Publications by authors named "Suqin Wu"

15 Publications

  • Page 1 of 1

Characteristics of human papillomavirus infection among women with cervical cytological abnormalities in the Zhoupu District, Shanghai City, China, 2014-2019.

Virol J 2021 Mar 8;18(1):51. Epub 2021 Mar 8.

Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China.

Background: Human papillomavirus (HPV) infection is currently the main cause of cervical cancer and precancerous lesions in female patients. By analyzing 6-year patient data from Shanghai Zhoupu Hospital in China, we retrospectively analyzed the epidemiological characteristics of women to determine the relationship between HPV genotype and cytological test results.

Methods: From 2014 to 2019, 23,724 cases of cervical shedding were collected from Zhoupu Hospital in Shanghai, China. By comparing the results of HPV and ThinPrep cytology test (TCT), the HPV infection rate of patients was retrospectively analyzed. HPV genotyping using commercial kits can detect 21 HPV subtypes (15 high-risk and 6 low-risk). According to the definition of the Bethesda system, seven types of cervical cytology results were involved.

Results: 3816 among 23,724 women, nearly 16.08%, were infected with HPV. The top three highest HPV prevalence rates were high-risk type infection, including HPV52 (3.19%), 58 (2.47%) and 16 (2.34%). The number of single-type HPV infections (3480 (91.20%)) was much larger than the number of multi-type ones (336 (8.8%)). Single-type infections were mainly in women aged 50-60 (16.63%) and women under 30 (15.37%), while multi-type infections were more common in women over 60 (2.67%). By analyzing the long-term trends, between 2014 and 2019, HPV52, 58, and 16 subtypes changed significantly, and the HPV positive rate also changed significantly during this period. Among 4502 TCT positive women, 15 (4.04%), 125 (2.64%),159 (1.54%), 4202 (17.71%) and 1 (0.004%) had atypical glandular cells (AGC), high-grade squamous intraepithelial lesions (HSIL), low-grade squamous intraepithelial lesions (LSIL), atypical squamous cells (ASC)and cervical adenocarcinoma, respectively. The HPV infection rates were 66.08%, 63.99%, 115.20%, 119.50%, and 31.72% for NILM, AGCs, HSILs LSILs and ASCs, respectively.

Conclusions: HPV and TCT screening were very important steps in the secondary prevention of cervical cancer. Through the tracking and analysis of HPV and TCT results in this study, it can provide valuable information for Shanghai's HPV screening and prevention strategies, and provide references for clinical decision-making in the treatment of cervical cancer and precancerous lesions.
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http://dx.doi.org/10.1186/s12985-021-01518-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7938559PMC
March 2021

Changes in clinical trials of endocrine disorder and metabolism and nutrition disorder drugs in mainland China over 2010-2019.

Pharmacol Res Perspect 2021 04;9(2):e00729

Clinical Trials Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

With the improvements in relevant policies, laws, and regulations regarding drug clinical trials in China, the quantity and quality of drug clinical trials have gradually improved, and the development prospects of drug clinical trials for endocrine disorders and metabolism and nutrition disorders are promising. Based on information from the clinical trials from the online drug clinical trial registration platform of the National Medical Products Administration, we aimed to review and evaluate the development of clinical trials of drugs for endocrine disorders and metabolism and nutrition disorders in mainland China from 2010 to 2019, as well as the trends over time. A total of 861 trials were carried out on 254 types of drugs for endocrine disorders and metabolism and nutrition disorders, among which 531 (61.67%) involved endocrine disorders, and 330 (38.33%) addressed metabolism and nutrition disorders. The annual number of clinical trials has been increasing gradually, with a significant increase in 2017. Among them, the proportion of clinical trials with Chinese epidemiological characteristics was relatively large (Wu, Annual Report on Development Health Management and Health Industry in China, 2018). The largest number of trials were for diabetes drugs (55.63%), followed by trials of drugs for hyperlipidemia (19.4%) and those for hyperuricemia (7.9%). It was found that the geographical area of the leading units also showed obvious unevenness according to the analysis of the test unit data. Based on the statistics and evaluation of the data, comprehensive information is provided to support the cooperation of global pharmaceutical R&D companies and research units in China and the development of international multicenter clinical trials in China. This work additionally provides clinical trial units with a self-evaluation of scientific research competitiveness and hospital development strategies. At the same time, it provides a reference with basic data for sponsors and stakeholders in these trials to determine their development strategy goals.
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http://dx.doi.org/10.1002/prp2.729DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7931124PMC
April 2021

