Publications by authors named "Chun-Lin Chen"

122 Publications

Three-Dimensional Computed Tomography Scanning of Temporal Vessels to Assess the Safety of Filler Injections.

Aesthet Surg J 2021 Feb 27. Epub 2021 Feb 27.

Department of Plastic and Reconstructive Surgery, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong, China.

Background: Temple filler injection is one of the most common minimally invasive cosmetic procedures involving the face; however, vascular complications are not uncommon.

Objectives: This study aimed to investigate the anatomy of the temporal vessels and provide a more accurate protocol for temple filler injection.

Methods: Computed tomography (CT) scans of 56 cadaveric heads injected with lead oxide were obtained. We then used Mimics software to construct 3-dimensional (3D) images of the temporal vessels described by a coordinate system based on the bilateral tragus and right lateral canthus.

Results: In the XOY plane, the superficial temporal artery (STA), middle temporal artery (MTA), zygomatico-orbital artery (ZOA), posterior branch of the deep temporal artery (PDTA), and lateral margin of the orbital rim divide the temple into 4 parts (A, B, C, and D). The probabilities of the STA, MTA, ZOA, and PDTA appearing in parts A, B, C, and D were 30.73%, 37.06%, 39.48%, and 77.18%, respectively. In 3D images, these vessels together compose an arterial network that is anastomosed with other vessels, such as the external carotid, facial, and ocular arteries.

Conclusions: 3D CT images can digitally elucidate the exact positions of temporal vessels in a coordinate system, improving the safety of temple filler injections in a clinical setting.
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http://dx.doi.org/10.1093/asj/sjaa371DOI Listing
February 2021

Garcimultiflorone K from Garcinia multiflora attenuates hepatocellular carcinoma metastasis by suppressing transforming growth factor-β signaling.

Phytomedicine 2021 Apr 12;84:153502. Epub 2021 Feb 12.

Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung 80424, Taiwan ROC; Department of Biotechnology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan ROC; Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung 80708, Taiwan ROC. Electronic address:

Background: Transforming growth factor‑β (TGF-β) signaling is a crucial inducer of tissue fibrosis and extracellular matrix accumulation and a vital suppressor of epithelial cell proliferation and cancer metastasis. The nature of this multifunctional cytokine has prompted the development of TGF-β signaling inhibitors as therapeutic agents. Our research group has recently isolated the polyprenylated polycyclic acylphloroglucinol garcimultiflorone K (GMK) from the stems of Garcinia multiflora; GMK exhibits antiangiogenic activity in endothelial cells.

Purpose: In the current study, we aimed to explore the antitumor effect and detailed mechanisms of Garcimultiflorone K in hepatocellular carcinoma cells.

Methods: Cell proliferation and viability were evaluated using the MTT assay. The migratory ability of HepG2 cells was measured using wound healing assays. The inhibitory effect of GMK against the nuclear translocation of Smad by TGF-β was assessed through immunofluorescence staining and Western blotting. To investigate TGF-β-dependent gene expression profiles upon GMK stimulation, RNA transcript levels were determined using reverse transcription polymerase chain reaction. The effects of GMK in Smad2-driven transcriptomic activities were studied using a reporter gene assay. Protein levels were detected using Western blotting.

Results: Our data revealed that GMK inhibited TGF-β-induced cellular responses, including Smad protein phosphorylation, cell migration, and extracellular matrix production, during epithelial-mesenchymal transition (EMT). Mechanistic studies further demonstrated that GMK suppressed TGF-β signaling by downregulating TGF-β receptor II (TβRII).

Conclusion: These findings elucidate that TβRII expression in hepatic cells can be specifically suppressed by GMK to attenuate metastasis and the disease-promoting effects of EMT, representing a therapeutic approach.
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http://dx.doi.org/10.1016/j.phymed.2021.153502DOI Listing
April 2021

The Effect of Previous Irradiation for Patients With Prosthetic Breast Reconstruction: A Meta-Analysis.

Aesthet Surg J 2021 Feb 23. Epub 2021 Feb 23.

Department of Plastic and Reconstructive Surgery, Guangdong Second Provincial General Hospital, Guangzhou, China.

Background: Results regarding immediate prosthetic breast reconstruction after postmastectomy radiation therapy (PMRT) have been inconsistent.

Objectives: The authors aimed to assess the efficacy and safety of PMRT before immediate prosthetic breast reconstruction for patients with breast cancer.

Methods: Electronic databases (PubMed, EmBase, and the Cochrane Library) were systematically searched to identify eligible studies from their inception until March 2020. The pooled odds ratio (OR) with 95% confidence intervals (CIs) was applied as an effect estimate and calculated using the random-effects model.

Results: Nineteen studies including a total of 6757 patients were selected for final meta-analysis. The pooled OR showed that PMRT was associated with a higher incidence of reconstruction failure (OR = 2.57; 95% CI =1.55-4.26; P < 0.001), capsular contracture (OR = 5.99; 95% CI = 3.12-11.47; P < 0.001), and overall complications (OR = 2.52; 95% CI = 1.68-3.79; P < 0.001). It was also associated with a lower incidence of patient satisfaction (OR = 0.29; 95% CI = 0.16-0.52; P < 0.001) and good aesthetic results (OR = 0.25; 95% CI = 0.12-0.52; P < 0.001) compared with those who did not undergo PMRT. These significant associations could be affected by study design, mean age, stage of immediate breast reconstruction, follow-up, and study quality.

Conclusions: Although PMRT is the standard adjuvant therapy for mastectomy patients treated with immediate implant-based breast reconstruction, PMRT for patients undergoing immediate implant-based breast reconstruction has been associated with high risks of reconstruction failure, capsular contracture, and overall complications as well as low incidences of patient satisfaction and good aesthetic results.

Level Of Evidence: 4:
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http://dx.doi.org/10.1093/asj/sjaa372DOI Listing
February 2021

Recent progress in TGF-β inhibitors for cancer therapy.

Biomed Pharmacother 2021 Feb 16;134:111046. Epub 2020 Dec 16.

