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Objective: Midpalatal expansion (MPE) is routinely employed to treat transverse maxillary arch deficiency. Neutrophils are indispensable for recruiting bone marrow stromal cells (BMSCs) at the initial stage of bone regeneration. This study aimed to explore whether neutrophils participate in MPE and how they function during bone formation under mechanical stretching. Materials and Methods: The presence and phenotype of neutrophils in the midpalatal suture during expansion were detected by flow cytometry and immunofluorescence staining. The possible mechanism of neutrophil recruitment and polarization was explored in vitro by exposing vascular endothelial cells (VECs) to cyclic tensile strain. Results: The number of neutrophils in the distracted suture peaked on Day 3, and N2‐type neutrophils significantly increased on Day 5 after force application. The depletion of circulatory neutrophils reduced bone volume by 43.6% after 7‐day expansion. The stretched VECs recruited neutrophils via a CXCR2 mechanism in vitro, which then promoted BMSC osteogenic differentiation through the VEGFA/VEGFR2 axis. Consistently, these neutrophils showed higher expression of canonical N2 phenotype genes, including CD206 and Arg1. Conclusions: These results suggested that neutrophils participated in early bone formation during MPE. Based on these findings, we propose that stretched VECs recruited and polarized neutrophils, which, in turn, induced BMSC osteogenic differentiation. [ABSTRACT FROM AUTHOR]

Hyperlipidemia is a risk factor for stroke, and worsens neurological outcome after stroke. Endothelial progenitor cells (EPCs), which become dysfunctional in cerebral ischemia, hold capacity to promote revascularization. We investigated the role of dyslipidemia in impairment of EPC-mediated angiogenesis in cerebral ischemic mice. The high fat diet (HFD)-fed mice following by ischemic stroke exhibited increased infarct volumes and neurological severity scores, and poorer angiogenesis. Bone marrow-EPCs treated with palmitic acid (PA) showed impaired functions and inhibited activity of AMP-activated protein kinase (AMPK). Notably, AMPK deficiency aggravated EPC dysfunction, further decreased mitochondrial membrane potential, and increased reactive oxygen species level in EPCs with PA treatment. Furthermore, the expression of fatty acid oxidation (FAO)-related genes was remarkably reduced, and carnitine palmitoyltransferase 1A (CPT1A) protein expression was downregulated in AMPK-deficient EPCs. AMPK deficiency aggravated neurological severity scores and angiogenesis in ischemic brain of HFD-fed mice, accompanied by suppressed protein level of CPT1A. EPC transplantation corrected impaired neurological severity scores and angiogenesis in AMPK-deficient mice. Our findings suggest that AMPK deficiency aggravates poor angiogenesis in ischemic brain by mediating FAO and oxidative stress thereby inducing EPC dysfunction in hyperlipidemic mice. [ABSTRACT FROM AUTHOR]

Simple Summary: This study presented an artificial intelligence-based classification emphasizing error identification and quantification of cellularity and nuclear morphological features in digital pathological images of common astrocytic tumors. The identification of incorrect predictions was essential for the subsequent development of better techniques. Quantifying cellularity and nuclear morphological features brought deeper insights into neoplastic morphology and paved the way for further development of a scoring system for objective classification and precision diagnosis to improve interobserver variations. Interobserver variations in the pathology of common astrocytic tumors impact diagnosis and subsequent treatment decisions. This study leveraged a residual neural network-50 (ResNet-50) in digital pathological images of diffuse astrocytoma, anaplastic astrocytoma, and glioblastoma to recognize characteristic pathological features and perform classification at the patch and case levels with identification of incorrect predictions. In addition, cellularity and nuclear morphological features, including axis ratio, circularity, entropy, area, irregularity, and perimeter, were quantified via a hybrid task cascade (HTC) framework and compared between different characteristic pathological features with importance weighting. A total of 95 cases, including 15 cases of diffuse astrocytoma, 11 cases of anaplastic astrocytoma, and 69 cases of glioblastoma, were collected in Taiwan Hualien Tzu Chi Hospital from January 2000 to December 2021. The results revealed that an optimized ResNet-50 model could recognize characteristic pathological features at the patch level and assist in diagnosis at the case level with accuracies of 0.916 and 0.846, respectively. Incorrect predictions were mainly due to indistinguishable morphologic overlap between anaplastic astrocytoma and glioblastoma tumor cell area, zones of scant vascular lumen with compact endothelial cells in the glioblastoma microvascular proliferation area mimicking the glioblastoma tumor cell area, and certain regions in diffuse astrocytoma with too low cellularity being misrecognized as the glioblastoma necrosis area. Significant differences were observed in cellularity and each nuclear morphological feature among different characteristic pathological features. Furthermore, using the extreme gradient boosting (XGBoost) algorithm, we found that entropy was the most important feature for classification, followed by cellularity, area, circularity, axis ratio, perimeter, and irregularity. Identifying incorrect predictions provided valuable feedback to machine learning design to further enhance accuracy and reduce errors in classification. Moreover, quantifying cellularity and nuclear morphological features with importance weighting provided the basis for developing an innovative scoring system to achieve objective classification and precision diagnosis among common astrocytic tumors. [ABSTRACT FROM AUTHOR]

Background: This study aims to explore the clinical value of low disease activity state (LDAS) in the treat-to-target strategy of pediatric systemic lupus erythematosus (pSLE) and find the risk factors for never reaching LDAS. Methods: A total of 272 children with SLE who were diagnosed and followed up in two tertiary hospitals in China during the period from January 2012 to December 2019 were involved in this study, and the clinical presentation, pathology, and treatment were retrospectively studied. Results: The male-to-female ratio was 1:5.2, the age at diagnosis was 11.1 years (IQR, 9.8-13.1 years), the disease duration was 1.0 month (IQR, 0.5-2.0 months), and follow-up was 36.5 months (IQR, 25.7-50.9 months). During follow-up, 230 children achieved LDAS, and 42 were never been in. Male (P = 0.018), mucosal ulcer (P = 0.048), liver function damage (P = 0.026), cardiac effusion (P = 0.034), anemia (P = 0.048), urine red blood cells (P = 0.017), urinary leukocytes (P = 0.032), and endothelial cell proliferation in renal biopsy (P = 0.004)--these indexes have statistical differences between the two groups in the baseline. At baseline, endothelial cell proliferation (P = 0.02) is an independent risk factor for never achieving LDAS by multivariate logistic analysis. During follow-up, non-compliance was a risk factor for never achieving LDAS by comparing between groups. Children with biologics achieved LDAS at a higher rate than children without biologics (P = 0.038). The proportion of organ damage in patients never been in LDAS was significantly higher than that in patients who achieved LDAS (P < 0.001). Conclusion: Endothelial cell proliferation in renal biopsy and non-compliance during follow-up were independent risk factors for never achieving LDAS. At the end of the follow-up, the organ damage in the remission group was similar to that in the LDAS group, indicating that LDAS can be used as a target for pSLE treatment. [ABSTRACT FROM AUTHOR]

