Publications by authors named "Yanfeng Song"

46 Publications

Acute and long-term effects of VX in rat brain cell aggregate culture.

Toxicol In Vitro 2021 Oct 12;78:105256. Epub 2021 Oct 12.

Defence Research & Development Canada, Suffield Research Centre, Box 4000, Medicine Hat, Alberta T1A 8K6, Canada.

The contact poison VX (O-ethyl S-(2-diisopropylaminoethyl) methylphosphonothioate) is a chemical warfare agent that is one of the most toxic organophosphorus compounds known. Its primary mechanism of toxic action is through the inhibition of acetylcholinesterase and resultant respiratory paralysis. The majority of work on VX has thus concentrated on its potent anticholinesterase activity and acute toxicity, with few studies investigating potential long-term effects. In this report we describe the effects of VX in aggregating rat brain cell cultures out to 28 days post-exposure. Cholinesterase activity was rapidly inhibited (60 min IC = 0.73 +/- 0.27 nM), but recovered towards baseline values over the next four weeks. Apoptotic cell death, as measured using caspase-3 activity was evident only at 100 μM concentrations. Cell type specific enzymatic markers (glutamine synthase, choline acetyltransferase and 2',3'-cyclic nucleotide 3'-phosphodiesterase) showed no significant changes. Total Akt levels were unchanged, while an increased phosphorylation of this protein was noted only at the highest VX concentration on the first day post-exposure. In contrast, significant and delayed (28 days post-exposure) decreases were noted in vascular endothelial growth factor (VEGF) levels, a protein whose reduced levels are known to contribute to neurodegenerative disorders. These observations may indicate that the long-term effects noted in some survivors of nerve agent intoxication may be due to VX-induced declines in brain VEGF levels.
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http://dx.doi.org/10.1016/j.tiv.2021.105256DOI Listing
October 2021

Sulphur mustard induces progressive toxicity and demyelination in brain cell aggregate culture.

Neurotoxicology 2021 05 19;84:114-124. Epub 2021 Mar 19.

Defence Research & Development Canada, Suffield Research Centre, Box 4000, Medicine Hat, Alberta, T1A 8K6, Canada.

Sulphur mustard (H; bis(2-chloroethyl) sulphide) is a vesicant chemical warfare (CW) agent that has been well documented as causing acute injury to the skin, eyes and respiratory system. Although a great deal of research effort has been expended to understand how H exerts these effects, its mechanism of action is still poorly understood. At high exposures, H also causes systemic toxicity with chronic and long-term effects to the immune, cardiovascular and central nervous systems, and these aspects of H poisoning are much less studied and comprehended. Rat aggregate cultures comprised of multiple brain cell types were exposed to H and followed for four weeks post-exposure to assess neurotoxicity. Toxicity (LDH, caspase-3 and aggregate diameter) was progressive with time post-exposure. In addition, statistically significant changes in neurofilament heavy chain (NFH), glial fibrillary acidic protein (GFAP), Akt phosphorylation, IL-6, GRO-KC and TNF-α were noted that were time- and concentration-dependent. Myelin basic protein, CNPase and vascular endothelial growth factor (VEGF) were found to be especially sensitive to H exposure in a time- and concentration-dependent fashion, with levels falling to ∼50 % of control values at ∼10 μM H by 8 days post-exposure. Demyelination and VEGF inhibition may be causal in the long-term neuropsychological illnesses that have been documented in casualties exposed to high concentrations of H, and may also play a role in the peripheral neuropathy that has been observed in some of these individuals.
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http://dx.doi.org/10.1016/j.neuro.2021.03.004DOI Listing
May 2021

Roles of galectin‑3 in the tumor microenvironment and tumor metabolism (Review).

Oncol Rep 2020 11 22;44(5):1799-1809. Epub 2020 Sep 22.

School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 73000, P.R. China.

Galectin‑3 is expressed in various tissues and plays an important role in the tumor microenvironment (TME). Galectin‑3 has been found to be overexpressed in a variety of cancers and is associated with tumor progression and metastasis. Over the past decades, emerging evidence has suggested that the TME may induce galectin‑3 expression to maintain cellular homeostasis and promote cell survival. Furthermore, galectin‑3 regulates immune cell function to promote tumor‑driven immunosuppression through several mechanisms. In the TME, intracellular and extracellular galectin‑3 has different functions. In addition, it has been reported that galectin‑3 is associated with glycolysis and mitochondrial metabolism in tumors, and it is involved in the regulation of relevant signaling pathways, thus promoting cancer cell survival via adapting to the TME. The aim of the present review was to summarize the current knowledge on galectin‑3 production and its function in the TME, its effect on TME immunosuppression, its association with tumor metabolism and relevant signaling pathways, and to report common types of cancer in which galectin‑3 is highly expressed, in order to ensure a comprehensive understanding of the critical effects of galectin‑3 on tumor progression and metastasis.
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http://dx.doi.org/10.3892/or.2020.7777DOI Listing
November 2020

Uncovering the Potential Differentially Expressed miRNAs and mRNAs in Ischemic Stroke Based on Integrated Analysis in the Gene Expression Omnibus Database.