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan, ROC; Department of Biotechnology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan ROC; Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung 80708, Taiwan ROC. Electronic address:

Transforming growth factor-β (TGF-β) is a multifunctional cytokine that is involved in proliferation, metastasis, and many other important processes in malignancy. Inhibitors targeting TGF-β have been considered by pharmaceutical companies for cancer therapy, and some of them are in clinical trial now. Unfortunately, several of these programs have recently been relinquished, and most companies that remain in the contest are progressing slowly and cautiously. This review summarizes the TGF-β signal transduction pathway, its roles in oncogenesis and fibrotic diseases, and advancements in antibodies and small-molecule inhibitors of TGF-β.
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http://dx.doi.org/10.1016/j.biopha.2020.111046DOI Listing
February 2021

Three-Dimensional Computed Tomographic Study on the Vessels of the Zygomatic Region: Arterial Variations and Clinical Relevance.

Plast Reconstr Surg 2021 Feb;147(2):328-336

From the Department of Plastic and Reconstructive Surgery, Guangdong Second Provincial People's Hospital.

Background: Injection-based techniques for "cheek augmentation" have gained popularity in recent years. The aim of this study was to perform a topographic analysis of the depth and distribution of the vessels in the zygomatic region to facilitate clinical procedures.

Methods: The external carotid arteries of seven cadaveric heads were infused with lead oxide contrast medium. The facial and superficial temporal arteries of another 12 cadaveric heads were injected sequentially with the same medium. Computed tomographic scanning was then performed, and three-dimensional computed tomographic scans were reconstructed using validated algorithms.

Results: The vessels on the zygomatic arch received a double blood supply from across the upper and lower borders of the arch, and the number of the vessels varied from one to four. Ninety percent of the vessels on the zygomatic arch were at a depth of 1 to 2.5 mm, and 75 percent were at a depth of 10 to 30 percent of the soft-tissue thickness. The vessels were concentrated on the midline of the zygomatic arch and the lateral margin of the frontal process. All samples showed a vessel travel along the lateral margin of the frontal process that eventually merged into the superior marginal arcades.

Conclusions: This study reported a topographic analysis of the depth and distribution of the vessels in the zygomatic region based on three-dimensional scanning. The results indicated that injection on the zygomatic arch should be performed deep to the bone, and the vascular zones anterior or posterior to the midline of the zygomatic arch were relatively safe injection areas.
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http://dx.doi.org/10.1097/PRS.0000000000007519DOI Listing
February 2021

UBE2C is a Potential Biomarker for Tumorigenesis and Prognosis in Tongue Squamous Cell Carcinoma.

Diagnostics (Basel) 2020 Sep 4;10(9). Epub 2020 Sep 4.

Department of Otorhinolaryngology-Head and Neck Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.

Ubiquitin-conjugating enzyme 2C (UBE2C) involves in numerous cellular processes and the tumor progression in many cancers. However, its role in oral squamous cell carcinoma (OSCC) is unclear. We aimed to investigate the role and clinical significance of UBE2C in OSCC. The expression levels of UBE2C were examined by immunohistochemistry in 185 buccal mucosa squamous cell carcinomas, 247 tongue squamous cell carcinomas (TSCCs) and 75 lip squamous cell carcinomas. The roles of UBE2C in cell growth, invasion/migration and cancer stemness were also examined in OSCC cells. The expression levels of UBE2C protein were higher in tumor tissues than they were in the corresponding tumor adjacent normal tissues from OSCC patients. Higher UBE2C expression was associated with poor cell differentiation and lymph node invasion in OSCC patients. High UBE2C expression was also correlated with shorter disease-specific survival in TSCC patients having poor cell differentiation, advanced pathological stages, lymph node metastasis as well as receiving radiation therapy. Compared to control cells, OSCC cells in which UBE2C was silenced showed decreased cell proliferation, migration/invasion and colony formation and they exhibited lower expression levels of the following cancer stemness markers-ALDH1/A2, CD44, CD166 and EpCAM. High co-expression levels of UBE2C/CD44, UBE2C/CD166 and UBE2C/EpCAM were associated with poor prognosis in oral cancer patients from The Cancer Genome Atlas database. Our findings indicated that UBE2C might be a potential biomarker for tumorigenesis and prognosis in TSCC.
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http://dx.doi.org/10.3390/diagnostics10090674DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555092PMC
September 2020

In vivo monitoring of carbonic anhydrase expression during the growth of larval zebrafish: a new environment-sensitive fluorophore for responsive turn-on fluorescence.

Chem Commun (Camb) 2020 Sep 25;56(76):11307-11310. Epub 2020 Aug 25.

Department of Chemistry, National Sun Yat-sen University, Kaohsiung 80424, Taiwan.

This study monitors the dynamic progress of a newly developed background-free, target responsive strategy; 2,3-dihydroquinolin-4-imine (DQI) that can instantly respond to environmental changes with fluorescence enhancement, revealing a comprehensive platform for in vivo fluorescence bioimaging of mebrane-bound carbonic anhydrase II in HeLa cells and its expression during the growth of larval zebrafish.
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http://dx.doi.org/10.1039/d0cc03090bDOI Listing
September 2020

Association of early vertebroplasty with risk of hip replacement: A nationwide population-based cohort study in Taiwan.

Medicine (Baltimore) 2020 Jul;99(27):e20926

Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei.

Studies show that vertebral fractures could predict the risk of hip fractures. We aimed to evaluate the potential benefits of whether the timing of vertebroplasty (VP) for vertebral fracture associated with the risk of hip fracture for hip replacement.We identified 142,782 patients from the Taiwan National Health Insurance Database with thoracolumbar vertebral fracture (International Classification of Diseases, Ninth Revision, Clinical Modification:805.2-805.9) who were followed up from 2000 to 2013. These patients were divided into those who underwent VP (VP group) (International Classification of Diseases, Ninth Revision, Clinical Modification : 78.49) within 3 months and those who did not (non-VP group). After adjusting for the confounding factors, the Cox proportional hazards analysis was used to estimate the effect of early VP on reducing the risk of hip fracture. The difference in the risk of hip replacement, between the VP group and non-VP group was estimated using the Kaplan-Meier method with the log-rank test.In the 14-year follow-up, the cumulative incidence rate of hip replacement in the VP group was lower than that in the non-VP group (0.362% and 0.533%, respectively, long-rank P < .001). There was a significant difference between the 2 groups since the first-year follow-up.Our study showed that early VP performed to avoid progression of the kyphotic changes following thoracolumbar vertebral fracture may reduce the risk of hip fracture. These results, obtained from retrospective data, indicate that a prospective study is warranted.
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http://dx.doi.org/10.1097/MD.0000000000020926DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337416PMC
July 2020

5-HT7 Receptor Inhibition Transiently Improves Respiratory Function Following Daily Acute Intermittent Hypercapnic-Hypoxia in Rats With Chronic Midcervical Spinal Cord Contusion.