Thrombophlebitis is the inflammatory condition characterized by obstruction of one or more vessels, commonly in the legs, due to the formation of blood clots. It has been reported that traditional Chinese medicine, including Mailuoning injection, is advantageous for treating inflammatory and blood disorders. This research assessed the therapeutic efficacy of Mailuoning injection in the treatment of thrombophlebitis in rodents, as well as investigated its impact on fibrinolysis, inflammation, and coagulation. An experimental setup for thrombophlebitis was established in rodents via modified ligation technique. Five groups comprised the animals: sham operation group, model group, and three Mailuoning treatment groups (low, medium, and high dosages). The pain response, edema, coagulation parameters (PT, APTT, TT, FIB), serum inflammatory markers (IL‐6, TNF‐α, CRP), and expression levels of endothelial markers (ICAM‐1, VCAM‐1, NF‐κB) were evaluated. Blood flow and vascular function were further assessed by measuring hemorheological parameters and the concentrations of TXB2, ET, and 6‐k‐PGF1α. In contrast to the sham group, model group demonstrated statistically significant increases in endothelial expression levels, coagulation latencies, and inflammatory markers (p < 0.05). The administration of mailing, specifically at high and medium dosages, resulted in a substantial reduction in inflammatory markers, enhancement of coagulation parameters, suppression of ICAM‐1 and VCAM‐1 expression, and restoration of hemorheological measurements to baseline (p < 0.05). Significantly higher concentrations of 6‐k‐PGF1α and lower levels of TXB2 and ET were observed in high‐dose group, suggesting that pro‐ and anti‐thrombotic factors were restored to equilibrium. Utilization of Mailuoning injection in rat model of thrombophlebitis exhibited significant therapeutic impact. This effect was manifested through pain alleviation, diminished inflammation, enhanced blood viscosity and facilitation of fibrinolysis. The study indicated that Mailuoning injection may serve as a viable therapeutic option for thrombophlebitis, potentially aiding in the improvement of wound healing by virtue of its anti‐inflammatory and blood flow‐enhancing characteristics. [ABSTRACT FROM AUTHOR]

Objective. To determine prognostic role of endothelial progenitor cells (EPCs) in intensive care patients with acute myocardial infarction (AMI). Materials and Methods. From December 2018 to July 2021, a total of 91 eligible patients with AMI were consecutively examined in a single intensive care unit (ICU) in China. Patients with a history of acute coronary artery disease were excluded from the study. Samples were collected within 24 hr of onset of symptoms. EPCs, defined as coexpression of CD34+/CD133+ cells or CD133+/CD34+/KDR+, were studied using flow cytometry and categorized by quartiles. Based on the 28-days mortality outcome, the patients were further divided into two groups: death and survival. The study incorporated various variables, including cardiovascular risk factors such as body mass index, hypertension, diabetes, hypercholesterolemia, atherosclerotic burden, and medication history, as well as clinical characteristics such as APACHEⅡscore, central venous-arterial carbon dioxide difference (GAP), homocysteine, creatinine, C-reactive protein, HbAlc, and cardiac index. Cox regression analysis was employed to conduct a multivariate analysis. Results. A total of 91 patients with AMI who were admitted to the ICU were deemed eligible for inclusion in the study. Among these patients, 23 (25.3%) died from various causes during the follow-up period. The counts of EPCs were found to be significantly higher in the survival group compared to the death group (P < 0.05). In the univariate analysis, it was observed that the 28-days mortality rate was associated with the several factors, including the APACHEⅡscore (P = 0.00), vasoactive inotropic score (P = 0.03), GAP (P = 0.00), HCY (P = 0.00), creatinine (P = 0.00), C-reactive protein (P = 0.00), HbAlc (P = 0.00), CI (P = 0.01), quartiles of CD34+/CD133+ cells (P = 0.00), and quartiles of CD34+/CD133+/KDR+ cells (P = 0.00). CD34+/CD133+/KDR+ cells retained statistical significance in Cox regression models even after controlling for clinical variables (HR: 6.258 × 10−10 and P = 0.001). Nevertheless, no significant correlation was observed between CD34+/CD133+ cells and all-cause mortality. Conclusions. The decreased EPCs levels, especially for CD34+/CD133+/KDR+ cells subsets, were an independent risk factor for 28-days mortality in AMI patients. [ABSTRACT FROM AUTHOR]

To investigate the regularity and characteristics of adverse drug reaction (ADR) of reactive cutaneous capillary endothelial proliferation caused by Camrelizumab, so as to provide reference for clinical rational use of drugs. Searching for case reports of Camrelizumab-induced reactive cutaneous capillary endothelial proliferation (RCCEP) in databases such as China Biology Medicine disc, VIP Database, CNKI, Wanfang Medical, PubMed, Wiley online library, Embase with "Carritzumab/Ericab," "SHR-1210," "Reactive cutaneous capillary endothelial proliferation," "Reactive capillary hemangiomas," and "Capillary proliferation" as search terms. The retrieval time is from the establishment of the database to February 2022. After eliminating clinical trials and incomplete literature, information of patients included in the literature was analyzed, which included gender, age, reason for medication, usage and dosage, time of ADR, concomitant medication, clinical manifestations, intervention measures, outcomes of patients, etc. A total of 11 articles involving 16 patients were included, including 11 males and five females, with an average age of 60.5 years. Reasons for medication included nine cases of non-small cell lung cancer (NSCLC), four cases of liver cancer, one case of small cell lung cancer (SCLC), one case of synovial sarcoma, and one case of Hodgkin lymphoma. Thirteen patients recorded in detail that the dosage of Camrelizumab was 200 mg, and the frequency of medication was q2w~q4w. Eight patients were treated with Camrelizumab alone, and eight patients were treated with combined medication. RCCEP occurred in nine patients after the first medication, and in seven patients after two-four cycles of medication, the average medication cycle was two cycles, and the average occurrence time was 12.5 days after the last medication. The main clinical manifestations were that several different sizes of growths such as red nevus-like, pearl-like, and mulberry-like growths appear on the head, face, neck, torso, limbs, and other parts of the body, all of which were grade 1-2. The RCCEP of all patients was controlled after treatment. During the treatment, 11 patients were stable and five patients were local remission. RCCEP is caused by Camrelizumabis a special skin immune response, which will not cause life-threatening to patients. However, clinicians and pharmacists should be familiar with the characteristics and regularities of the adverse reaction, to do a good job in medication monitoring and management, as for ensuring the safety of patients with medication. [ABSTRACT FROM AUTHOR]

Background. In this meta-analysis, we aimed to systematically compare the efficacy and safety of phacoemulsification and laser peripheral iridotomy (LPI) in the treatment of primary angle-closure glaucoma (PACG). Method. We searched PubMed, MEDLINE, EMBASE, the Cochrane Library, the Chinese Journal Full-text Database (CNKI), the Wanfang database, and the China Science and Technology Journal Database for randomized controlled trials (RCTs) of phacoemulsification and LPI in the treatment of PACG published up to September 30, 2022. Postoperative intraocular pressure (IOP), anterior chamber depth (ACD), complications, corneal endothelial cell count, and best-corrected visual acuity (BCVA) were compared. The effective quantity of measurement data was measured by the mean difference (MD) and 95% confidence interval (CI). The effect of counting data was measured by the odds ratio (OR). Result. A total of 1731 potential studies were identified, and after screening, 8 RCT studies were included. The results of the meta-analysis showed that, compared to the LPI group, the patients in the phacoemulsification group showed lower IOP six and twelve months after operation (MD-3.39, 95% CI −4.15∼−2.63, P < 0.00001 ; −2.29, −3.52∼−1.06, 0.0003). The ACD in the phacoemulsification group was significantly deeper than that in the LPI group (1.59, 1.10∼2.09, 0.00001). Meanwhile, the incidence of complications in the phacoemulsification group was lower than that in the LPI group (OR = 0.46, 0.29∼0.72, 0.0006). There was no statistically significant difference between the phacoemulsification group and the LPI group in corneal endothelial cell count and BCVA at 6 and 12 months after operation (P = 0.38 ; 0.11; 0.81). Conclusion. Compared with LPI, phacoemulsification is safer and more effective in the treatment of PACG, especially in controlling IOP and minimizing postoperative complications. [ABSTRACT FROM AUTHOR]

Increasing evidence highlights that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has long-term effects on cognitive function, which may cause neurodegenerative diseases like Alzheimer's disease (AD) in the future. We performed an analysis of a possible link between SARSCoV-2 infection and AD risk and proposed several hypotheses for its possible mechanism, including systemic inflammation, neuroinflammation, vascular endothelial injury, direct viral infection, and abnormal amyloid precursor protein metabolism. The purpose of this review is to highlight the impact of infection with SASR-CoV-2 on the future risk of AD, to provide recommendations on medical strategies during the pandemic, and to propose strategies to address the risk of AD induced by SASR-CoV-2. We call for the establishment of a follow-up system for survivors to help researchers better understand the occurrence, natural history, and optimal management of SARS-CoV-2-related AD and prepare for the future. [ABSTRACT FROM AUTHOR]

