Protective autophagy enhances antistress ability through AMPK/ULK1 signaling pathway in human immortalized keratinocytes.

Keratinocytes, located in the outermost layer of human skin, are pivotal cells to resist environmental damage. Cellular autophagy plays a critical role in eliminating damaged organelles and maintaining skin cell homeostasis. Low-dose 5-Aminolevulinic acid photodynamic therapy (ALA-PDT) has been demonstrated to enhance skin's antistress ability; however, the regulatory mechanisms of autophagy in keratinocytes remain unclear. In this study, we treated immortalized human keratinocytes (HaCaT cells) with low-dose ALA-PDT (0.5 mmol/L, 3 J/cm2). Through RNA-sequencing analysis, we identified that low-dose ALA-PDT modulated autophagy-related pathways in keratinocytes and pinpointed Unc-51-like kinase 1 (ULK1) as a key gene involved. Western blot results revealed that low-dose ALA-PDT treatment upregulated the expression of autophagy-related proteins Beclin-1 and LC3-II/LC3-I ratio. Notably, low-dose ALA-PDT regulated autophagy by inducing an appropriate level of reactive oxygen species (ROS), transiently reducing mitochondrial membrane potential, and decreasing adenosine triphosphate production; all these processes functioned on the AMP-activated protein kinase (AMPK)/ULK1 pathway to activate autophagy. Finally, we simulated external environmental damage using ultraviolet B (UVB) at a dose of 60 mJ/cm2 and observed that low-dose ALA-PDT mitigated UVB-induced cell apoptosis; however, this protective effect was reversed when using the autophagy inhibitor 3-methyladenine. Overall, these findings highlight how low-dose ALA-PDT enhances antistress ability in HaCaT cells through controlling ROS generation and activating the AMPK/ULK1 pathway to arouse cellular autophagy.

Site-Selective Tyrosine Reaction for Antibody-Cell Conjugation and Targeted Immunotherapy.

Targeted immunotherapies capitalize on the exceptional binding capabilities of antibodies to stimulate a host response that effectuates long-lived tumor destruction. One example is the conjugation of immunoglobulins (IgGs) to immune effector cells, which equips the cells with the ability to recognize and accurately kill malignant cells through a process called antibody-dependent cellular cytotoxicity (ADCC). In this study, a chemoenzymatic reaction is developed that specifically functionalizes a single tyrosine (Tyr, Y) residue, Y296, in the Fc domain of therapeutic IgGs. A one-pot reaction that combines the tyrosinase-catalyzed oxidation of tyrosine to o-quinone with a subsequent [3+2] photoaddition with vinyl ether is employed. This reaction installs fluorescent molecules or bioorthogonal groups at Y296 of IgGs or the C-terminal Y-tag of an engineered nanobody. The Tyr-specific reaction is utilized in constructing monofunctionalized antibody-drug conjugates (ADCs) and antibody/nanobody-conjugated effector cells, such as natural killer cells or macrophages. These results demonstrate the potential of site-selective antibody reactions for enhancing targeted cancer immunotherapy.

A fast multi-residue analysis of twenty-four classes of pesticide in sesame (Sesamum indicum L.) and their migration into processed products.

Sesame is widely used as a nutritional supplement or condiment because of its nutritious properties and palatable flavor. However, the extensive use of pesticides in sesame fields has paradoxically decreased the nutritional vantage. The current study used QuEChERS with a low-temperature freezing method to develop a multi-residue analytical approach to detect target analytes (pesticides) in sesame seed, sesame oil, sesame paste, and sesame meal. The migration ability of target pesticides during oil processing was investigated using HPLC-MS/MS and GC-MS: 35% of pesticides decreased, with processing factors (PFs) lower than 0.98, whereas 65% migrated from the seed to the oil during processing. The migration success of methoxyfenozide was the highest, while clothianidin and pymetrozine demonstrated a significantly lower rate of transfer. The results provide insight into the types of pesticides that should be used in farming practices of sesame to decrease the impact on human health.