Interleukin-33 promotes proliferation and inhibits apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis.

Clin Exp Rheumatol 2021 Jul-Aug;39(4):844-851. Epub 2020 Oct 9.

Department of Clinical Pharmacy, China Medical University, Shenyang, China.

Objectives: The aim of our study was to determine the effect of interleukin (IL)-33 on the proliferation, apoptosis, and secretion of inflammatory cytokines by fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) and to investigate the underlying mechanisms.

Methods: Cultured RA FLSs and osteoarthritis (OA) FLSs were cocultured with different concentrations of IL-33. TUNEL assay and flow cytometry were used to detect apoptosis. Western blotting and Real-time (RT)-PCR were used to detect the expression levels of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax), while the Cell Counting Kit-8 was used to determine cell proliferation in each cocultured group. Enzyme-linked immunosorbent assay was used to detect the expression levels of tumour necrosis factor (TNF)-α and IL-6 in the supernatant from each cell culture. Western blot analysis was used to determine the phosphorylated expression levels of the nuclear factor-kappa light chain enhancer of the activated B cells (NF-κB) pathway in each group.

Results: IL-33 inhibited RA FLS apoptosis, promoted FLS proliferation, increased Bcl-2 protein expression levels, and decreased Bax protein expression levels. It also increased the expression levels of inflammatory cytokines TNF-α and IL-6 and increased the expression levels of P-NF-κ B in FLSs.

Conclusions: IL-33 inhibited apoptosis and promoted proliferation of FLSs; in addition, IL-33 increased the serum levels of inflammatory cytokines. The effect of IL-33 on RA FLSs was likely mediated via the NF-κB pathway.
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July 2021

miR-194-5p inhibits SLC40A1 expression to induce cisplatin resistance in ovarian cancer.

Pathol Res Pract 2020 Jul 28;216(7):152979. Epub 2020 Apr 28.

Department of Gynaecology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China. Electronic address:

Background: miR-194-5p has been associated with drug resistance in many cancers. However, the role of miR-194-5p in cisplatin resistance in ovarian cancer is still unclear.

Materials And Methods: To study the role and mechanism of miR-194-5p in cisplatin resistance, qRT-PCR was performed to determine the expression of miR-194-5p and SLC40A1 in ovarian cancer. Cell Counting Kit-8 (CCK8) assay was used to analyse cell viability after cisplatin treatment. Dual-luciferase reporter gene assay was performed to examine the relationship between miR-194-5p and SLC40A1. The genes downstream of SLC40A1 were investigated through bioinformatics analysis.

Results: Compared to cisplatin-sensitive ovarian cancer cells, higher miR-194-5p expression and lower SLC40A1 expression were found in cisplatin-resistant ovarian cancer cells. Moreover, this study demonstrated that over-expression of miR-194-5p inhibited SLC40A1 expression, and knockdown of miR-194-5p promoted SLC40A1 expression. In addition, dual-luciferase reporter gene assay further confirmed the negative correlation between miR-194-5p and SLC40A1. Furthermore, we found that over-expression of miR-194-5p resulted in cisplatin resistance. When miR-194-5p and SLC40A1 were simultaneously up-regulated, cisplatin sensitivity increased, while down-regulation of miR-194-5p sensitised ovarian cancer cells to cisplatin. However, when miR-194-5p and SLC40A1 were simultaneously down-regulated, cisplatin sensitivity was decreased. These data suggested that miR-194-5p inhibited SLC40A1 expression to induce cisplatin resistance. In addition, bioinformatics analysis indicated a positive correlation of SLC40A1 with hephaestin (HEPH), and homeostatic iron regulator (HFE). However, we found that HEPH and HFE were associated with cisplatin resistance, suggesting that their role in drug resistance is induced by miR-194-5p/SLC40A1.