Mulberry (Morus alba L.) has a special significance in the history of agriculture and economic plant cultivation. Mulberry has strong environmental adaptability, a wide planting range, and abundant output. It is not only an important resource for silkworm breeding but also a raw ingredient for various foods and has great potential for the development of biological resources. The bioactivities of mulberry in different planting areas are not the same, which is an obstacle to the development of mulberry. This study collected information on the planting conditions of mulberry branches in 12 planting areas, such as altitude, temperature difference, and precipitation. A comparison of the levels of 12 constituents of mulberry branches from mulberry grown in different planting areas was then made. An in vitro model was used to study the bioactivities of mulberry branches in the 12 planting areas, and mathematical analysis was used to explain the possible reasons for the differences in the composition and bioactivities of mulberry branches in different planting areas. After studying mulberry samples from 12 planting areas in China, it was found that a small temperature difference could affect the antiapoptotic effect of mulberry branch on microvascular endothelial cells by changing the levels and proportions of rutin, hyperoside, and morusin. Adequate irrigation can promote the antioxidation of the mulberry branch on microvascular endothelial cells by changing the levels and proportions of scopoletin and quercitrin. The results of the analysis of planting conditions and the levels of active constituents and their correlation with bioactivities support the improvement of mulberry planting conditions and have great significance in the rational development of mulberry resources. This is the first time that a mathematical analysis method was used to analyze the effects of planting conditions on mulberry biological activity. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a serious health hazard that lacks effective treatment strategies. This study aims to investigate baicalin's effect on tight junctions and immune cell infiltration after ischemic stroke injury. Rat brain microvascular endothelial cells (BMECs) were treated with OGD/R to establish an in vitro model. Caspase-3, Bax, Bcl-2, zonula occludens-1 (ZO-1), occludin, claudin-5, tumor necrosis factor (TNF)- α , interleukin (IL)-6, inducible nitric oxide synthase (iNOS), Toll-like receptor (TLR) 2, TLR4, and nuclear factor-kappa B (NF- κ B) expressions were detected using qRT-PCR and western blotting. ZO-1, TNF- α , iNOS, IL6, CD31, and ZO-1 expressions were examined using immunofluorescence. A tube formation assay was performed to measure angiogenesis. An ischemia-reperfusion model in rats was established by middle cerebral artery occlusion. The infarct volume was observed using 2,3,5-triphenyltetrazolium chloride staining. TNF- α , iNOS, and IL6 levels in the serum were tested using ELISA. Flow cytometry was performed to examine immune cell inflammatory infiltration. Baicalin had no significant effect on the proliferation of normal BMECs. Baicalin inhibited apoptosis, protected against tight junction injury, and alleviated the inflammatory response in OGD/R-induced BMECs and IR rats, with the highest dose (25 μ g/mL) exerting a superior effect. Baicalin decreased the neurological function score, infarct volume, and brain water content, relieved brain morphological changes, and inhibited immune cell infiltration in vivo. In conclusion, baicalin could reduce BMECs apoptosis, protect tight junctions, and resist immune cell infiltration, thereby alleviating ischemic stroke. Our findings potentially provide a novel treatment strategy for ischemic stroke. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy (DR) is one of the more serious complications of diabetes. However, the mechanisms involved in DR are complex and still need to be investigated. The beneficial effects of fisetin have been widely reported, but whether it is beneficial in DR is not clear yet. This study was designed to investigate the regulatory role of fisetin in regulating DR and explore the involved mechanism. First, 30 mM glucose was used to establish DR cell model in vitro. Cell counting kit 8 (CCK8) assay was utilized to study the effects of fisetin on cell viability through treating human retinal microvascular endothelial cells (HRMECs) with 25, 50, and 100 μM fisetin. Transwell and wound healing assays were used to detect the function of fisetin on the migration and angiogenesis on HG-induced HRMECs. Finally, OE-VEGF was used as a mimic of VEGF, and western blotting (WB) was used to verify the targeting genes of fisetin. HG induced an increase in cell viability, cell migration, and angiogenesis in HRMECs, whereas fisetin inhibited these enhancements induced by HG through inhibiting VEGF. In conclusion, fisetin prevents angiogenesis in DR by downregulating VEGF. [ABSTRACT FROM AUTHOR]

Objective. This research aimed at better understanding the histopathological development of precancerous lesions of gastric cancer (PLGC) and organelle ultrastructure changes. Methods. Sprague-Dawley rats were randomly assigned to the model and control groups. Model rats drank N-methyl-N′-nitro-N-nitrosoguanidine solution, while control rats drank pure water ad libitum. At 1, 3, 5, 6, and 8 months after the start of feeding, eight rats were randomly chosen from each group, and gastric mucosa tissues were removed for histopathological analysis. H&E staining was applied to analyze the pathological histological structure of the rat gastric mucosa via a light microscope, and the ultrastructural changes were observed via a transmission electron microscope. Results. Gastric mucosal pathologies of model rats such as mucosal atrophy, intestinal metaplasia, inflammatory lesions, and even intraepithelial neoplasia deteriorated over time. The endoplasmic reticulum gap widened, the mitochondrial endothelial cristae were disrupted, the nuclear membrane thickened, and chromatin condensed with heterotypic alterations in the main and parietal cells. Additionally, endothelial cell enlargement and thickening of the microvascular intima were seen. Conclusion. Our research showed that the PLGC progression of rats is correlated with the pathological alteration axis of "normal gastric mucosa-gastric mucosa inflammatory changes-intestinal metaplasia with mild dysplasia-moderate to severe dysplasia." Ultrastructure analysis of model rats is compatible with the structural changes in the gastric mucosa with spleen deficiency and blood stasis. The pathological evolutionary axis and ultrastructural analysis are helpful for evaluating potential novel herbal therapies for PLGC. [ABSTRACT FROM AUTHOR]

Exposure to airborne particulate matter (PM2.5) is associated with cardiovascular diseases. In order to investigate the molecular mechanisms of air pollution-induced CVDs toxicity, human umbilical vein endothelial cells (HUVECs) were exposed to PM2.5 collected from January, 2016 winter in Beijing, China. We performed RNA sequencing to elucidate key molecular mechanism of PM 2.5-mediated toxicity in HUVECs. A total of 1753 genes, 864 up-regulated and 889 down-regulated, were observed to be differentially expressed genes (DEGs). Among these, genes involved in metabolic response, oxidative stress, inflammatory response, and vascular dysfunction were significantly differentially expressed (log2 FC > 4). The results were validated by quantitative real-time PCR (qPCR) and Western blot for CYP1B1, HMOX1, IL8, and GJA4. Pathway analysis revealed that DEGs were involved in the biological processes related to metabolism, inflammation, and host defense against environmental insults. This research is providing a further understanding of the mechanisms underlying PM2.5-induced cardiovascular diseases (CVDs). [ABSTRACT FROM AUTHOR]

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Purpose. To explore the effect of oral tranexamic acid treatment on the blood transfusion rate and the incidence of deep vein thromboembolism after total knee arthroplasty (TKA). Methods. 90 patients undergoing TKA admitted to First People's Hospital of Changshu City from January 2019 to January 2020 were selected and randomized into the control group and the experimental group accordingly (45 cases in each group). The control group intravenously received 20 mL/kg tranexamic acid before the incision was closed. The experimental group was given 1 g of tranexamic acid orally before anesthesia, 6 h and 12 h after the operation. Results. The experimental group witnessed better perioperative indexes in relation to the control group. The experimental group displayed better postoperative coagulation function indexes as compared to the control group (P < 0.05). Remarkably lower postoperative vascular endothelial function indexes in the experimental group than in the control group were observed. The experimental group experienced a markedly lower incidence of deep vein thromboembolism in comparison with the control group (P < 0.05). The postoperative knee society score (KSS) score of the experimental group was significantly higher than that of the control group. A significantly higher postoperative modified rivermead mobility index (MRMI) score was yielded in the experimental group in contrast to the control group (P < 0.05). The experimental group obtained lower numerical rating scale (NRS) scores at T2 and T3 as compared to the control group. Conclusion. Oral tranexamic acid is a suitable alternative for patients undergoing TKA in terms of reducing the blood transfusion rate, relieving pain, and accelerating the recovery of the patient's limbs. [ABSTRACT FROM AUTHOR]