Neurorehabil Neural Repair 2020 04 26;34(4):333-343. Epub 2020 Feb 26.

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.

. Intermittent hypoxia can induce respiratory neuroplasticity to enhance respiratory motor outputs following hypoxic treatment. This type of respiratory neuroplasticity is primarily mediated by the activation of Gq-protein-coupled 5-HT2 receptors and constrained by Gs-protein-coupled 5-HT7 receptors. . The present study hypothesized that the blockade of 5-HT7 receptors can potentiate the effect of intermittent hypercapnic-hypoxia on respiratory function after cervical spinal cord contusion injury. . The ventilatory behaviors of unanesthetized rats with midcervical spinal cord contusions were measured before, during, and after daily acute intermittent hypercapnic-hypoxia (10 episodes of 5 minutes of hypoxia [10% O, 4% CO, 86% N] with 5 minutes of normoxia intervals for 5 days) at 8 weeks postinjury. On a daily basis, 5 minutes before intermittent hypercapnic-hypoxia, rats received either a 5-HT7 receptor antagonist (SB269970, 4 mg/kg, intraperitoneal) or a vehicle (dimethyl sulfoxide). . Treatment with intermittent hypercapnic-hypoxia induced a similar increase in tidal volume between rats that received SB269970 and those that received dimethyl sulfoxide within 60 minutes post-hypoxia on the first day. However, after 2 to 3 days of daily acute intermittent hypercapnic-hypoxia, the baseline tidal volumes of rats treated with SB269970 increased significantly. . These results suggest that inhibiting the 5-HT7 receptor can transiently improve daily intermittent hypercapnic-hypoxia-induced tidal volume increase in midcervical spinal contused animals. Therefore, combining pharmacological treatment with rehabilitative intermittent hypercapnic-hypoxia training may be an effective strategy for synergistically enhancing respiratory neuroplasticity to improve respiratory function following chronic cervical spinal cord injury.
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http://dx.doi.org/10.1177/1545968320905806DOI Listing
April 2020

Retinal blood vessel-origin yes-associated protein (YAP) governs astrocytic maturation via leukaemia inhibitory factor (LIF).

Cell Prolif 2020 Feb 8;53(2):e12757. Epub 2020 Jan 8.

Department of Ophthalmology, Research Institute of Surgery & Daping Hospital, Army Medical Center of PLA, Army Medical University, Chongqing, China.

Objectives: To testify that endothelial cells (ECs) induce astrocyte maturation by leukaemia inhibitory factor (LIF) secretion.

Materials And Methods: In vivo experiments, mice bearing floxed alleles of YAP were crossed with mice expressing a Cre recombinase driven by the endothelial Tek promoter (Tek-Cre) to finally obtain the following three genotypes: YAP , Tek-Cre; YAP , Tek-Cre; and YAP . Retinal vascularization and astrocyte network were evaluated by whole-mount fluorescence and Western blotting. In vitro, experiments were performed in an astrocyte and human microvascular endothelial cell (HMEC-1) coculture model to analyse the mechanisms underlying the effect of endothelial YAP on astrocytes.

Results: In vivo, YAP ;Tek-Cre mice showed delayed angiogenesis, sparse vessels and decreased glial fibrillary acidic protein (GFAP)+ astrocytes but aberrant growth of endothelial networks and immature astrocytes (platelet-derived growth factor A, PDGFRA+ astrocytes) overgrowth. In vitro, Yap deletion attenuated the LIF release that delayed the maturation of retinal astrocyte which was consistent with the results of HMEC-1-astrocyte coculture. The effect of YAP overexpression on LIF-LIFR axis in HMEC-1 interferes the GFAP expression of astrocyte. In contrast, LIF protein rescues the astrocytic GFAP expression when EC YAP was inhibited by siRNAs.

Conclusions: We show that EC yes-associated protein (YAP) is not only a critical coactivator of Hippo signalling in retinal vessel development but also plays an essential role in retinal astrocyte maturation by regulating LIF production.
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http://dx.doi.org/10.1111/cpr.12757DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7046482PMC
February 2020

Roles of Myosin-Mediated Membrane Trafficking in TGF-β Signaling.

Int J Mol Sci 2019 Aug 12;20(16). Epub 2019 Aug 12.

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan.

Recent findings have revealed the role of membrane traffic in the signaling of transforming growth factor-β (TGF-β). These findings originate from the pivotal function of TGF-β in development, cell proliferation, tumor metastasis, and many other processes essential in malignancy. Actin and unconventional myosin have crucial roles in subcellular trafficking of receptors; research has also revealed a growing number of unconventional myosins that have crucial roles in TGF-β signaling. Unconventional myosins modulate the spatial organization of endocytic trafficking and tether membranes or transport them along the actin cytoskeletons. Current models do not fully explain how membrane traffic forms a bridge between TGF-β and the downstream effectors that produce its functional responsiveness, such as cell migration. In this review, we present a brief overview of the current knowledge of the TGF-β signaling pathway and the molecular components that comprise the core pathway as follows: ligands, receptors, and Smad mediators. Second, we highlight key role(s) of myosin motor-mediated protein trafficking and membrane domain segregation in the modulation of the TGF-β signaling pathway. Finally, we review future challenges and provide future prospects in this field.
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http://dx.doi.org/10.3390/ijms20163913DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719161PMC
August 2019

Neogenin-loss in neural crest cells results in persistent hyperplastic primary vitreous formation.

J Mol Cell Biol 2020 01;12(1):17-31

Department of Neuroscience & Regenerative Medicine and Department of Neurology, Augusta University, Augusta, GA 30912, USA.