Conclusion: In conclusion, we found that miR-194-5p inhibited SLC40A1 expression to induce cisplatin resistance in ovarian cancer. This study suggests that miR-194-5p could be a potential therapeutic target and a prognostic biomarker for ovarian cancer, with important implications for future research.
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http://dx.doi.org/10.1016/j.prp.2020.152979DOI Listing
July 2020

Systematic Assessment of the Effect of Internal Library in Targeted Analysis of SWATH-MS.

J Proteome Res 2020 01 15;19(1):477-492. Epub 2019 Nov 15.

State Key Laboratory of Cellular Stress Biology, Innovation Center for Cellular Signaling Network, School of Life Sciences , Xiamen University , Xiamen 361102 , China.

Targeted analysis of sequential window acquisition of all theoretical mass spectra (SWATH-MS) requires the spectral library, which can be generated by shotgun mass spectrometry (MS) or by the pseudo-spectra files directly obtained from SWATH-MS data. The external library generated by shotgun MS is employed in most SWATH-MS research. However, performance of the internal library, which is constructed by pseudo-spectra files, in the targeted analysis of SWATH-MS has not been systemically evaluated. Here, we show that up to 40% of the peptides detected by the internal library were not overlapped with those detected by the external library for most SWATH-MS data sets. However, the internal library did not identify extra phosphopeptides compared with the external library for phosphoproteomic SWATH-MS data. Therefore, the internal library should be incorporated into the external library for targeted analysis of nonphosphoproteomic SWATH-MS, given that it can significantly increase the number of peptides of SWATH-MS without requiring additional instrument measurement time.
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http://dx.doi.org/10.1021/acs.jproteome.9b00669DOI Listing
January 2020

Nrf2 induced cisplatin resistance in ovarian cancer by promoting CD99 expression.

Biochem Biophys Res Commun 2019 10 28;518(4):698-705. Epub 2019 Aug 28.

Department of Gynecology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China. Electronic address:

Cisplatin resistance is a vital obstacle for the prognosis of ovarian cancer. However, the mechanism of cisplatin resistance is still unknown. This research was performed to explore the role of Nrf2 (nuclear factor, erythroid 2 like 2) and CD99 (CD99 molecule) in cisplatin resistance in ovarian cancer. QRT-PCR and Western blot were used to detect the expression of CD99 in ovarian cancer cells and tissues with different cisplatin sensitivities. Cell viability was analyzed by the Cell Counting Kit-8 (CCK8). The relationship of Nrf2 and CD99 was assessed by dual-luciferase reporter gene assay and chromatin immunoprecipitation (ChIP). Bioinformatics analysis was performed to search for the downstream gene of CD99. In this study, it was revealed that CD99 was highly expressed in cisplatin-resistant ovarian cancer cells and tissues, while lower CD99 expression was found in cisplatin-sensitive ovarian cancer cells and tissues. In addition, the overexpression of CD99 resulted in cisplatin resistance; on the other hand, knockdown of CD99 sensitized ovarian cancer to cisplatin. Furthermore, survival analysis indicated that overall survival (OS) and progression-free survival (PFS) of patients with higher CD99 expression were shorter than those with lower CD99 expression. It was also found that when Nrf2 was upregulated in cisplatin-sensitive ovarian cells, CD99 expression and cell viability increased after cisplatin treatment. Knockdown of CD99 could reverse cisplatin resistance induced by Nrf2. Conversely, when Nrf2 was knocked down in cisplatin-resistant ovarian cancer cells, CD99 expression and cell viability with cisplatin treatment decreased, while simultaneously upregulating CD99 reactivated cisplatin resistance in ovarian cancer cells. The dual-luciferase reporter gene assay and ChIP analysis suggested CD99 was a downstream gene of Nrf2, and Nrf2 positively regulated the expression of CD99 at the transcriptional level. In conclusion, Nrf2 induced cisplatin resistance in ovarian cancer cells by promoting CD99 expression. Targeted CD99 might be an effective way to reverse cisplatin resistance in ovarian cancer.
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http://dx.doi.org/10.1016/j.bbrc.2019.08.113DOI Listing
October 2019