Purpose. To evaluate the outcomes of femtosecond laser, modified capsular tension ring, and iris hook-assisted surgical treatment of lens subluxation in patients with elevated intraocular pressure (IOP). Methods. Fifteen patients with lens subluxation and elevated IOP were enrolled in this study. All patients underwent femtosecond-laser-assisted cataract surgery/phacoemulsification/intraocular lens implantation/modified capsular tension ring (MCTR) implantation with iris hook assistance. Uncorrected visual acuity (UCVA), best corrected visual acuity (BCVA), IOP, number of glaucoma medication complications, endothelial cell density (ECD), and tilt of the lens were recorded before and after surgery. All patients were observed for 24 months postoperatively. Results. UCVA and BCVA increased significantly at 1 month, 6 months, 12 months, and 24 months, compared with preoperative UCVA and BCVA (P < 0.001). IOP significantly decreased at 1 month, 3 months, 6 months, 12 months, and 24 months, compared with preoperative IOP (P < 0.001). 3 patients received glaucoma medications to control IOP after surgery. All medications were discontinued at 3 months postoperatively. Conjunctival redness or hemorrhage was observed in 11 patients (73.3%); transient corneal edema was observed in 3 patients (20.0%); and posterior capsule opacification occurred in 1 patient (6.67%). The ECD and tilt of the lens are within an acceptable range. Conclusion. The combined use of a femtosecond laser, MCTR, and iris hooks is an effective and safe method for treating patients with lens subluxation and elevated IOP. [ABSTRACT FROM AUTHOR]

Background: Knee osteoarthritis (KOA) is one of the most common chronic musculoskeletal disorders worldwide, for which exosomes derived from stem cells may provide an effective treatment. Purpose: To assess the effect of exosomes derived from human urine–derived stem cells (hUSCs) overexpressing miR-140-5p (miR means microRNA) on KOA in an in vitro interleukin 1β (IL-1β)–induced osteoarthritis (OA) model and an in vivo rat KOA model. Study Design: Controlled laboratory study. Methods: Exosomes derived from hUSCs (hUSC-Exos) were isolated and validated. The hUSCs were transfected with miR-140s using lentivirus, and exosomes secreted from such cells (hUSC-140-Exos) were collected. The roles of hUSC-Exos and hUSC-140-Exos in protecting chondrocytes against IL-1β treatment were compared by analyzing the proliferation, migration, apoptosis, and secretion of extracellular matrix (ECM) in chondrocytes. After vascular endothelial growth factor A (VEGFA) was identified as a target of miR-140, the mechanism by which VEGFA can mediate the beneficial effect of miR-140 on OA was investigated using small interfering RNA transfection or chemical drugs. The expression of VEGFA in cartilage and synovial fluid from patients with KOA was measured and compared with that of healthy controls. Surgery for anterior cruciate ligament transection and destabilization of the medial meniscus were performed on the knee joints of Sprague-Dawley rats to establish an animal model of OA, and intra-articular (IA) injection of hUSC-Exos or hUSC-140-Exos was conducted at 4 to 8 weeks after the surgery. Cartilage regeneration and subchondral bone remodeling were evaluated through histological staining and micro–computed tomography analysis. Results: Proliferation and migration ability were enhanced and apoptosis was inhibited in chondrocytes treated with IL-1β via hUSC-Exos, with the side effect of decreased ECM secretion. hUSC-140-Exos not only retained the advantages of hUSC-Exos but also increased the secretion of ECM by targeting VEGFA, including collagen II and aggrecan. Increased expression of VEGFA during the progression of KOA was also confirmed in cartilage and synovial fluid samples obtained from patients with OA. In the rat OA model, IA injection of hUSC-140-Exos enhanced cartilage regeneration and subchondral bone remodeling. Conclusion: Our results demonstrated the superiority of hUSC-Exos overexpressing miR-140-5p for treating OA compared with the hUSC-Exos. The effect of hUSC-140-Exos for suppressing the progression of KOA is in part mediated by VEGFA. Clinical Relevance: Exosomes derived from stem cells may provide a promising treatment for KOA, and our study can advance the related basic research. [ABSTRACT FROM AUTHOR]

Background and Purpose: SIRT1 was associated with AS risk and EPCs were reported to participate in the endothelial repair in Coronary Atherosclerosis (CAS). In this study, we explored the role of SIRT1 in AS mice and also its modulation in EPCs. Methods and Materials: ApoE−/−mice were fed on high-fat and high-glucose diet to establish the AS animal model with the normally-raised C57BL/6 mice as a control group. SIRT1 activator, SRT 2104 was injected intravenously into 5 ApoE−/−mice and its inhibitor Nicotinamide was injected in tail in another 5 ApoE−/− mice. Weight changes were recorded. Blood samples were taken from posterior orbital venous plexus and were detected by automatic biochemical analyzer. HE staining displayed the pathological conditions while Immunohistochemistry (IHC) evaluated the CD34+/VEGFR2+ relative density in the aorta tissues. EPCs were isolated from bone marrow and verified using immunofluorescence staining (IFS). The modulatory mechanism of SIRT1 in EPCs were studied by using RT-PCR, MTT, Western Blot and colony formation, scratch methods. Results: SIRT1 activator negatively regulated the weight and TC, TG and LDL levels, alleviated the lesion conditions and decreased the CD34+/VEGFR2+ density compared to the AS control. In vitro, SIRT1 activator promoted the proliferation and migration of EPCs and activated wnt/β-catenin/GSK3β signaling pathway. SIRT1 activator also inhibited the autophagy biomarkers ATG1 and LC3II. Furthermore, inhibitor of autophagy promoted SIRT1 expression and induced EPC proliferation, migration and activated wnt/β-catenin/GSK3β pathway. The suppression of the wnt/β-catenin/GSK3β pathway inhibited SIRT1 expression in EPCs, attenuated the proliferation and migration and promoted autophagy of EPCs. Conclusion: SIRT1 activation might be protective in AS mice through autophagy inhibition in EPCs via wnt/β-catenin/GSK3β signaling pathway. [ABSTRACT FROM AUTHOR]

Banxia Baizhu Tianma decoction (BBTD), a six-herb Chinese medicine formula first described approximately 1732 AD, is commonly prescribed for Hypertension with Phlegm-dampness Stagnation (HPDS) as an adjuvant therapy in China. Obesity is an important risk factor for the increasing prevalence of hypertension year by year in China. In Traditional Chinese medicine, obesity is often differentiated as the syndrome of excessive phlegm-dampness.Vascular endothelial cell injury plays an important role in the development and occurrence of HPDS. In this study, the protective effects of 18 batches of BBTD samples from different origins on HUVEC cells were evaluated, including antioxidant and anti-inflammatory activities. Ultrahigh performance liquid chromatography (UPLC) was used to establish fingerprints, and combined with pharmacodynamic indexes, the protective components of BBTD on endothelial cells were analyzed. Antioxidant and anti-inflammatory activities were evaluated by ROS and Hs-CRP models, respectively. Hierarchical cluster analysis (HCA) and Bivariate correlation analysis (BCA) were used to investigate the potential correlation between chemical components and endothelial cell protection. The results indicated that BBTD could reduce ROS and hs-CRP levels in HUVEC cells, and the pharmacological activities in 18 batches of BBTD samples were significantly different. The results of BCA indicated that Gastrodin, Liquiritin, Hesperidin, Isoliquiritin, Hesperetin, and Isoliquiritigenin might be the active constituents to activate ROS and suppress hs-CRP as determined by spectrum-effect relationships. The antioxidant and anti-inflammatory activities of the 6 components at different concentration were verified, and the results showed that all of them had good antioxidant and anti-inflammatory activities in a concentration-dependent manner. This study showed that activity determination and spectral correlation can be used to search for active substances in Chinese medicine formula and provide data support for quality control of Traditional Chinese medicine (TCM). [ABSTRACT FROM AUTHOR]