Neogenin is a transmembrane receptor critical for multiple cellular processes, including neurogenesis, astrogliogenesis, endochondral bone formation, and iron homeostasis. Here we present evidence that loss of neogenin contributes to pathogenesis of persistent hyperplastic primary vitreous (PHPV) formation, a genetic disorder accounting for ~ 5% of blindness in the USA. Selective loss of neogenin in neural crest cells (as observed in Wnt1-Cre; Neof/f mice), but not neural stem cells (as observed in GFAP-Cre and Nestin-Cre; Neof/f mice), resulted in a dysregulation of neural crest cell migration or delamination, exhibiting features of PHPV-like pathology (e.g. elevated retrolental mass), unclosed retinal fissure, and microphthalmia. These results demonstrate an unrecognized function of neogenin in preventing PHPV pathogenesis, implicating neogenin regulation of neural crest cell delamination/migration and retinal fissure formation as potential underlying mechanisms of PHPV.
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http://dx.doi.org/10.1093/jmcb/mjz076DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053014PMC
January 2020

Dulaglutide Modulates the Development of Tissue-Infiltrating Th1/Th17 Cells and the Pathogenicity of Encephalitogenic Th1 Cells in the Central Nervous System.

Int J Mol Sci 2019 Mar 29;20(7). Epub 2019 Mar 29.

Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung City 807, Taiwan.

GLP-1 (glucagon-like peptide-1) has been reported to play a vital role in neuroprotection. Experimental autoimmune encephalomyelitis (EAE) is a well-established animal model widely used to study human multiple sclerosis, a chronic demyelination disease in the central nervous system (CNS). Recently, important studies have designated that the signaling axis of GLP-1 and its receptor controls the clinical manifestations and pathogenesis of EAE. However, it is elusive whether GLP-1 receptor signaling regulates the phenotype of autoreactive T cells in the CNS. We administered dulaglutide, a well-established GLP-1 receptor agonist (GLP-1 RA), to treat EAE mice prophylactically or semi-therapeutically and subsequently analyzed the mononuclear cells of the CNS. In this study, dulaglutide treatment significantly alleviates the clinical manifestations and histopathological outcomes of EAE. Dulaglutide decreases incidences of encephalitogenic Th1/Th17 cells and Th1 granulocyte-macrophage-colony-stimulating factor (GM-CSF) expression in the CNS. Administration of dulaglutide failed to control the chemotactic abilities of encephalitogenic Th1 and Th17 cells; however, prophylactic treatment considerably decreased the populations of dendritic cells and macrophages in the CNS parenchyma. These results obtained indicate that dulaglutide modulates the differentiation of encephalitogenic Th1/Th17 and the pathogenicity of Th1 cells by influencing antigen presenting cells quantities, providing mechanism insight on T cells regulation in ameliorating EAE by GLP-1.
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http://dx.doi.org/10.3390/ijms20071584DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6479396PMC
March 2019

Optimal Use Ratio of the Stromal Vascular Fraction (SVF): An Animal Experiment Based on Micro-CT Dynamic Detection After Large-Volume Fat Grafting.

Aesthet Surg J 2019 05;39(6):NP213-NP224

Department of Plastic and Reconstructive Surgery, Guangdong Second Provincial General Hospital, Guangzhou City, China.

Background: The addition of the stromal vascular fraction (SVF) can enhance the postoperative survival rate of fat. However, a universal SVF application method is currently unavailable. Therefore, a simple and convenient guideline for SVF addition is needed for its clinical application.

Objectives: The authors sought to evaluate whether SVF can improve fat survival after large-volume fat grafting and to find a simple and convenient standard for the clinical use of SVF.

Methods: Patient fat samples were obtained after liposuction for SVF preparation and grafting. Four types of grafts were prepared with different SVF ratios: 0:1, 1:1, 2:1, and 4:1 SVF:fat. After intensive mixing, fat grafts (5 mL) were randomly injected into both sides of the backs of athymic rats (n = 15). At 24 hours and 1, 3, 6, and 9 months after the operation, microcomputed tomography scanning was performed to calculate the fat survival rate.

Results: Nine months after the operation, the survival rates of fat in the 4 groups were 8.89 ± 1.62% (0:1), 18.26 ± 3.85% (1:1), 8.83 ± 1.46% (2:1), and 7.96 ± 1.31% (4:1). The 1:1 group exhibited the greatest survival rate (P < 0.01), and the adipose tissue histological patterns and blood vessel quality were enhanced compared with those in the other groups.

Conclusions: An appropriate SVF ratio can increase the fat survival rate after large-volume fat grafting, but no linear relationship exists between the SVF ratio and fat survival. The optimal SVF:fat ratio for grafting is 1:1.
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http://dx.doi.org/10.1093/asj/sjy266DOI Listing
May 2019

Using 3D MRI can potentially enhance the ability of trained surgeons to more precisely diagnose Mullerian duct anomalies compared to MR alone.

Eur J Obstet Gynecol Reprod Biol 2018 Sep 9;228:313-318. Epub 2018 Jul 9.

Department of Obstetrics and Gynecology, Nan Fang Hospital of Southern Medical University, Guangzhou, Guangdong 510515, PR China. Electronic address:

Objective: The aim of this study was to examine if the advanced tool of 3D MRI model provides more precise information on the anatomy of pelvic organs than MRI alone, and compare to clinical and operative finding of patients with vagina in Müllerian duct anomalies.

Study Design: One hundred and ten patients with clinically and operatively proven Müllerian duct anomalies were included. The consistency of diagnosis of Mullerian tract anomalies by MRI and 3D MRI compared to clinically and surgically proven anomalies defined according to ASRM classification.

Results: We successfully reconstructed retrospectively all 110 patients' three-dimensional models from the simple MRI scans. Eighty-six of the patients (78.2%) showed an agenesis of the uterus, four patients presented with uterine didephys (3.6%). Septate uterus was detectable in 8 of 110 cases (7.3%). Arcuate uterus was detectable in 3 of 110 cases (2.7%). The remaining patients presented with either unilateral (n = 4; 3.6%) or bilateral (n = 5; 4.5%) uterine horns. Reviewed by radiologists, comparing the agreement rate between 3D- MRI reconstruction models and simple MRI, there was a trend towards but not significant difference (P = 0.064). Reviewed by trained surgeons, the agreement between three-dimensional MRI reconstruction models and MRI, there was significant difference (P = 0.003).

Conclusion: 3D MRI model is a non-expensive add-on software tool that enhance the ability of expert surgeon to reach a more precise diagnosis of the pelvic anatomy structures, compared to MRI alone. Getting a more precise description of the pelvic anatomy allows a better planning of the corrective procedure needed and preoperative assessment of the expected prognosis.
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http://dx.doi.org/10.1016/j.ejogrb.2018.07.007DOI Listing
September 2018

Morphine Induces Fibroblast Activation through Up-regulation of Connexin 43 Expression: Implication of Fibrosis in Wound Healing.