Maternal thyroid function during late pregnancy is not a risk factor for postpartum depression.

Psychiatry Res 2019 09 6;279:387-388. Epub 2019 May 6.

Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning 110000, China. Electronic address:

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http://dx.doi.org/10.1016/j.psychres.2019.04.027DOI Listing
September 2019

Interleukin-35 inhibits angiogenesis through STAT1 signalling in rheumatoid synoviocytes.

Clin Exp Rheumatol 2018 Mar-Apr;36(2):223-227. Epub 2017 Aug 28.

Department of Rheumatology, 1st Affiliated Hospital of China Medical University, Shenyang, China.

Objectives: We studied the anti-angiogenic effect of interleukin-35 (IL-35) by investigating its effects on signal transmission through the Janus kinase signal transducer and activator of transcription (JAK-STAT) pathway in fibroblast-like synoviocytes (FLS).

Methods: Using the collagen-induced arthritis (CIA) model of rheumatoid arthritis (RA), we derived and cultured FLS, stimulated FLS with IL-35 at different concentrations and examined the expression levels of mRNA and protein of both vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), endostatin, TNF-α, and IL-6 using reverse transcription polymerase chain reaction (RT-PCR) and immunoblotting. We used Western blotting to study the effects of IL-35 on the function of the JAK-STAT pathway in FLS.

Results: IL-35 treatment inhibited the expression of VEGF, FGF-2, TNF-α and IL-6, and increased the expression of endostatin in FLS. Western blotting showed that IL-35 treatment of CIA-derived FLS resulted in signalling through STAT1, but not through STAT3 or STAT5.

Conclusions: IL-35 signalling through STAT1 and inhibition of the expression of mediators of angiogenesis and inflammation in FLS provide a likely mechanism for anti-angiogenic effects seen in experimental models of RA. Our data suggest that IL-35 and its signalling pathway represent a therapeutic target for the treatment of RA and other angiogenesis-related diseases.
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June 2018

IL-35 Inhibits Angiogenesis through VEGF/Ang2/Tie2 Pathway in Rheumatoid Arthritis.

Cell Physiol Biochem 2016 14;40(5):1105-1116. Epub 2016 Dec 14.

Department of Rheumatology and Immunology, the First Affiliated Hospital of China Medical University, Shenyang, PR China.

Background/aims: The pro-angiogenic factors vascular endothelial growth factor (VEGF) and angiopoietins (Angs) play a prominent role in synovial angiogenesis, an early and critical event in the pathogenesis of rheumatoid arthritis (RA). Interleukin (IL)-35 is an anti-inflammatory cytokine that attenuates collagen-induced arthritis, however, the mechanisms involved are not fully understood.

Methods: The effects of IL-35 on endothelial cell migration, adhesion, and tube formation were examined using human umbilical vein endothelial cells (HUVEC) in vitro. The effects of IL-35 on vessel formation in vivo were examined using a murine Matrigel plugs model. MMP2/MMP9 and IL-6/IL-8 secretion were assessed by zymography and ELISA, respectively. The crosstalk between IL-35, VEGF, and Ang2 in HUVECs and RA synovial tissue explants was investigated.