Objectives. We aimed to investigate the effects of Shen-Yuan-Dan (SYD), a Chinese medicine preparation, on periprocedural myocardial injury (PMI) and the number of peripheral blood endothelial progenitor cells (EPCs) in patients with unstable angina pectoris (UA) who underwent elective percutaneous coronary intervention (PCI). Methods. Patients were randomly divided into the experimental (group A) and control (group B) groups through the random number table method. In group A, patients concurrently received the conventional western treatment and SYD orally (4 capsules/time, 3 times/d, from 3 d before surgery to 7 d after surgery). In group B, patients received conventional Western medicine treatment. Both groups underwent coronary angiography, and patients undergoing PCI were eventually included in the study. The following patient data were collected: incidence of PMI, serum CK-MB content before PCI, 4 h, 24 h, and 7 d after PCI, number of CD45dim/-CD34+CD309+ peripheral venous EPCs, and number of CD184 coexpressed EPCs. The incidence of adverse reactions and 30-day major adverse cardiovascular events (MACEs) were also recorded. Results. Sixty-two patients were finally included in this study, with 32 and 30 in groups A and B, respectively. In group A, the number of peripheral blood EPCs and the number of CD184 coexpressed EPCs at 1 h before surgery were higher than those at 3 d before surgery (37.24 ± 25.20 vs. 22.78 ± 9.60/ml; P < 0.001 and 23.38 ± 15.30 vs. 13.54 ± 8.08/ml; P < 0.001 , resp.). The number of peripheral blood EPCs and number of CD184 coexpressed EPCs at 4 h after surgery were lower than those at 1 h before surgery (25.30 ± 11.90 vs. 37.24 ± 25.20/ml; P = 0.019 and 15.38 ± 8.78 vs. 23.38 ± 15.30/ml; P = 0.013 , resp.), but there was no difference at 24 h and at 7 d after surgery in comparison with that at 1 h before surgery (P > 0.05). In group B, compared with that at 1 h before surgery, there existed a decline in the number of EPCs in peripheral blood and the number of CD184 coexpressed EPCs at 4 h after surgery, but without a statistical difference (P > 0.05). Comparing both groups, it was found that the incidence of PMI in group A was lower (6.25% vs. 26.67%; P = 0.04), and the serum CK-MB content at 4 and 24 h after surgery was also lower than that in group B (17.33 ± 5.83 vs. 20.38 ± 4.32 U/l; P = 0.048 and 15.79 ± 5.32 vs. 19.10 ± 4.93 U/l; P = 0.030 , resp.). The number of EPCs in peripheral blood and the number of CD184 coexpressed EPCs in group A were higher than those in group B at 1 h before surgery (37.24 ± 25.20 vs. 22.36 ± 12.26/ml; P = 0.034 and 23.38 ± 15.30 vs. 13.12 ± 14.62/ml; P = 0.013 , resp.). In addition, there were no obvious adverse reactions and no 30-day MACEs in both groups during the trial. Conclusion. SYD can reduce PMI and promote the mobilization of EPCs in the perioperative period of elective PCI in patients with UA. [ABSTRACT FROM AUTHOR]

Background. Vascular endothelial cell injury is not only the initiating factor of cardiovascular and cerebrovascular diseases but also the essence of blood stasis. Levistilide A (LA), a natural component isolated from the traditional Chinese herb, Ligusticum chuanxiong Hort, has traditional effects on improving blood circulation and removing stasis. In this study, the effects and potential mechanisms of LA in the rat model of blood stasis and the mechanism in endothelial cell injury have been explored. Materials and Methods. In this experiment, the effects of LA on the model of acute blood stasis in rats were explored. The blood samples were collected for the measurement of coagulation and hemorheological indices, and the carotid arteries were also excised from rats for hematoxylin-eosin (HE) staining and immunohistochemistry (IHC). In addition, the improvement effects of LA on the H2O2-induced human umbilical vein endothelial cell (HUVEC) injury model were evaluated. And the cell viability detection was conducted by the CCK8 assay, and the pathway-related protein expressions were detected by western blotting. Results. In vivo, compared with the model group, the treatment of LA (10 mg/kg) could reduce the FIB (fibrinogen) content (P < 0.01), increase the INR (international normalized ratio) and PT (prothrombin time) (P < 0.01), and reduce the plasma viscosity (P < 0.05) and whole blood viscosities of low, medium, and high shear rates in the blood of blood stasis model rats (P < 0.01). In vitro, the cell viability in the LA-pretreated group was higher than that of the model group (P < 0.05). The expression levels of PI3K, AKT, and eNOs in the LA-pretreated group were increased (P < 0.01) as compared to the model group. Conclusion. These findings demonstrated that LA has the ability to improve blood hypercoagulation and blood viscosity, and enhance the viability of cells. It is more likely that it exerts a protective effect on the endothelial cell through the PI3K-AKT-eNOs pathway. These results indicate LA will be a potential candidate to cure blood stasis with endothelial cell injury. [ABSTRACT FROM AUTHOR]

In China, cardiovascular disease (CVD) has surpassed malignant tumours to become the disease with the highest mortality rate, and atherosclerosis (AS) is an important pathological cause of CVD. Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone in circulating human blood and is a precursor of estrogen and androgen. DHEA is converted into a series of sex hormones in local peripheral tissues where its acts physiologically. DHEA also acts therapeutically, thereby avoiding the adverse systemic reactions to sex hormones. DHEA inhibits AS, thus inhibiting the development of CVD, and it improves the prognosis for CVD. The incidence of CVD in postmenopausal women is substantially higher than that in premenopausal women, and that incidence is believed to be related to a decrease in ovarian function. The current review analyzes the mechanisms of postmenopausal women's susceptibility to AS. They tend to have dyslipidemia, and their vascular smooth muscle cells (VSMCs) proliferate and migrate more. In addition, oxidative stress and the inflammatory response of endothelial cells (ECs) are more serious in postmenopausal women. This review also discusses how DHEA combats AS by countering these mechanisms, which include regulating the blood lipid status, protecting ECs (including coping with oxidative stress and inflammatory reactions of the vascular endothelium, inhibiting apoptosis of ECs, and inducing NO production) and inhibiting the proliferation and migration of VSMCs. As a result, DHEA has great value in preventing AS and inhibiting its progression in postmenopausal women. [ABSTRACT FROM AUTHOR]