Int J Med Sci 2018 4;15(9):875-882. Epub 2018 Jun 4.

Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung, Taiwan.

Morphine is the most effective drugs for attenuating various types of severe pain, but morphine abuse carries a high risk of systemic fibrosis. Our previous have indicated that systemic administration of morphine hinders angiogenesis and delays wound healing. Here we have explained the pathological mechanism underlying the effect of morphine on wound healing. To determine how morphine affects wound healing, we first created a wound in mice treated them with a combination of a low doses (5 mg/kg/day) and high doses (20 or 30 mg/kg/day) of morphine. An study revealed that high-dose morphine-induced abnormal myofibroblasts persist after the end of wound healing because of connexin 43 (Cx43) upregulation. High-dose morphine-induced Cx43 increased the expression levels of focal adhesion molecules, namely fibronectin and alpha-smooth muscle actin (α-SMA) through the activation of transforming growth factor (TGF)-β1 signaling. In addition, we found that Cx43 contributed to TGF-βRII/ Smad2/3 signaling for regulating the differentiation of fibroblasts into myofibroblasts during high-dose morphine exposure. In conclusion, the abnormal regulation of Cx43 by morphine may induce systemic fibrosis because of abnormal myofibroblast function.
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http://dx.doi.org/10.7150/ijms.23074DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036091PMC
January 2019

Four IVa bHLH Transcription Factors Are Novel Interactors of FIT and Mediate JA Inhibition of Iron Uptake in Arabidopsis.

Mol Plant 2018 09 28;11(9):1166-1183. Epub 2018 Jun 28.

The State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address:

Plants have evolved sophisticated genetic networks to regulate iron (Fe) homeostasis for their survival. Several classes of plant hormones including jasmonic acid (JA) have been shown to be involved in regulating the expression of iron uptake and/or deficiency-responsive genes in plants. However, the molecular mechanisms by which JA regulates iron uptake remain unclear. In this study, we found that JA negatively modulates iron uptake by downregulating the expression of FIT (bHLH29), bHLH38, bHLH39, bHLH100, and bHLH101 and promoting the degradation of FIT protein, a key regulator of iron uptake in Arabidopsis. We further demonstrated that the subgroup IVa bHLH proteins, bHLH18, bHLH19, bHLH20, and bHLH25, are novel interactors of FIT, which promote JA-induced FIT protein degradation. These four IVa bHLHs function redundantly to antagonize the activity of the Ib bHLHs (such as bHLH38) in regulating FIT protein stability under iron deficiency. The four IVa bHLH genes are primarily expressed in roots, and are inducible by JA treatment. Moreover, we found that MYC2 and JAR1, two critical components of the JA signaling pathway, play critical roles in mediating JA suppression of the expression of FIT and Ib bHLH genes, whereas they differentially modulate the expression of bHLH18, bHLH19, bHLH20, and bHLH25 to regulate FIT accumulation under iron deficiency. Taken together, these results indicate that by transcriptionally regulating the expression of different sets of bHLH genes JA signaling promotes FIT degradation, resulting in reduced expression of iron-uptake genes, IRT1 and FRO2, and increased sensitivity to iron deficiency. Our data suggest that there is a multilayered inhibition of iron-deficiency response in the presence JA in Arabidopsis.
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http://dx.doi.org/10.1016/j.molp.2018.06.005DOI Listing
September 2018

Four New 2-(2-Phenylethyl)-4H-chromen-4-one Derivatives from the Resinous Wood of Aquilaria sinensis and Their Inhibitory Activities on Neutrophil Pro-Inflammatory Responses.

Planta Med 2018 Dec 28;84(18):1340-1347. Epub 2018 Jun 28.

Faculty of Pharmacy, School of Pharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan.

Four new 2-(2-phenylethyl)-4-chromen-4-one derivatives, 6-hydroxy-5-methoxy-2-[2-(4'-methoxyphenyl)ethyl]chromone (1: ), 6,7-dimethoxy-2-[2-(2'-hydroxyphenyl)ethyl]chromone (2: ), 5-hydroxy-6-methoxy-2-[2-(3'-methoxyphenyl)ethyl]-chromone (3: ), and 7-chloro-8-hydroxy-2-[2-(4'-methoxyphenyl)ethyl]chromone (4: ), have been isolated from the resinous wood of , together with 16 known compounds (5: -20: ). Among these, 7-methoxy-2-[2-(4'-methoxyphenyl)ethyl]chromone (5: ) was isolated from a natural source for the first time. The structures of the new compounds were established by spectroscopic analyses (1D and 2D NMR, HR-ESI-MS, IR, UV). Nine compounds, including 1: showed more than 80% inhibition of superoxide anion generation by human neutrophils in response to formyl-L-methionyl-L-leucyl-L-phenylalanine at 50 µM.
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http://dx.doi.org/10.1055/a-0645-1437DOI Listing
December 2018

Study on the cephalopelvic relationship with cephalic presentation in nulliparous full-term Chinese pregnant women by MRI with three-dimensional reconstruction.

Arch Gynecol Obstet 2018 08 13;298(2):433-441. Epub 2018 Jun 13.

Department of Obstetrics and Gynecology of Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

Purpose: To analyze the relationship between fetal head size and maternal pelvis size using magnetic resonance imaging (MRI) with a 3-D reconstruction technique.

Methods: A total of 301 nulliparous full-term Chinese pregnant women with cephalic presentation were enrolled and received MRI examinations before labor onset. Data were collected and imported into Mimics software to reconstruct the maternal pelvis and fetus.

Results: Of 301 pregnant women, 212 underwent vaginal delivery and 32 received cesarean section. The body mass index (BMI) was significantly different between the vaginal delivery group and the suspected cephalopelvic disproportion (CPD) group; the larger the BMI, the higher was the risk of CPD. The transverse diameter of the pelvic inlet and the posterior sagittal diameter of the midpelvis were significantly larger in the vaginal delivery group, compared with the suspected CPD group. Fetal weight > 3.5 kg could be used as a diagnostic indicator for CPD.