Photo-Responsive Phase-Separating Fluorescent Molecules for Intracellular Protein Delivery.

Cellular membranes, including the plasma and endosome membranes, are barriers to outside proteins. Various vehicles have been devised to deliver proteins across the plasma membrane, but in many cases, the payload gets trapped in the endosome. Here we designed a photo-responsive phase-separating fluorescent molecule (PPFM) with a molecular weight of 666.8 daltons. The PPFM compound condensates as fluorescent droplets in the aqueous solution by liquid-liquid phase separation (LLPS), which disintegrate upon photoirradiation with a 405 nm light-emitting diode (LED) lamp within 20 min or a 405 nm laser within 3 min. The PPFM coacervates recruit a wide range of peptides and proteins and deliver them into mammalian cells. Photolysis disperses the payload from condensates into the cytosolic space. Altogether, a type of small molecules that are photo-responsive and phase separating are discovered; their coacervates can serve as transmembrane vehicles for intracellular delivery of proteins, whereas photo illumination triggers the cytosolic distribution of the payload.

The multifaceted role of placental growth factor in the pathogenesis and progression of bronchial asthma and pulmonary fibrosis: Therapeutic implications.

Placental growth factor (PlGF) is a glycosylated dimeric protein that is homologous to vascular endothelial growth factor (VEGF). PlGF expression is upregulated in patients with bronchial asthma, suggesting that it plays a role in the pathogenesis of asthma. Bronchial asthma is characterized by chronic airway inflammation and airway hyperresponsiveness (AHR). After recurrent asthma attacks, pulmonary fibrosis develops and leads to airway remodeling and a further decline in lung function. In this review, we focused on the pivotal role of PlGF in chronic airway inflammation, AHR, and airway remodeling during bronchial asthma. Furthermore, we summarized data showing that PlGF may be a potential therapeutic target in bronchial asthma.

Design, Synthesis, Application and Research Progress of Fluorescent Probes.

Fluorescent probes are sensitive, selective, nontoxic in detection and thus provided a new solution in biomedical, environmental monitoring, and food safety. In order to expand the application of fluorescent probes in various fields, the paper discusses the design, synthesis, and characterization of fluorescent probes, explores new design and development trends of fluorescent probes in various fields, and improves the performance and applicability of fluorescent probes by using new materials and technologies to meet the evolving demands of molecular detection in various fields.

Down-regulation of HuR inhibits pathological angiogenesis in oxygen-induced retinopathy.

HuR (also known as ELAV1), a ubiquitous RNA-binding protein, is implicated in the pathogenesis of diverse diseases via the mechanism of post-transcriptional regulation. Whether it is involved in pathological angiogenesis in oxygen-induced retinopathy is not clear. In this study, we detected HuR expression was increased in the retina of mouse model of oxygen-induced retinopathy (OIR) as well as in vascular endothelial cells exposed to hypoxia. With gain-of-function and loss-of-function studies using adenovirus infection, we found HuR over-expression promoted while HuR knockdown inhibited the migration, proliferation and tube formation of vascular endothelial cells. Moreover, HuR regulated the expression of VEGFA in vascular endothelial cells. We also found the retinal pathological angiogenesis in mouse OIR model was greatly reduced with HuR knockdown using recombinant AAV expressing HuR specific shRNA which was administered by intravitreal injection. The results of this study suggest HuR is involved in pathological angiogenesis via regulating angiogenic behaviors of endothelial cells, providing a potential target for the treatment of retinopathy of prematurity.

Macular Vascular Complexity Analysis of Diabetes Mellitus by Swept-Source Optical Coherence Tomographic Angiography.