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Background: Lei-gong-gen formula granule (LFG) is a folk prescription derived from Zhuang nationality, the largest ethnic minority among 56 nationalities in China. It consists of three herbs, namely Eclipta prostrata (L.) L., Smilax glabra Roxb, and Centella asiatica (L.) Urb. It has been widely used as health protection tea for hundreds of years to prevent hypertension in Guangxi Zhuang Autonomous Region. The purpose of this study is to validate the antihypertensive effect of LFG on the spontaneously hypertensive rat (SHR) model, and to further identify the effective components and anti-hypertension mechanism of LFG. Methods: The effects of LFG on blood pressure, body weight, and heart rate were investigated in vivo using the SHR model. The levels of NO, ANG II, and ET-1 in the serum were measured, and pathological changes in the heart were examined by H&E staining. The main active components of LFG, their corresponding targets, and hypertension associated pathways were discerned through network pharmacology analysis based on the Traditional Chinese Medicine Systems Pharmacology (TCMSP), Traditional Chinese Medicine Integrated Database (TCMID), and the Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine (BATMAN-TCM). Then the predicted results were further verified by molecular biology experiments such as RT-qPCR and western blot. Additionally, the potential active compounds were predicted by molecular docking technology, and the chemical constituents of LFG were analyzed and identified by UPLC-QTOF/MS technology. Finally, an in vitro assay was performed to investigate the protective effects of potential active compounds against hydrogen peroxide (H2O2) induced oxidative damage in human umbilical vein endothelial cells (HUVEC). Results: LFG could effectively reduce blood pressure and increase serum NO content in SHR model. Histological results showed that LFG could ameliorate pathological changes such as cardiac hypertrophy and interstitial inflammation. From network pharmacology analysis, 53 candidate active compounds of LFG were collected, which linked to 765 potential targets, and 828 hypertension associated targets were retrieved, from which 12 overlapped targets both related to candidate active compounds from LFG and hypertension were screened and used as the potential targets of LFG on antihypertensive effect. The molecular biology experiments of the 12 overlapped targets showed that LFG could upregulate the mRNA and protein expressions of NOS3 and proto-oncogene tyrosine-protein kinase SRC (SRC) in the thoracic aorta. Pathway enrichment analysis showed that the PI3K-AKT signaling pathway was closely related to the expression of NOS3 and SRC. Moreover, western blot results showed that LFG significantly increased the protein expression levels of PI3K and phosphorylated AKT in SHR model, suggesting that LFG may active the PI3K-AKT signaling pathway to decrease hypertension. Molecular docking study further supported that p-hydroxybenzoic acid, cedar acid, shikimic acid, salicylic acid, nicotinic acid, linalool, and histidine can be well binding with NOS3, SRC, PI3K, and AKT. UPLC-QTOF/MS analysis confirmed that p-hydroxybenzoic acid, shikimic acid, salicylic acid, and nicotinic acid existed in LFG. Pre-treatment of HUVEC with nicotinic acid could alleviate the effect on cell viability induced by H2O2 and increase the NO level in cell supernatants. Conclusions: LFG can reduce the blood pressure in SHR model, which might be attributed to increasing the NO level in serum for promoting vasodilation via upregulating SRC expression level and activating the PI3K-AKT-NOS3 signaling pathway. Nicotinic acid might be the potential compound for LFG antihypertensive effect. [ABSTRACT FROM AUTHOR]

Objective: To investigate effects of Shengmai injection (SMI) postconditioning on myocardial ischemia-reperfusion injury (MIRI) in isolated rat hearts. Materials and methods: A total of thirty isolated hearts were randomly divided into three groups: Sham group, I/R group and SMI group. Sham group was continuously perfused with K-H solution for 120 minutes. I/R group and SMI group were given balanced perfusion for 30 min followed by reperfusion for 60 min, with an interval of 30 min, and those in the SMI group were given postconditioning with 1% SMI during the first 10 min of reperfusion. The left ventricular function, markers of myocardial injury, endothelial cell injury and oxidative stress injury were measured at 30 minutes after equilibration (t0), 30 minutes after ischemia (t2) and 60 minutes after reperfusion (t3). Results: The results showed that there was no significant difference for all observation indexes at t0. Compared with the Sham group, real portfolio project and coronary arterial flow rate and the activity of superoxide dismutase were significantly decreased in the I/R group, whereas those in the SMI group were significantly higher. Left ventricular end-diastolic pressure, the concentrate of malondialdehyde, lactate dehydrogenase, cTn-I, hyaluronic acid, heparin sulphate, syndecan-1 in the I/R group were markedly higher than those in the Sham group, whereas those in the SMI group were significantly lower. Conclusion: In summary, the present study indicated that 1% SMI postconditioning can alleviate the detachment of endothelial cell glycoprotein envelope induced by myocardial ischemia-reperfusion injury, and its mechanism is probably related to the inhibition of the oxidative stress injury. [ABSTRACT FROM AUTHOR]

Calcium, as a second messenger, plays an important role in the pathogenesis of cardiovascular diseases (CVDs). The malfunction of calcium signaling in endothelial cells and vascular smooth muscle cells promotes hypertension. In cardiomyocytes, calcium overload induces apoptosis, leading to myocardial infarction and arrhythmias. Moreover, the calcium–calcineurin–nuclear factor of activated T cells (NFAT) pathway is essential for expressing the cardiac pro-hypertrophic gene. Heart failure is also characterized by reduced calcium transient amplitude and enhanced sarcoplasmic reticulum (SR) calcium leakage. Traditional Chinese medicine (TCM) has been used to treat CVDs for thousands of years in China. Because of its multicomponent and multitarget characteristics, TCM's unique advantages in CVD treatment are closely related to the modulation of multiple calcium handling proteins and calcium signaling pathways in different types of cells involved in distinct CVDs. Thus, we systematically review the diverse mechanisms of TCM in regulating calcium pathways to treat various types of CVDs, ranging from hypertrophic cardiomyopathy to diabetic heart disease. [ABSTRACT FROM AUTHOR]

Tanshinone IIa (TSA) has been approved to treat cardiovascular diseases by the China State Food and Drug Administration. TSA has exhibited a variety of pharmacological effects, including vasodilator, antioxidant, anti-inflammatory, and anti-tumor properties. Endothelial cells play an important physiological role in vascular homeostasis and control inflammation, coagulation, and thrombosis. Accumulating studies have shown that TSA can improve endothelial function through various pathways. The PubMed database was reviewed for relevant papers published up to 2020. This review summarizes the current clinical and pharmaceutical studies to provide a systemic overview of the pharmacological and therapeutic effects of TSA on endothelial cells. TSA is a representative monomeric compound extracted from Danshen and it exhibits significant pharmacological and therapeutic properties to improve endothelial cell function, including alleviating oxidative stress, attenuating inflammatory injury, modulating ion channels and so on. TSA represents a spectrum of agents that are extracted from plants and can restore the endothelial function to establish the beneficial and harmless molecular therapeutics. This also suggests the possible detection of endothelial cells for very early diagnosis of diseases. In future, precise therapeutic methods will be developed to repair endothelial cells injury and recover endothelial dysfunction. [ABSTRACT FROM AUTHOR]

Objective: To investigate the clinicopathological features, classification, and genetic characteristics of common lymphatic malformation (CLM) in superficial soft tissue. Methods: A retrospective study of 110 patients with the diagnosis of CLM at the Henan Province People's Hospital, China from August 2019 to August 2022 was performed. The clinicopathological features, relevant immunohistochemical (IHC) staining results, and fluorescence quantitative PCR of PIK3CA mutation were analyzed, and patients were followed up. Results: Among the 110 CLM patients, there were 53 males and 57 females; 65 cases (65/110, 59.1%) were first detected when the patients were≤2 years old. The most common location was the head and neck in 41 cases (41/110, 37.3%). Clinically, 102 cases (102/110, 92.7%) were solitary, 83 cases (83/110, 75.5%) were skin-colored, 69 cases (69/110, 62.7%) had indistinct borders, and 10 cases (10/110, 9.1%) had diffuse and severe macroscopic manifestations. There were 52 macrocystic type (52/110, 47.3%), 23 microcystic type (23/110, 20.9%), and 35 combined type (35/110, 31.8%). The macrocystic CLM presented as soft, translucent masses with large cystic cavities on the cut surface, and histologically they were composed of large, irregularly dilated channels that were thicker with irregular smooth muscle and lymphocytic infiltration. Microcystic CLM showed wartlike projections or translucent blisters on the skin, with small honeycomb structures on the cut surface, and histologically consisted of round or angular dilated small lymphatic vessels with little or no smooth muscle. The combined CLM had both macrocystic and microcystic morphologies. IHC staining showed that the lymphatic endothelial cells were positive for LYVE-1, D2-40, PROX1, CD31, and VEGFR3 but negative for CD34; in the macrocystic and combined CLM vessel walls were positive for SMA. Eight of 13 CLM had PIK3CA mutation. All patients were followed up, and 24 (24/110, 21.8%) had relapses, which more frequently occurred in combined type, followed by microcystic type. Conclusions: CLM is a congenital vascular malformation composed of dilated, abnormal lymphatic channels, with PIK3CA mutation. There are significant differences in clinicopathological characteristics among the different types. Since microcystic and combined CLM are prone to recurrence, accurate pathological subtyping is necessary to guide treatment and to predict prognosis.