Conclusions: BMI is a risk factor for CPD, and fetal weight < 3.5 kg is an important diagnostic indicator for natural delivery in Chinese pregnant women.
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http://dx.doi.org/10.1007/s00404-018-4814-5DOI Listing
August 2018

Preparation and application of magnetic molecularly imprinted polymers for the isolation of chelerythrine from Macleaya cordata.

J Sep Sci 2018 Aug 3;41(16):3318-3327. Epub 2018 Jul 3.

Ningbo Institute of Materials Technology & Engineering, Chinese Academy of Sciences, Ningbo, P. R. China.

A novel type of magnetic molecularly imprinted polymer was prepared for the selective enrichment and isolation of chelerythrine from Macleaya cordata (Willd) R. Br. The magnetic molecularly imprinted polymers were prepared using functional Fe O @SiO as a magnetic support, chelerythrine as template, methacrylic acid as functional monomer, and ethylene glycol dimethacrylate as cross-linker. Density functional theory at the B3LYP/6-31G (d, p) level with Gaussian 09 software was applied to calculate the interaction energies of chelerythrine, methacrylic acid and the complexes formed from chelerythrine and methacrylic acid in different ratios. The structural features and morphology of the synthesized polymers were characterized by using Fourier transform infrared spectroscopy, X-ray diffraction, transmission electron microscopy, and vibration sample magnetometry. Adsorption experiments revealed that the magnetic molecularly imprinted polymers possessed rapid kinetics, high selectivity, and a higher binding capacity (7.96 mg/g) to chelerythrine than magnetic molecularly non-imprinted polymers (2.36 mg/g). The adsorption process was in good agreement with the Langmuir adsorption isotherm and pseudo-second-order kinetics models. Furthermore, the magnetic molecularly imprinted polymers were successfully employed as adsorbents for the extraction and enrichment of chelerythrine from Macleaya cordata (Willd) R. Br. The results indicated that the magnetic molecularly imprinted polymers were suitable for the selective adsorption of chelerythrine from complex samples such as natural medical plants.
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http://dx.doi.org/10.1002/jssc.201800245DOI Listing
August 2018

BMP-2 restoration aids in recovery from liver fibrosis by attenuating TGF-β1 signaling.

Lab Invest 2018 08 22;98(8):999-1013. Epub 2018 May 22.

Institute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.

Transforming growth factor-β (TGF-β) plays a central role in hepatic fibrogenesis. This study investigated the function and mechanism of bone morphogenetic protein-2 (BMP-2) in regulation of hepatic fibrogenesis. BMP-2 expression in fibrotic liver was measured in human tissue microarray and mouse models of liver fibrosis induced by bile duct ligation surgery or carbon tetrachloride administration. Adenovirus-mediated BMP-2 gene delivery was used to test the prophylactic effect on liver fibrosis. Primary hepatic stellate cells (HSC), HSC-T6 and clone-9 cell lines were used to study the interplay between BMP-2 and TGF-β1. Hepatic BMP-2 was localized in parenchymal hepatocytes and activated HSCs and significantly decreased in human and mouse fibrotic livers, showing an opposite pattern of hepatic TGF-β1 contents. BMP-2 gene delivery alleviated the elevations of serum hepatic enzymes, cholangiocyte marker CK19, HSC activation markers, and liver fibrosis in both models. Mechanistically, exogenous TGF-β1 dose dependently reduced BMP-2 expression, whereas BMP-2 significantly suppressed expression of TGF-β and its cognate type I and II receptor peptides, as well as the induced Smad3 phosphorylation levels in primary mouse HSCs. Aside from its suppressive effects on cell proliferation and migration, BMP-2 treatment prominently attenuated the TGF-β1-stimulated α-SMA and fibronectin expression, and reversed the TGF-β1-modulated epithelial-to-mesenchymal transition marker expression in mouse HSCs. The mutual regulation between BMP-2 and TGF-β1 signaling axes may constitute the anti-fibrogenic mechanism of BMP-2 in the pathogenesis of liver fibrosis. BMP-2 may potentially serve as a novel therapeutic target for treatment of liver fibrosis.
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http://dx.doi.org/10.1038/s41374-018-0069-9DOI Listing
August 2018

Pentabromopseudilin: a myosin V inhibitor suppresses TGF-β activity by recruiting the type II TGF-β receptor to lysosomal degradation.

J Enzyme Inhib Med Chem 2018 Dec;33(1):920-935

a Department of Biological Sciences , National Sun Yat-sen University , Kaohsiung , Taiwan, ROC.

Pentabromopseudilin (PBrP) is a marine antibiotic isolated from the marine bacteria Pseudomonas bromoutilis and Alteromonas luteoviolaceus. PBrP exhibits antimicrobial, anti-tumour, and phytotoxic activities. In mammalian cells, PBrP is known to act as a reversible and allosteric inhibitor of myosin Va (MyoVa). In this study, we report that PBrP is a potent inhibitor of transforming growth factor-β (TGF-β) activity. PBrP inhibits TGF-β-stimulated Smad2/3 phosphorylation, plasminogen activator inhibitor-1 (PAI-1) protein production and blocks TGF-β-induced epithelial-mesenchymal transition in epithelial cells. PBrP inhibits TGF-β signalling by reducing the cell-surface expression of type II TGF-β receptor (TβRII) and promotes receptor degradation. Gene silencing approaches suggest that MyoVa plays a crucial role in PBrP-induced TβRII turnover and the subsequent reduction of TGF-β signalling. Because, TGF-β signalling is crucial in the regulation of diverse pathophysiological processes such as tissue fibrosis and cancer development, PBrP should be further explored for its therapeutic role in treating fibrotic diseases and cancer.
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http://dx.doi.org/10.1080/14756366.2018.1465416DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6009923PMC
December 2018

[Development of a near-infrared fluorescence imaging system based on fluorescence properties of methylene blue].

Nan Fang Yi Ke Da Xue Xue Bao 2018 Apr;38(4):414-420

Department of Biomedical Engineering, Southern Medical University, Guangzhou 510515, China. E-mail:

Objective: To develop a near-infrared fluorescence imaging system based on the fluorescence properties of methylene blue.

Methods: According to the optical properties of methylene blue, we used a custom-made specific LED light source and an interference filter, a CCD camera and other relevant components to construct the near-infrared fluorescence imaging system. We tested the signal-to-background ratio (SBR) of this imaging system for detecting methylene blue under different experimental conditions and analyzed the SBR in urine samples collected from 15 Wistar rats with intravenous injection of methylene blue at the doses of 0, 1.4, 1.6, 1.8, or 2.0 0 mg/kg methylene blue.