PURPOSE: This study was designed to evaluate the associations between retinal vascular complexity features, including fractal dimension (FD) and blood vessel tortuosity (BVT), and the severity of diabetic retinopathy (DR) by using optical coherence tomographic angiography (OCTA). METHODS: In this prospective cross-sectional study, 1,282 ocular-treatment-naive patients with type 2 diabetes mellitus (DM) (1,059 without DR and 223 with DR) registered in the community of Guangzhou, China, were enrolled. OCTA was used to measure FD and BVT in the superficial capillary plexus (SCP) and the deep capillary plexus (DCP). Univariate and multivariate linear regression analyses were performed to analyze the correlation of FD and BVT in different layers with DR severity. RESULTS: In this study, 1,282 patients with DM (1,282 eyes), with a mean age of 64.2 ± 7.8 years, were included. FD in the DCP decreased and BVT in the DCP increased in patients with DR compared with those in patients without DR, even after adjusting for confounding factors (p < 0.05). Trend analysis showed a significant decrease in the FD values as the DR progressed, whereas the BVT progressively increased with worsening DR severity (p < 0.01). The FD in DCP had a statistically significant positive correlation with FD in SCP and a negative correlation with BVT in SCP and BVT in DCP in all of the participants, including the non-DR group, moderate DR group, and severe DR group (p < 0.01). CONCLUSIONS: FD and BVT determined using OCTA might be useful parameters for objectively distinguishing DR from non-DR and indicating DR progression.

Panaxatriol saponin ameliorates myocardial infarction-induced cardiac fibrosis by targeting Keap1/Nrf2 to regulate oxidative stress and inhibit cardiac-fibroblast activation and proliferation.

Cardiac fibrosis is a common precursor of ventricular dysfunction and heart failure. We investigated the role of oxidative stress in myocardial fibrosis and the protective effect of panaxatriol saponin (PTS) against myocardial infarction (MI)-induced cardiac fibrosis and explored the underlying mechanisms. In vitro, cell viability was tested using a cell counting kit. The reactive oxygen species (ROS) levels including hydrogen peroxide (H2O2) and superoxide anion (O2•-) were determined. Antioxidant enzyme levels were determined by immunofluorescence and Western blotting. Enzyme-linked immunosorbent assays, echocardiography, histological analysis, immunofluorescence staining, and molecular analysis were performed. Nuclear factor erythroid 2-related factor 2 (Nrf2) activation was evaluated by molecular docking and immunoprecipitation. Finally, the mechanism by which PTS inhibits cardiac fibrosis was investigated using the Nrf2 activator ML334 and a small interfering RNA for Nrf2. Ang II-induced differentiation of cardiac fibroblasts was associated with oxidative stress, characterized by upregulation of α-smooth muscle actin, increased reactive oxygen species production, and inhibition of superoxide dismutase-1 and heme oxygenase expression. In addition, PTS improved cardiac function and ameliorated cardiac fibrosis in MI rats. It also reduced Ang II-induced fibroblast differentiation and proliferation, suppressed oxidative stress, and disrupted the Kelch-like ECH-associated protein 1 (Keap1)-Nrf2 interaction by directly blocking the Nrf2 binding site in Keap1. Overexpression of Nrf2 by ML334 enhanced the antifibrotic effect of PTS. However, genetic ablation of Nrf2 abrogated the antifibrotic effect of PTS in cardiac fibrosis. Taken together, our findings suggest that Nrf2 has promise as a target and PTS as a therapeutic agent for cardiac fibrosis.

Pretreatment with Panaxatriol Saponin Attenuates Mitochondrial Apoptosis and Oxidative Stress to Facilitate Treatment of Myocardial Ischemia-Reperfusion Injury via the Regulation of Keap1/Nrf2 Activity.