Purpose. To investigate the long-term changes of corneal endothelial cells (EC) in anterior chamber intraocular lens- (AC-IOL-) implanted eyes. Methods. Retrospective study. We included 37 eyes (25 patients) that received AC-IOL implantation previously in the Eye and ENT Hospital of Fudan University between 1995 and 2016. Follow-up outcomes included the best-corrected visual acuity (BCVA), endothelial cell density, hexagonality, coefficient of variance, and central corneal thickness. Results. In total, 23 eyes (62.16%) with phakic and 14 eyes (37.84%) with aphakic AC-IOLs were included. Among these, 3 eyes (8.11%) were angle-supported AC-IOLs and 34 eyes (91.89%) were Artisan iris-fixated AC-IOLs. The mean age of patients was 41.40 ± 17.17 years, and the mean follow-up time was 12.12 ± 4.71 years in our study. At the follow-up time, corneal decompensation existed in 3 angle-supported AC-IOL eyes with a rate of 100% and 15 iris-fixated AC-IOL eyes with a rate of 44.12%. AC-IOL displacement occurred in 14 (41.18%) iris-fixated AC-IOL eyes. In the 19 iris-fixated AC-IOL eyes without corneal decompensation, significant changes also took place in corneal endothelial cells. The endothelial cell density decreased from 2843.26 ± 300.76 to 2015.58 ± 567.99 cells/mm2 (29.1% loss, P < 0.001) and hexagonality decreased from 51.21 ± 7.83 to 42.53 ± 9.17 (%) (16.9% loss, P < 0.001). The Kaplan–Meier survival curve also demonstrated the accumulated expectation rates of corneal endothelial cell decomposition for AC-IOLs with a median survival time of 12 years. Conclusion. We reported a significant chronic loss and long-term decompensation destiny of corneal endothelial cells in AC-IOL eyes. Semiannual or annual follow-up and evaluation of endothelial cells should be conducted in AC-IOL-implanted patients. [ABSTRACT FROM AUTHOR]

In a retrospective study of 39 COVID-19 patients and 32 control participants in China, we collected clinical data and examined the expression of endothelial cell adhesion molecules by enzyme-linked immunosorbent assays. Serum levels of fractalkine, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular adhesion protein-1 (VAP-1) were elevated in patients with mild disease, dramatically elevated in severe cases, and decreased in the convalescence phase. We conclude the increased expression of endothelial cell adhesion molecules is related to COVID-19 disease severity and may contribute to coagulation dysfunction. [ABSTRACT FROM AUTHOR]

Three new compounds, namely massonside C (1), massonianoside F (2), and 3, 8-dimethyl- herbacetin-7-O-β-D-glucopyranoside (3), together with five known compounds (4–8), were isolated from the fresh needles of Pinus massoniana. Their structures were established by 1D, 2D NMR, HRMS and comparison with the literature data. The absolute configuration of 1 was confirmed by a combination of X-ray single crystal analysis. All isolated compounds were evaluated for the protective effect of human umbilical vein endothelial cells against oxidative damage. [ABSTRACT FROM AUTHOR]

Background: Tufted angioma is a rare benign lesion with vascular proliferation.Aim: To retrospectively analyze the clinicopathological manifestations and immunohistochemical features of tufted angioma.Methods: Clinical and histopathological features of tufted angioma (n = 54) were evaluated and analyzed retrospectively in the Department of Dermatology, Xijing Hospital from 2003 to 2014.Results: Clinically, tufted angioma usually presented as erythematous plaques and papules on the head and neck (n = 11), trunk (n = 21) and extremities (n = 22), mainly in children (n = 48), without gender difference (24 males and 30 females). A total of 45 cases showed solitary lesions and nine cases showed multiple lesions. Common symptoms included pain (n = 11), tenderness (n = 7), itching (n = 1), hypertrichosis (n = 7), hyperhidrosis (n = 6) and Kasabach-Merritt phenomenon (n = 1). Histopathologically, typical tufted angioma (n = 37) showed proliferation of endothelial cells in a so-called cannonball pattern, while in the early (n = 4) and regressed (n = 13) stages the tufted appearance was not prominent. The proliferated endothelial cells were diffusely positive for CD31 and Wilms tumor 1, focally positive for D2-40 and Prox1, and negative for Glut-1.Limitations: Our research was confined to patients of Chinese origin and our sample size was limited.Conclusions: Tufted angioma is a rare vascular neoplasm with diverse clinical manifestations and unique pathological features. It should be recognized as a vascular tumor with lymphatic differentiation. We emphasize the importance of considering tufted angioma in the differential diagnoses of any congenital or acquired vascular tumor. [ABSTRACT FROM AUTHOR]

Context: Ferulic acid (FA) is an active principle derived from the traditional Chinese medicine Angelica sinensis, which has been used for the treatment of cardiovascular and cerebrovascular diseases in China for many years. However, a thorough understanding of effects on vascular function by FA has not been investigated. Aims: The aim of the present study was to investigate the potential mechanism of FA by suppressing Transient receptor potential cation channel subfamily M member 8 (TRPM8) channels and regulating endothelial nitric oxide (NO) pathway to ameliorate cold explore injury in human umbilical vascular endothelial cells (HUVECs). Subjects and Methods: The effects of cold exposure and FA on cell viability were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) assay. Quantitative polymerase chain reaction and Western blot were utilized to detect TRPM8, hypoxia-inducible factor-alpha (HIF-1α), endothelin-1 (ET-1), inducible NO synthase (iNOS), endothelial NO synthase (eNOS) messenger RNA, and protein expression in HUVECs. Enzyme-linked immunosorbent assay method was used to detect the concentration of ET-1 in culture supernatants of HUVECs. Results: Cold exposure at 18°C had no significant effect on cell morphology but increased secretion of LDH and ET-1 and the expression of TRPM8, HIF-1α, iNOS, and ET-1. Treatment with FA decreased all of these changes. The levels of NO and eNOS decreased in cold stress model, while FA treatment attenuated the cold-induced decrease of NO and eNOS. Conclusion: Cold stress can cause an increase in vasoconstrictors such as TRPM8 and ET-1 and reducing cell viability, but FA can prevent cold stress-related cardiovascular disease by regulating the expression of these substances in cells. [ABSTRACT FROM AUTHOR]

"Shexiang Baoxin Pill" (SBP), a commonly used traditional Chinese medicine, has been used to treat angina, myocardial infarction and coronary heart disease in China for thirty years. SBP has been proven to promote angiogenesis in a rat model of myocardial infarction (MI). The aim of the present study was to determine the pro-angiogenic effects and mechanism of SBP during inflammation or ischemic pathological conditions and elucidate its regulatory effects on endothelial cell function and signaling pathways mediated by macrophages. We used a polyvinyl alcohol (PVA) sponge implantation mouse model as an inflammatory angiogenesis model and utilized a mouse femoral artery ligation model as a hind limb ischemia model. We also performed cell proliferation, cell migration and tubule formation in vitro experiments to assess the effects of SBP on endothelial cell function and signaling pathways by stimulating macrophage activity. The in vitro experiment results showed that SBP could significantly increase the expression of mRNAs and proteins associated with angiogenesis in endothelial cells by activating macrophages to release pro-angiogenic factors such as Vegf-a. Activation of macrophages by SBP eventually led to endothelial cell proliferation, migration and tubule formation and increased the expression of p-Akt and p-Erk1/2 proteins in the downstream PI3K/Akt and MAPK/Erk1/2 signaling pathways related to angiogenesis, respectively. The in vivo experiment results indicated that SBP had angiogenesis effects in both inflammatory and ischemic angiogenesis models with dose- and time-dependent effects. Shexiang Baoxin Pills can promote angiogenesis by activating macrophages to regulate endothelial cell function and signal transduction pathways. Image 1 • SBP increases expression of mRNAs and proteins in endothelial cells by activating macrophages. • SBP leads to endothelial cell proliferation, migration and tubule formation through activation of macrophages. • SBP increases expression of the p-Akt and p-Erk1/2 proteins through activation of macrophages. • SBP promotes the expression of VEGF-A mRNA, VEGF protein release and microvessel formation in an inflammatory angiogenesis model. • SBP promotes neovessel formation and prevents necrosis of acutely ischemic tissues in a hind limb ischemia model. [ABSTRACT FROM AUTHOR]