Results: The SBR of this imaging system for detecting methylene blue was affected by the concentration of methylene blue and the distance from the sample (P<0.05). In the urine samples from Wistar rats, the SBR varied with the the injection dose, and the rats injected with 1.6 mg/kg methylene blue showed the highest SBR (8.71∓0.20) in the urine (P<0.05).

Conclusion: This near-infrared fluorescence imaging system is useful for fluorescence detection of methylene blue and can be used for real-time recognition of ureters during abdominal surgery.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6765651PMC
April 2018

Sorafenib suppresses TGF-β responses by inducing caveolae/lipid raft-mediated internalization/degradation of cell-surface type II TGF-β receptors: Implications in development of effective adjunctive therapy for hepatocellular carcinoma.

Biochem Pharmacol 2018 08 18;154:39-53. Epub 2018 Apr 18.

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan, ROC; Doctoral Degree Program in Marine Biotechnology, National Sun Yat-sen University and Academia Sinica, Kaohsiung 80424, Taiwan, ROC. Electronic address:

Sorafenib is the only FDA approved drug for the treatment of advanced hepatocellular carcinoma (HCC) and other malignancies. Studies indicate that TGF-β signalling is associated with tumour progression in HCC. Autocrine and paracrine TGF-β promotes tumour growth and malignancy by inducing epithelial-mesenchymal transition (EMT). Sorafenib is believed to antagonize tumour progression by inhibiting TGF-β-induced EMT. It improves survival of patients but HCC later develops resistance and relapses. The underlying mechanism of resistance is unknown. Understanding of the molecular mechanism of sorafenib inhibition of TGF-β-induced signalling or responses in HCC may lead to development of adjunctive effective therapy for HCC. In this study, we demonstrate that sorafenib suppresses TGF-β responsiveness in hepatoma cells, hepatocytes, and animal liver, mainly by downregulating cell-surface type II TGF-β receptors (TβRII) localized in caveolae/lipid rafts and non-lipid raft microdomains via caveolae/lipid rafts-mediated internalization and degradation. Furthermore, sorafenib-induced downregulation and degradation of cell-surface TβRII is prevented by simultaneous treatment with a caveolae disruptor or lysosomal inhibitors. On the other hand, sorafenib only downregulates cell-surface TβRII localized in caveolae/lipid rafts but not localized in non-lipid raft microdomains in hepatic stellate cells. These results suggest that sorafenib inhibits TGF-β signalling mainly by inducing caveolae/lipid raft-mediated internalization and degradation of cell-surface TβR-II in target cells. They may also imply that treatment with agents which promote formation of caveolae/lipid rafts, TGF-β receptor kinase inhibitors (e.g., LY2157299) or TGF-β peptide antagonists (by liver-targeting delivery) may be considered as effective adjunct therapy with sorafenib for HCC.
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http://dx.doi.org/10.1016/j.bcp.2018.04.014DOI Listing
August 2018

A FIT-binding protein is involved in modulating iron and zinc homeostasis in Arabidopsis.

Plant Cell Environ 2018 07 23;41(7):1698-1714. Epub 2018 May 23.

The State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, 100101, China.

Fe and Zn are essential micronutrients for plant growth, and the interrelationship regarding their homeostasis is very complicated. In this study, we identified a FIT-binding protein (FBP) using the yeast two-hybrid system. The C-terminus of FBP binds to the bHLH domain of FIT, abolishing the DNA-binding capacity of FIT. Knockout of FBP results in an enhanced expression of NAS genes and a higher nicotianamine content, and the fbp mutant exhibits tolerance to excessive Zn. Physiological analyses reveal that the mutant fbp retains a larger amount of Zn in roots and transfers a greater proportion of Fe to shoots than that in wild type under Zn-excessive stress. As FBP is expressed in the root stele, the negative regulation caused by sequestration of FIT is restricted to this tissue, whereas other FIT-regulated genes, such as IRT1 and FRO2, which mainly expressed in root epidermis, do not show transcriptional upregulation in the fbp mutant. As an antagonistic partner, FBP offers a new approach to spatially fine-tune the expression of genes controlled by FIT. In conclusion, our findings provide a new insight to understand the interrelationship of Fe and Zn homeostasis in plants.
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http://dx.doi.org/10.1111/pce.13321DOI Listing
July 2018

Polyprenylated polycyclic acylphloroglucinol: Angiogenesis inhibitor from Garcinia multiflora.

Bioorg Med Chem Lett 2018 06 6;28(10):1860-1863. Epub 2018 Apr 6.

Faculty of Pharmacy, School of Pharmaceutical Sciences, National Yang-Ming University, Taipei 112, Taiwan; Department of Medical Research, China Medical University Hospital, Taichung 404, Taiwan. Electronic address:

A new polyprenylated polycyclic acylphloroglucinol, garcimultiflorone K (1), has been isolated from the stems of Garcinia multiflora, together with two known compounds, garcimultiflorone A (2) and garcimultiflorone B (3). The structure of new compound 1 was determined through spectroscopic methods including 1D and 2D NMR and MS analyses. The anti-angiogenic and anti-cancer effects of compounds 1-3 were evaluated in human endothelial progenitor cells (EPCs) and cancer cells. Of these, garcimultiflorone K (1) displayed the most potent anti-angiogenic property by suppressing cell growth and tube formation of EPCs. Compound 1 also exhibited growth-inhibitory activities against human hepatocellular carcinoma cell line SK-Hep-1 and hormone refractory prostate cancer cell line PC-3 with GI values of 4.3 ± 1.6 and 6.6 ± 0.4 μM, respectively.
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http://dx.doi.org/10.1016/j.bmcl.2018.04.006DOI Listing
June 2018

Pentachloropseudilin Inhibits Transforming Growth Factor-β (TGF-β) Activity by Accelerating Cell-Surface Type II TGF-β Receptor Turnover in Target Cells.

Chembiochem 2018 04 2;19(8):851-864. Epub 2018 Mar 2.

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung, 80424 ROC, Taiwan.