Myocardial ischemia-reperfusion injury (MIRI) is a type of severe injury to the ischemic myocardium that can occur following recovery of blood flow, and for which, there is no effective treatment. Panaxatriol saponin (PTS), a major active component of P. notoginseng, has been used clinically to treat ischemia-related encephalopathy due to its antioxidant activity, but its effect on ischemic cardiomyopathy and underlying mechanism of action is still unclear. This study was performed to investigate the protective effect of PTS against MIRI and explore the potential underlying mechanisms. Hydrogen peroxide (H2O2) was used to stimulate cardiomyocytes, to mimic MIRI in vitro. Cell viability was tested using the CCK-8 method. The antioxidant activity of PTS in the H9c2 rat cardiomyocyte cell line was examined using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). The levels of superoxide dismutase-1 (SOD1), SOD2, and heme oxygenase (HO-1) were determined by Western blotting and/or immunofluorescence. The antiapoptotic effect of PTS was determined. In addition, mitochondrial permeability transition pore (mPTP) opening and mitochondrial membrane potential (ΔΨm) changes were assessed. Changes in Keap1/Nrf2 activation were evaluated by Western blotting analysis, molecular docking, and immunoprecipitation. An in vivo MIRI model was established in rats, and the myocardial infarct size was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Myocardial enzyme activities were determined by ELISA or biochemical analyses. Furthermore, changes in Nrf2 activation were evaluated, and the regulatory effect of PTS on cardiomyocyte apoptosis was examined using the Nrf2 blocker, ML385. The results showed that PTS ameliorated the cardiomyocyte injury induced by H2O2, characterized by increased cell viability, decreased reactive oxygen species (ROS) production, and promotion of SOD1, SOD2, and HO1 expression. PTS inhibited cardiomyocyte apoptosis in vivo and in vitro. PTS also reduced mPTP opening and stabilized ΔΨm in H9c2 cells. Molecular docking and immunoprecipitation study revealed that PTS can disrupt Keap1/Nrf2 interaction by directly blocking the binding site of Nrf2 in the Keap1 protein. In vivo, PTS decreased the area of myocardial infarction and attenuated pathological damage in ischemia-reperfusion (I/R) rats. In addition, the activities of myocardial injury markers were decreased by PTS. Finally, PTS regulated nuclear translocation of Nrf2, and ML385 blocked the therapeutic effect of PTS in vivo and in vitro. These results suggested that PTS has therapeutic potential for MIRI by targeting Keap1/Nrf2 activity.

Data Augmentation Using Bitplane Information Recombination Model.

The performance of deep learning heavily depend on the quantity and quality of training data. But in many fields, well-annotated data are so difficult to collect, which makes the data scale hard to meet the needs of network training. To deal with this issue, a novel data augmentation method using the bitplane information recombination model (termed as BIRD) is proposed in this paper. Considering each bitplane can provide different structural information at different levels of detail, this method divides the internal hierarchical structure of a given image into different bitplanes, and reorganizes them by bitplane extraction, bitplane selection and bitplane recombination, to form an augmented data with different image details. This method can generate up to 62 times of the training data, for a given 8-bits image. In addition, this generalized method is model free, parameter free and easy to combine with various neural networks, without changing the original annotated data. Taking the task of target detection for remotely sensed images and classification for natural images as an example, experimental results on DOTA dataset and CIFAR-100 dataset demonstrated that, our proposed method is not only effective for data augmentation, but also helpful to improve the accuracy of target detection and image classification.

Bcl-2 interacting protein 3 (BNIP3) promotes tumor growth in breast cancer under hypoxic conditions through an autophagy-dependent pathway.

Hypoxia-induced autophagy has been implicated in many cancers. Bcl-2 interacting protein 3 (BNIP3) has been associated with hypoxia, whose aberrant expression is involved in the carcinogenesis of breast cancer (BC). Here, we aim to investigate the role of hypoxia-induced autophagy and the mechanistic actions of the bioinformatically identified BNIP3 in BC. The expression pattern of BNIP3 in BC tissues and cell lines was examined using RT-qPCR and Western blot analyses. The binding affinity among BNIP3, BECN1 and BCL-2 was characterized by co-immunoprecipitation. BNIP3 expression was manipulated to assess its effects on BC cell malignant phenotypes, evaluated by cell counting kit-8, Transwell and wound healing assays, and on BC autophagy under hypoxic conditions. A BC tumor xenografts mouse model was further established to substantiate in vitro findings. Up-regulated expression of BNIP3 was found in BC tissues and cell lines, and BNIP3 expression was positively correlated with hypoxia exposure duration. BNIP3 knockdown restricted BC cell proliferation, invasion, and migration under hypoxic conditions. BNIP3 activated BC cell autophagy by inhibiting the binding between BCL-2 and BECN1 under hypoxic conditions. BNIP3-induced autophagy activation enhanced malignant phenotypes of BC cells, thus accelerating the tumorigenesis of BC cells in vivo. These data collectively supported the tumor-promoting role of BNIP3 in autophagy activation of BC under hypoxic conditions, highlighting a potential therapeutic target against BC.