To evaluate the effectiveness and safety of hypothermic perfusion in the phacoemulsification of hard nuclear cataract. Tertiary opthalmology center, China. Laboratory study and prospective randomized clinical trial. Rabbits and patients with hard nuclear cataract underwent phacoemulsification with perfusion temperatures at 4°C or 24°C. Anterior segment optical coherence tomography (AS-OCT), corneal endothelial cell count (ECC), and cornea sections were observed before the rabbits' operation and 1 day and 7 days postoperatively. AS-OCT, corneal ECC, and anterior chamber (AC) inflammation were observed before the patients' operation and 1 day, 7 days, and 30 days postoperatively. The study comprised 40 rabbits and 80 patients. In the animal models, the mean central corneal thickness (CCT) in the 4°C group (370.4 μm ± 45.5 [SD]) was thinner than in the 24°C group (496.7 ± 121.5 μm) 1 day postoperatively (P <.001). The mean AC inflammation reaction grade in the 4°C group (1.1 ± 0.9) was lower than in the 24°C group (2.2 ± 0.8) (P =.0333). In clinical trials, the mean CCT and incisional corneal thicknesses in the 4°C group (600.7 ± 51.8 μm and 859.2 ± 177.8 μm, respectively) were thinner than in the 24°C group (655.3 ± 85.0 μm and 955.9 ± 196.7 μm, respectively) (P <.001). The endothelial cell density (P =.036) and hexagonality (P =.001) were higher in the 4°C group. The mean AC inflammation reaction grade in the 4°C group (0.6 ± 0.6) was lower than in the 24°C group (1.3 ± 1.0) 1 day postoperatively (P =.004). Hypothermic perfusion in phacoemulsification of hard nuclear cataract is safe and it can effectively protect corneal endothelium, decrease corneal edema, and reduce AC inflammation in the early postoperative stage. [ABSTRACT FROM AUTHOR]

Vascular endothelial growth factor (VEGF) is a heparin-specific growth factor specific for vascular endothelial cells and induces angiogenesis via binding to vascular endothelial growth factor receptor (VEGFR). Chronic kidney disease (CKD), accompanied by microvascular disease, is recognized as an irreversible reduction of renal function. The effects of VEGF on CKD risk were evaluated in this study. 121 CKD patients and 50 healthy volunteers were evaluated in the current study. Data mining using the China Biological Medicine (CBM) and NCBI/PubMed databases, was performed and applicable investigations were pursued. Pooled mean differences (MD) and pooled odds ratios (OR), with corresponding confidence intervals (CIs), were calculated by meta-analysis. The levels of Scr, BUN and VEGF in the CKD group were significantly higher, when compared with the control group (P < 0.01). For the meta-analysis, thirteen articles and our current study were evaluated. VEGF levels was found to be associated with CKD risk (P < 0.00001). In the sub-group meta-analysis, we found that the pooled MD of VEGF levels was related to the early CKD group, although the difference was not notable. However, the meta-analysis itself indicated that the pooled MD of VEGF levels were in accordance with severe CKD group (P < 0.00001). Furthermore, VEGF +936C/T T allele was not associated with CKD risk (P = 0.69). VEGF levels are apparently associated with CKD risk, especially in more severe CKD. Gene polymorphism analysis indicates that the VEGF +936C/T T allele is not associated with CKD risk.

High glucose (HG) induces vascular injury in diabetes. Hydroxysafflor yellow A (HSYA) has been used to ameliorate ischemic cardiovascular diseases in China for many years. In the present study, we assessed whether HSYA has a potential protective role in HG-induced human umbilical vein endothelial cell (HUVEC) injury. Cell viability was determined with an 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. Cell apoptosis was detected by fluorescein isothiocyanate/propidium iodide staining assay. The endothelial cell permeability was measured with a permeability assay. Cell adhesion molecule (CAM) expression, vascular endothelial growth factor, and basic fibroblast growth factor levels were detected with an enzyme-linked immunosorbent assay. Reactive oxygen species (ROS) formation was measured with a DCF-DA assay. Protein expression of NADPH oxidase 4 (NOX4) was measured by Western blotting. Our data indicated that HG increases HUVEC apoptosis, vascular permeability, monocyte adhesion, the level of CAMs, the formation of ROS, and NOX4 expression. Our data revealed that HG increases vascular injury, which is attenuated by HSYA. Because vascular inflammation has a key role in the development of diabetes mellitus, our results implied that HSYA is considered as a potential agent for diabetic vascular injury treatment. [ABSTRACT FROM AUTHOR]

Cooking oil fume-derived PM 2.5 (COF-PM 2.5) is a major source of indoor air contamination in China, which has been demonstrated to be a hazard factor of cardiovascular and cerebrovascular diseases. This study aimed to investigate the role of ROS-mediated PERK/ATF4 signaling activation in COF-PM 2.5 -inhibited extracorporeal tube formation in human umbilical vein endothelial cells (HUVECs). HUVECs were treated with 100 μg/mL COF-PM 2.5 at different times, with or without 100 nM PERK activity inhibitor GSK2606414 (GSK) or 200 μM antioxidant N-acetylcysteine (NAC) pretreatment. Our results showed that COF-PM 2.5 exposure can inhibit extracorporeal tube formation and down-regulate VEGFR2 expression in HUVECs. Furthermore, our data indicated that COF-PM 2.5 exposure can activate the PERK/ATF4 signaling in HUVECs. Mechanistically, pretreatment with GSK interdicted PERK/ATF4 signaling, thereby reversing COF-PM 2.5 -downregulated VEGFR2 protein expression in HUVECs. Furthermore, NAC reversed VEGFR2 expression downregulated induced by COF-PM 2.5 by inhibiting the upregulation of intracellular ROS levels and PERK/ATF4 signaling in HUVECs. As above, COF-PM 2.5 exposure could induce ROS release from HUVECs, which in turn activate the endoplasmic reticulum PERK/ATF4 signaling and inhibit tube formation of HUVECs. [Display omitted] • COF-PM 2.5 inhibits extracorporeal tube formation of HUVECs. • COF-PM 2.5 reduces VEGFR2 via ROS mediated PERK/ ATF4 signaling activation. • NAC reverses COF-PM 2.5 -reduced tube formation via downregulating ROS/PERK/ATF4 axis. [ABSTRACT FROM AUTHOR]

Purpose: To compare changes in endothelial morphology in the central and superior cornea in subjects wearing single-vision spectacles and orthokeratology lenses over two years.Methods: Endothelial images of the two locations of 99 subjects (6-12 years) from completed myopia control studies were analysed. Endothelial cell density (ECD), coefficient of variation in cell size (CV), and hexagonality (HEX) before and two years after treatment were compared between the two groups of subjects.Results: Baseline ECD and CV in the central cornea were slightly lower than those in the superior cornea, but no significant difference in HEX was found in the two corneal locations. After two years, reduction in ECD and increase in CV were only significant in the central cornea, but not in the superior cornea. Reduction in HEX was significant in both corneal locations. Subjects receiving orthokeratology had smaller reduction in ECD in the central cornea compared to the controls (orthokeratology: 56±94 cells/mm2; control: 98±91 cells/mm2, p=0.024), otherwise, there were no significant differences in the changes in endothelial morphology in the two corneal locations between the two groups of subjects.Conclusions: The current study confirmed that there were differences in endothelial morphology of central and superior cornea of Chinese children aged 6-12 years. The morphological response to normal ageing differed between the two corneal locations as reduction in cell density and polymegathism were found only in the central cornea whilst pleomorphism was found in both locations. Orthokeratology lens wear had minimal effect on the developmental changes in endothelial morphology. [ABSTRACT FROM AUTHOR]