Results: IL-35 inhibited basal and VEGF-induced HUVEC migration and adhesion in vitro as well as tube formation in vitro and in vivo. VEGF increased Ang2 secretion by HUVECs and RA synovial tissue explants, and exogenous Ang2 promoted HUVEC migration, adhesion, and tube formation with similar potency to VEGF. Blocking the Ang/Tie2 pathway with a Tie2 kinase antibody inhibited the proangiogenic effects of exogenous Ang2 and VEGF in HUVECs. IL-35 inhibited basal and VEGF-induced Ang2 secretion by HUVECs and RA synovial tissue explants; it also antagonized the proangiogenic effects of exogenous Ang2 in HUVECs. Moreover, IL-35 reduced basal and VEGF/Ang2-induced MMP2/MMP9 and IL-6/IL-8 secretion.

Conclusion: These results suggested that IL-35 restrains RA angiogenesis and inflammation by downregulating basal and VEGF-induced Ang2 secretion as well as disrupting Ang2/Tie2 signal transduction. Our findings extend current understanding of mechanisms regulating RA angiogenesis and may support development of novel angiogenesis-targeting therapeutics for RA treatment.
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http://dx.doi.org/10.1159/000453165DOI Listing
February 2017

Interleukin-35 (IL-35) inhibits proliferation and promotes apoptosis of fibroblast-like synoviocytes isolated from mice with collagen-induced arthritis.

Mol Biol Rep 2016 Sep 5;43(9):947-56. Epub 2016 Jul 5.

Department of Rheumatology and Immunology, The First Affiliated Hospital of China Medical University, 155 Nanjing North Street, Heping District, Shenyang, 110001, People's Republic of China.

Rheumatoid arthritis (RA) is an inflammatory disorder of the joints that affects 0.5-1 % of adults. Excessive growth of the fibroblast-like synoviocytes (FLS) promotes hyperplasia of synovial tissues and causes its invasion into the bone and cartilage, which eventually causes deformity and dysfunction of affected joints. Interleukin 35 (IL-35) was shown to suppress the inflammatory responses to collagen-induced arthritis (CIA) via upregulation of T regulatory cells and suppression of T helper type 17 cells in a mouse model. To study the effects of IL-35 on the proliferation and apoptosis frequency of cultured FLS isolated from mice with CIA as well as to examine the effects of IL-35 on CIA in vivo. Thirty DBA/1 J mice, which are used as an animal model for RA, were divided randomly (ten mice per group) to a CIA group (collagen treatment), a CIA + IL-35 group (collagen and IL-35 treatments), and a control group (no treatment). Starting on the 24th day after collagen administration, IL-35 was injected intraperitoneally into mice of the CIA + IL-35 group once per day for 10 days. An arthritis index was calculated, and pathological analysis of synovial tissue was performed. FLS isolated from CIA mice were treated with various concentrations of IL-35 (12.5-100 ng/ml). The MTT assay was used to examine FLS proliferation, and apoptosis frequency of FLS was detected by flow cytometry. On day 24, the CIA mice began to exhibit arthritis symptoms, and the symptoms rapidly progressed with time. Treatment with IL-35 significantly alleviated arthritis symptoms and reduced the synovial tissue inflammation. In addition, IL-35 treatment inhibited proliferation and promoted apoptosis in cultured FLS from CIA mice in a dose-dependent manner. IL-35 could ameliorate the symptoms of arthritis in the CIA mouse model in vivo and inhibited FLS proliferation while promoting FLS apoptosis in vitro, thereby exhibited the potential in inhibiting the progression of RA.
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http://dx.doi.org/10.1007/s11033-016-4034-7DOI Listing
September 2016

Interleukin-35 attenuates collagen-induced arthritis through suppression of vascular endothelial growth factor and its receptors.

Int Immunopharmacol 2016 May 26;34:71-77. Epub 2016 Feb 26.