Impact of procedural variability and study design quality on the efficacy of cell-based therapies for heart failure - a meta-analysis.

BACKGROUND: Cell-based therapy has long been considered a promising strategy for the treatment of heart failure (HF). However, its effectiveness in the clinical setting is now doubted. Because previous meta-analyses provided conflicting results, we sought to review all available data focusing on cell type and trial design. METHODS AND FINDINGS: The electronic databases PubMed, Cochrane library, ClinicalTrials.gov, and EudraCT were searched for randomized controlled trials (RCTs) utilizing cell therapy for HF patients from January 1, 2000 to December 31, 2020. Forty-three RCTs with 2855 participants were identified. The quality of the reported study design was assessed by evaluating the risk-of-bias (ROB). Primary outcomes were defined as mortality rate and left ventricular ejection fraction (LVEF) change from baseline. Secondary outcomes included both heart function data and clinical symptoms/events. Between-study heterogeneity was assessed using the I2 index. Subgroup analysis was performed based on HF type, cell source, cell origin, cell type, cell processing, type of surgical intervention, cell delivery routes, cell dose, and follow-up duration. Only 10 of the 43 studies had a low ROB for all method- and outcome parameters. A higher ROB was associated with a greater increase in LVEF. Overall, there was no impact on mortality for up to 12 months follow-up, and a clinically irrelevant average LVEF increase by LVEF (2.4%, 95% CI = 0.75-4.05, p = 0.004). Freshly isolated, primary cells tended to produce better outcomes than cultured cell products, but there was no clear impact of the cell source tissue, bone marrow cell phenotype or cell chricdose (raw or normalized for CD34+ cells). A meaningful increase in LVEF was only observed when cell therapy was combined with myocardial revascularization. CONCLUSIONS: The published results suggest a small increase in LVEF following cell therapy for heart failure, but publication bias and methodologic shortcomings need to be taken into account. Given that cardiac cell therapy has now been pursued for 20 years without real progress, further efforts should not be made. STUDY REGISTRY NUMBER: This meta-analysis is registered at the international prospective register of systematic reviews, number CRD42019118872.

Changes in Conjunctival Microbiota Associated With HIV Infection and Antiretroviral Therapy.

Purpose: HIV infection is associated with a variety of ocular surface diseases. Understanding the difference of the ocular microbiota between HIV-infected and healthy individuals as well as the influence of antiretroviral therapy will help to investigate the pathogenesis of these conditions. Methods: A cross-sectional study was conducted on subjects including HIV-negative individuals, untreated HIV-infected individuals, and HIV-infected individuals with antiretroviral therapy. Conjunctival microbiota was assessed by bacterial 16S rRNA sequencing of the samples obtained from the conjunctival swab. Results: The microbial richness in ocular surface was similar in HIV-negative, untreated HIV-positive, and highly active antiretroviral therapy (HAART) subjects. The bacterial compositions were similar in the two HIV infection groups but were significantly different from the HIV-negative group. HAART changed the beta diversity of bacterial community as determined by Shannon index. CD4+ T cell count had no significant influence on the diversity of ocular microbiota in HIV-infected individuals. Conclusions: The data revealed the compositional and structural difference in conjunctival microbial community in subjects with and without HIV infection, indicating that HIV infection or its treatment, may contribute to ocular surface dysbiosis.