Pentachloropseudilin (PClP) is a chlorinated phenylpyrrole compound that was first isolated from Actinoplanes (ATCC33002), and its structure has been confirmed by chemical synthesis. PClP shows broad antimicrobial activity against Gram-negative and Gram-positive bacteria, protozoa, fungi, and yeast. In mammalian cells, PClP is known to act as a reversible and allosteric inhibitor of myosin 1c (Myo1c). Herein, we report that PCIP is a potent inhibitor of transforming growth factor-β (TGF-β)-stimulated signaling. PCIP inhibits TGF-β-stimulated Smad2/3 phosphorylation and plasminogen activator inhibitor-1 (PAI-1) promoter activation with an IC of 0.1 μm in target cells (A549, HepG2, and Mv1Lu cells). In addition, PCIP attenuates TGF-β-stimulated expression of vimentin, N-cadherin, and fibronectin and, thus, blocks TGF-β-induced epithelial to mesenchymal transition (EMT) in these cells. Furthermore, cell-surface labeling and immunoblot analysis indicates that PCIP suppresses TGF-β-stimulated cellular responses by attenuating cell-surface expression of the type II TGF-β receptor through accelerating caveolae-mediated internalization followed by primarily lysosome-dependent degradation of the receptor, as demonstrated by sucrose density gradient analysis and immune fluorescence staining.
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http://dx.doi.org/10.1002/cbic.201700693DOI Listing
April 2018

The Efficacy of Therapeutic Plasma Exchange in Antiphospholipid Antibody-positive Patients With Spontaneous Intracerebral Hemorrhage and High D-dimer Levels.

Neurologist 2018 Jan;23(1):7-11

Department of Neurological Surgery.

Objective: We investigated the efficacy of plasma exchange (PE) in antiphospholipid antibody (aPL)-positive patients with a spontaneous intracerebral hemorrhage (ICH) and high D-dimer levels.

Materials And Methods: From May 2013 to May 2016, we evaluated 32 patients who were below the age of 50 and presented with spontaneous ICH. Five patients were positive for aPL antibody and 3 had a higher level of D-dimer. These 3 patients underwent 5 sessions of PE using fresh frozen plasma as replacement fluid. We analyzed the days postadmission until PE-start, the days of intensive care unit (ICU) hospitalization, D-dimer series, Glasgow Coma Scale (GCS) scores, and modified Rankin scale (mRS) scores. D-dimer levels and GCS scores were recorded at both pre-PE and post-PE stages. The mRS scores were recorded at pre-PE stage and 3 months post-PE.

Results: The mean postadmission period until PE-start was 8.33 days. The mean ICU hospitalization was 17.33 days. The D-dimer level pre-PE ranged from 2.34 to 5.44 mg/L fibrinogen equivalent unit (FEU). The D-dimer level post-PE ranged from 1.05 to 3.30 mg/L FEU. The amount of decline of the D-dimer level between pre-PE and post-PE ranged from 0.65 to 2.14 mg/L FEU. The GCS score pre-PE was between 7 and 8. The highest post-PE GCS score was 14. The improved GCS scores post-PE ranged from 3 to 6. The improved mRS scores of 3 months post-PE ranged from 3 to 4.

Conclusions: The concurrent presence of positive aPL and a higher D-dimer level may worsen the neurological outcome of patients with a spontaneous ICH. Aggressive PE is effective for the treatment of such patients, decreasing the extent of the ICU hospitalization.
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http://dx.doi.org/10.1097/NRL.0000000000000159DOI Listing
January 2018

TMED2 promotes epithelial ovarian cancer growth.

Oncotarget 2017 Nov 6;8(55):94151-94165. Epub 2017 Oct 6.

Department of Gynecology, Maternal and Child Health Hospital of Duanzhou District, Zhaoqing 526000, P.R. China.

TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell proliferation, migration and invasion. Silencing TMED2 inhibited ovarian cancer growth in mice. Silencing TMED2 inhibited IGF2/IGF1R/PI3K/Akt pathway. In agreement, ectopically expressed TMED2 activated IGF2/IGF1R/PI3K/Akt pathway. Mechanistic study revealed that TMED2 directly binds to AKT2, thereby facilitating its phosphorylation. We also found that TMED2 increased IGF1R expression by competing for miR-30a. Thus, TMED2 is oncogenic and a potential target for epithelial ovarian cancer therapy.
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http://dx.doi.org/10.18632/oncotarget.21593DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706863PMC
November 2017

Coral-Derived Natural Marine Compound GB9 Impairs Vascular Development in Zebrafish.

Int J Mol Sci 2017 Aug 3;18(8). Epub 2017 Aug 3.

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan.

Blood vessels in vertebrates are established and genetically controlled in an evolutionarily-conserved manner during embryogenesis. Disruption of vascular growth by chemical compounds or environmental hormones may cause developmental defects. This study analyzed the vascular impacts of marine compound GB9 in zebrafish. GB9 was isolated from the marine soft coral and had shown anti-neuroinflammatory and anti-nociceptive activities. However, the role of GB9 on vascular development has not been reported. We first tested the survival rate of embryos under exogenous 5, 7.5, 10, and 15 μM GB9 added to the medium and determined a sub-lethal dosage of 10 μM GB9 for further assay. Using transgenic () fish to examine vascular development, we found that GB9 treatment impaired intersegmental vessel (ISV) growth and caudal vein plexus (CVP) patterning at 25 hours post-fertilization (hpf) and 30 hpf. GB9 exposure caused pericardial edema and impaired circulation at 48-52 hpf, which are common secondary effects of vascular defects and suggest the effects of GB9 on vascular development. Apoptic cell death analysis showed that vascular defects were not caused by cell death, but were likely due to the inhibition of migration and/or proliferation by examining ISV cell numbers. To test the molecular mechanisms of vascular defects in GB9-treated embryos, we examined the expression of vascular markers and found the decreased expression of vascular specific markers , , , and . In addition, we examined whether GB9 treatment impairs vascular growth due to an imbalance of redox homeostasis. We found an enhanced effect of vascular defects during GB9 and H₂O₂ co-treatment. Moreover, exogenous -acetyl-cysteine (NAC) treatment rescued the vascular defects in GB9 treated embryos. Our results showed that GB9 exposure causes vascular defects likely mediated by the imbalance of redox homeostasis.
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http://dx.doi.org/10.3390/ijms18081696DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5578086PMC
August 2017