Department of Rheumatology and Immunology, the First Affiliated Hospital of China Medical University, 155 Nanjing North Street, Heping District, Shenyang 110001, PR China. Electronic address:

Objective: To investigate the effect of interleukin-35 (IL-35) on vascular endothelial growth factor (VEGF) and its receptors, Flt-1 and Flk-1, in a collagen-induced arthritis (CIA) mouse model of rheumatoid arthritis (RA).

Methods: We established a CIA mouse model and injected IL-35 intraperitoneally. The articular index (AI) was measured based on the amount of erythema, swelling, or joint rigidity and synovial histology was measured by hematoxylin and eosin staining (HE staining). The levels of VEGF, Flt-1, Flk-1, and von Willebrand factor (vWF) expression in CIA synovial tissue were determined by immunohistochemistry. The mRNA and protein expression levels of VEGF, Flt-1, Flk-1, TNF-α, and INF-γ were detected by reverse transcription PCR (RT-PCR) and western blots, respectively.

Results: The IL-35 treatment decreased the AI and the synovial histological scores of CIA mice. Immunohistochemistry results revealed that the IL-35 treatment downregulated VEGF, Flt-1, Flk-1, and vWF expression in the CIA mice. RT-PCR results showed that the IL-35-treated mice had lower levels of VEGF, Flt-1, Flk-1, and TNF-α mRNA expression than those of the PBS-treated mice. While there was no significant difference in the level of INF-γ mRNA expression between IL-35-treated and PBS-treated mice. Western blot results showed that the IL-35 treatment downregulated the levels of VEGF, Flt-1, Flk-1, and TNF-α in CIA mice, but the level of INF-γ was not significantly affected.

Conclusion: These findings show that IL-35 may represent a novel therapeutic agent for RA, and the probable mechanisms may rely on inhibiting VEGF and its receptors Flt-1 and Flk-1.
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http://dx.doi.org/10.1016/j.intimp.2016.02.018DOI Listing
May 2016

Recognition of cytosolic DNA attenuates glucose metabolism and induces AMPK mediated energy stress response.

Int J Biol Sci 2015 5;11(5):587-94. Epub 2015 Apr 5.

2. Translational Medicine Institute, Fujian Medical University, Fuzhou, Fujian, 350108, China. ; 5. Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

Both viral infection and DNA transfection expose single-stranded or double-stranded DNA to the cytoplasm of mammalian cells. Recognition of cytosolic DNA activates a series of cellular responses, including induction of pro-inflammatory genes such as type I interferon through the well-known cGAS-STING pathway. Here we show for the first time that intracellular administration of either single or double stranded interferon stimulating DNA (ISD), but not poly(dA) suppresses cell growth in many different cell types. Suppression of cell growth by cytosolic DNA is cGAS/STING independent and associated with inhibition of glucose metabolism, ATP depletion and subsequent cellular energy stress responses including activation of AMPK and inactivation of mTORC1. Our results suggest that in concert with but independent of innate immune response, recognition of cytosolic DNA induced cellular energy stress potentially functions as a metabolic barrier to viral replication.
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http://dx.doi.org/10.7150/ijbs.10945DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4400389PMC
January 2016

Binding characteristics of homogeneous molecularly imprinted polymers for acyclovir using an (acceptor-donor-donor)-(donor-acceptor-acceptor) hydrogen-bond strategy, and analytical applications for serum samples.

J Chromatogr A 2013 Apr 19;1285:124-31. Epub 2013 Feb 19.

School of Chemistry & Environment, South China Normal University, Guangzhou 510006, China.