Nanoparticle Delivery of CRISPR/Cas9 for Genome Editing.

The emerging clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated system (Cas) gene-editing system represents a promising tool for genome manipulation. However, its low intracellular delivery efficiency severely compromises its use and potency for clinical applications. Nanocarriers, such as liposomes, polymers, and inorganic nanoparticles, have shown great potential for gene delivery. The remarkable development of nanoparticles as non-viral carriers for the delivery of the CRISPR/Cas9 system has shown great promise for therapeutic applications. In this review, we briefly summarize the delivery components of the CRISPR/Cas9 system and report on the progress of nano-system development for CRISPR/Cas9 delivery. We also compare the advantages of various nano-delivery systems and their applications to deliver CRISPR/Cas9 for disease treatment. Nano-delivery systems can be modified to fulfill the tasks of targeting cells or tissues. We primarily emphasize the novel exosome-based CRISPR/Cas9 delivery system. Overall, we review the challenges, development trends, and application prospects of nanoparticle-based technology for CRISPR/Cas9 delivery.

Hierarchical responsive micelle facilitates intratumoral penetration by acid-activated positive charge surface and size contraction.

Integrating these features of acid-activated positively charged surface and size contraction into single nanoparticle would be an effective strategy for enhancing cellular uptake, intratumoral penetration and accumulation. Here, hierarchical responsive micelle (HVDMs) was developed via RAFT reaction as multifunctional polymer-drug conjugate for maximizing penetration and therapeutic effect against MCF-7 tumor by combining positively charged surface with size contraction: surface zeta-potential reversal (-2 to +12 mV) by protonation of PHEME and size contraction (~81-~41 nm) by simultaneous hydrophobic/hydrophilic conversion (pH ≈ 6.7); the disintegration of hydrazone bond between hydrophobic PVB and DOX triggered drug release (pH ≈ 5.0). The in vitro structural stabilization, cellular uptake and anti-proliferative efficiency were significantly higher than other control groups (CVDMs and HSDMs) at pH 6.7. The markedly increased penetration depth, cellular internalization and anti-tumor efficiency were confirmed in 3D MCSs spheroids at pH 6.7, and the ex vivo DOX fluorescence images further verified obvious penetration and accumulation in internal region of solid tumor. The antitumor effect in vivo demonstrated that HVDMs accelerated tumor atrophy, induced intratumoral cells apoptosis and alleviated system toxicity.

Integrated serum pharmacochemistry and network pharmacological analysis used to explore possible anti-rheumatoid arthritis mechanisms of the Shentong-Zhuyu decoction.

ETHNOPHARMACOLOGICAL RELEVANCE: Shentong-Zhuyu decoction (STZYD) has been recognized by the Chinese National Administration of Traditional Chinese Medicine (TCM) as a classic TCM formula. Use of STZYD has shown a satisfactory clinical therapeutic outcome for rheumatoid arthritis (RA); despite this, its bioactive chemical composition and relevant mechanism(s) of this action have not been clearly elucidated. AIM OF THE STUDY: To explore the bioactive chemical composition of STZYD used for RA treatment and its possible mechanism(s) of action. MATERIALS AND METHODS: Serum pharmacochemistry mediated by the UPLC-Q-Exactive MS/MS method was employed to identify the absorbed phytochemical compounds in serum derived from STZYD, which were commonly considered as the potential bioactive compounds. And then, these components were used to construct a compound-target network for RA using a network pharmacology approach, to predict the possible biological targets of STZYD along with potential signaling pathways. Afterwards, we established a Complete Freund's adjuvant (CFA)-induced RA rat model, and observed the anti-RA effect of STZYD by a series of indexes, including foot swelling, ankle diameter, arthritis score, morphological and radiographic analysis, serum inflammatory factors, and histopathological analysis of synovial tissues. Particularly, the predicted pathway by the combination of serum pharmacochemistry and network pharmacology was further validated using RT-qPCR, Western blot, and immunohistochemical analyses in animal experiment. RESULTS: Totally, 38 compounds derived from STZYD have been identified by serum sample analysis. Based on it, 387 genes related to these identified compounds in STZYD and 3807 genes related to RA were collected by network pharmacology. Critically, KEGG analysis indicated that the PI3K/AKT signaling pathway was recommended as one of the main pathway related to anti-RA effect of STZYD. Experimentally, STZYD significantly alleviated CFA-induced arthritis without any visible side-effects. Compared to the RA model group without any treatment, the treatment of STZYD significantly reduced the expression of both mRNA and protein targets in the PI3K/AKT signaling pathway. Furthermore, this result was also corroborated by immunohistochemistry analysis. All these studies could effectively corroborate the predicted result as above, suggested that the feasibility of this integrated strategy. CONCLUSION: This study provided a useful strategy to identify bioactive compounds and the potential mechanisms for TCM formula by integrating serum pharmacochemistry and network pharmacology.

