpoint programmed cell death receptor-1 (PD-1) and cytotoxic T lymphocyte-associated molecule-4 (CTLA-4) are currently utilized for wide variety of human cancers. Agonists of stimulatory checkpoints such as GITR, OX40, 4-1BB, ICOS, CD40 and STING are undergoing critical clinical trials. Immune checkpoint agonists that affect stimulatory checkpoint molecules develop rapidly, and immune agonist antibodies thus represent an important approach for solid tumor treatments.

Objective:To explore an early mobilization plan for oral cancer patients after free flap reconstruction and evaluate the application effect of the plan.Methods:This study was a prospective randomized controlled trial. A total of 173 patients undergoing free flap reconstruction surgery from December 2018 to December 2021 in the second ward of Peking University School and Hospital of Stomatology were selected. The patients were randomly divided into the control group (87 cases) and the intervention group (86 cases) by cluster randomized grouping. The control group received the routine nursing plan, that was, head immobilization for 4 days after surgery, and patients performed sat up and off-bed activity on the 5th day. The intervention group received the early mobilization plan, that was, patients sat up on the 2nd day after surgery and performed off-bed activity on the 3rd day. The incidence of vascular compromise, postoperative complications, sleep time in the first 5 days after surgery, catheter removal time, hospitalization duration and expenses were compared between the two groups.Results:The incidence of postoperative pulmonary infection, the daily sleep time in the first 5 days after surgery, the time for removing nasogastric tube, trachea cannula, and urinary catheter were 7.0%(6/86), (5.0 ± 1.0) h/d, (11.8 ± 7.3) d, (6.1 ± 3.2) d, (3.6 ± 0.6) d in the intervention group, and 13.8%(12/87), (4.4 ± 1.3) h/d, (14.2 ± 5.8) d, (7.3 ± 1.7) d, (4.0 ± 0.9) d in the control group, all differences were statistically significant ( χ2 = 3.89, t values were -3.57 - -2.44, all P<0.05). There was no significant difference in the incidence of rascular compromise, hospitalization duration and expenses between the two groups (all P>0.05). Conclusions:For patients undergoing free tissue flap reconstruction, it is safe to sit up on the 2nd day and get out of bed on the 3rd day, which can reduce the incidence of pulmonary infection, improve patient sleep, and shorten the indwelling time of nasogastric tube, trachea cannula and urinary catheter.