This paper demonstrates a novel approach to assembling homogeneous molecularly imprinted polymers (MIPs) based on mimicking multiple hydrogen bonds between nucleotide bases by preparing acyclovir (ACV) as a template and using coatings grafted on silica supports. (1)H NMR studies confirmed the AAD-DDA (A for acceptor, D for donor) hydrogen-bond array between template and functional monomer, while the resultant monodisperse molecularly imprinted microspheres (MIMs) were evaluated using a binding experiment, high performance liquid chromatography (HPLC), and solid phase extraction. The Langmuir isothermal model and the Langmuir-Freundlich isothermal model suggest that ACV-MIMs have more homogeneous binding sites than MIPs prepared through normal imprinting. In contrast to previous MIP-HPLC columns, there were no apparent tailings for the ACV peaks, and ACV-MIMs had excellent specific binding properties with a Ka peak of 3.44 × 10(5)M(-1). A complete baseline separation is obtained for ACV and structurally similar compounds. This work also successfully used MIMs as a specific sorbent for capturing ACV from serum samples. The detection limit and mean recovery of ACV was 1.8 ng/mL(-1) and 95.6%, respectively, for molecularly imprinted solid phase extraction coupled with HPLC. To our knowledge, this was the first example of MIPs using AAD-DDA hydrogen bonds.
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http://dx.doi.org/10.1016/j.chroma.2013.02.039DOI Listing
April 2013

The discovery of lymphatic stomata and its ultrastructure in mouse tunica vaginalis.

J Pediatr Surg 2012 Nov;47(11):2087-92

Institute of Cell Biology, Zhejiang University, Hangzhou 310058, China.

Background/purpose: The communicating hydrocele is caused by the failure of the processus vaginalis closure. After the patent processus vaginalis is closed, the hydrocele can subside spontaneously, but the mechanism responsible for the drainage of hydrocele has not been expounded. Former studies showed that lymphatic stomata between the mesothelial cells lining the peritoneum and pleura were responsible for the drainage of ascites and pleural effusion. Although the tunica vaginalis is also lined by mesothelial cells, the existence of lymphatic stomata in it has never been reported. Therefore, we investigated the presence and ultrastructure of lymphatic stomata in mouse tunica vaginalis.

Methods: We studied the ultrastructure of mouse tunica vaginalis by scanning and transmission electron microscopy. The submesothelial connective tissue with foramina were investigated after the mesothelial cells were digested by NaOH solution. Typan blue was used as a tracer to show the absorptive function of lymphatic stomata.

Results: The lymphatic stomata were found between the mesothelial cells. The trypan blue was directly absorbed by the lymphatic stomata. Milky spots which possessed immune function were observed, and the lymphatic stomata were found within the milky spots.

Conclusion: Our study is the first to report the presence and ultrastructure of lymphatic stomata in mouse tunica vaginalis. They might be related to the lymphatic drainage in the tunica vaginalis cavity.
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http://dx.doi.org/10.1016/j.jpedsurg.2012.06.015DOI Listing
November 2012

Recognition characteristics of molecularly imprinted microspheres for triazine herbicides using hydrogen-bond array strategy and their analytical applications for corn and soil samples.

J Chromatogr A 2011 Mar 11;1218(10):1340-6. Epub 2011 Jan 11.

School of Chemistry & Environment, South China Normal University, Guangzhou 510006, China.

The homogeneous molecularly imprinted microspheres (MIMs) based on a biologically inspired hydrogen-bond array were prepared using allobarbital as the novel functional monomer and divinylbenzene as the cross-linker. The host-guest binding characteristics were examined by molecular simulation and infrared spectroscopy. The resultant MIMs were evaluated using high performance liquid chromatography and solid-phase extraction. The results obtained demonstrate that the good imprinting effect and the excellent selectivity of MIMs are mainly due to the interaction involving the formation of three-point hydrogen bond between host and guest. The complete baseline separation was obtained for five triazine analogues and a metabolite on the MIM HPLC column. The MIMs were further successfully used as a specific sorbent for selective extraction of simetryne from corn and soil samples by molecularly imprinted solid phase extraction. Detection limits and recoveries were 5.8 μg/kg and 0.14 μg/kg and 87.4-105% and 94.6-101% for simetryne in corn and soil sample, respectively.
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http://dx.doi.org/10.1016/j.chroma.2011.01.008DOI Listing
March 2011
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