Anti-platelet aggregation of Panax notoginseng triol saponins by regulating GP1BA for ischemic stroke therapy.

BACKGROUND: Panax notoginseng triol saponins (PTS) has been used clinically for ischemic stroke therapy (IST) in China for more than 17 years due to its anti-platelet aggregation and neuro-protective effects, but its mechanism of action is not fully understand. In this study, anti-platelet aggregation-related protein analysis and computer simulations of drug-protein binding interactions were performed to explore the mechanism of the effects of PTS against ischemic stroke in an ischemia reperfusion model. METHODS: Three oral doses of PTS were administered in a model of middle cerebral artery occlusion (MCAO) in rats. Panax notoginseng total saponins (PNS) and a combination of PTS and aspirin were chosen for comparison. To evaluate therapeutic effects and explore possible mechanisms of anti-platelet aggregation, we measured cerebral infarct size and water content in brain tissue, histomorphological changes, expression of related factors (such as arachidonic acid metabolites) and platelet receptors in serum, as well as the binding affinity of PTS for platelet adhesion receptors. RESULTS: Compared with PNS, PTS showed a stronger and more potent anti-platelet aggregation effect in MCAO model rats. The combination of PTS and aspirin could reduce adverse gastrointestinal effects by regulating the TXA2/PGI2 ratio. We demonstrated for the first time that PTS was able to regulate Glycoprotein Ib-α (GP1BA) in a model animal. The binding of ginsenoside Rg1 and GP1BA could form a stable structure. Moreover, PTS could reduce von Willebrand factor (VWF)-mediated platelet adhesion to damaged vascular endothelium, and thus enhance the probability of anti-platelet aggregation and anti-thrombosis under pathological conditions. CONCLUSIONS: Our results showed that GP1BA was closely related to the anti-platelet aggregation action of PTS, which provided new scientific and molecular evidence for its clinical application.

A secondary iris cyst with 3 years of asymptomatic period following a blunt ocular trauma.

PURPOSE: To present a relatively uncommon case with a secondary iris cyst in the anterior chamber and its successful management with an anterior chamber mass excision surgery. CASE REPORT: A 46-year-old Chinese woman presented with a dark shadow in her left eye for 6 months without any other discomfort. She had a history of blunt ocular trauma by a badminton strike 3 years ago. Slit-lamp examination showed a small, nearly circular, sharply demarcated, and movable mass in the anterior chamber OS, which could change its position with head tilt. The anterior segment optical coherence tomography revealed a well-circumscribed cystic lesion in the anterior chamber with higher reflective outer layer and lower internal reflectivity. An anterior chamber mass removal surgery was performed without recurrence up to 1 year. CONCLUSION: Secondary free-floating iris cyst following a blunt trauma is rarely reported. It is relatively stable and nonprogressive so it may remain asymptomatic for a long time. Appropriate imaging techniques are necessary for facilitating diagnosis and therapy. Therapeutic management should be considered if visual symptoms arise, especially when complications occur.