Eur Neurol 2020 9;83(4):404-414. Epub 2020 Sep 9.

Department of Neurology, Liaocheng Second Hospital Affiliated to Shandong First Medical University, Linqing City, China.

Introduction: Ischemic stroke is the third leading cause of death. There is no known treatment or cure for the disease. Moreover, the pathological mechanism of ischemic stroke remains unclear.

Objective: We aimed to identify potential microRNAs (miRNAs) and mRNAs, contributing to understanding the pathology of ischemic stroke.

Methods: First, the data of miRNA and mRNA were downloaded for differential expression analysis. Then, the regulatory network between miRNA and mRNAs was constructed. Third, top 100 differentially expressed mRNAs were used to construct a protein-protein interaction network followed by the function annotation of mRNAs. In addition, in vitro experiment was used to validate the expression of mRNAs. Last, receiver operating characteristic diagnostic analysis of differentially methylated genes was performed.

Results: Totally, up to 26 differentially expressed miRNAs and 1,345 differentially expressed mRNAs were identified. Several regulatory interaction pairs between miRNA and mRNAs were identified, such as hsa-miR-206-HMGCR/PICALM, hsa-miR-4491-TMEM97, hsa-miR-3622b-5p/hsa-miR-548k-KLF12, and hsa-miR-302a-3p/hsa-miR-3145-3p-CTSS. MAPK signaling pathway (involved DUSP1) and the Notch signaling pathway (involved NUMB and CREBBP) were identified. The expression validation of KLF12, ARG1, ITGAM, SIRT4, SERPINH1, and DUSP1 was consistent with the bioinformatics analysis. Interestingly, hsa-miR-206, hsa-miR-4491, hsa-miR-3622b-5p, hsa-miR-548k, hsa-miR-302a-3p, hsa-miR-3145-3p, KLF12, and ID3 had the potential diagnostic value of ischemic stroke.

Conclusions: The identified differentially expressed miRNAs and mRNAs may be associated with the development of ischemic stroke.
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http://dx.doi.org/10.1159/000507364DOI Listing
February 2021

Loss of RAD6B induces degeneration of the cochlea in mice.

Biochem Biophys Res Commun 2020 10 28;531(3):402-408. Epub 2020 Aug 28.

Department of Anatomy and Histology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China. Electronic address:

Presbycusis is a form of age-related hearing loss (AHL). Many studies have shown that the degeneration of various structures in the cochlea of the inner ear is related to AHL, and DNA damage is an important factor leading to the above process. As an E2 ubiquitin-conjugated enzyme, RAD6B plays an important role in DNA damage repair (DDR) through histone ubiquitination. However, the molecular mechanism is still unclear. In this study, we investigated the role of RAD6B in the morphological changes and DDR mechanisms in aging-related degeneration of the cochlea of mice. We observed that the hair cells, stria vascularis and spiral ganglion in the cochlea of the RAD6B knockout mice showed significant degenerative changes and abnormal expression of proteins associated with DDR mechanisms compared with those of the littermate wild-type mice. In conclusion, our results suggest that the deletion of RAD6B may lead to abnormalities in DDR, thereby accelerating the degeneration of various structures in the cochlea and senescence and apoptosis of cochlea cells.
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http://dx.doi.org/10.1016/j.bbrc.2020.08.017DOI Listing
October 2020

RAD6B Plays a Critical Role in Neuronal DNA Damage Response to Resist Neurodegeneration.

Front Cell Neurosci 2019 23;13:392. Epub 2019 Aug 23.

Department of Anatomy and Histology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China.

RAD6 participates in DNA double-strand breaks (DSBs) repair by ubiquitinating histone H2B in mitotic cells. In terminally differentiated cells, however, the mechanisms of DNA damage repair are less well known. In this study, we investigate whether RAD6B is involved in DSBs repair in neurons and effects of RAD6B deficiency on neuronal survival. We compared neurons of RAD6B-deficient mice with those of littermate wild type (WT) mice and induced DNA damage by X-ray irradiation. We provide evidence that RAD6B is essential for neural DDR and RAD6B deficiency results in increased genomic instability and neurodegeneration. Moreover, higher levels of p53 and p21 are present in the brains of RAD6B-deficient mice, which may be responsible for neuronal senescence, and degeneration. In addition, behavioral experiments show that RAD6B-deficient mice exhibit marked learning and memory deficits. In conclusion, these findings suggest that RAD6B is critical for neural integrity and that the absence of RAD6B accelerates neurodegeneration in mice.
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http://dx.doi.org/10.3389/fncel.2019.00392DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6716356PMC
August 2019

Biochar can mitigate methane emissions by improving methanotrophs for prolonged period in fertilized paddy soils.

Environ Pollut 2019 Oct 16;253:1038-1046. Epub 2019 Jul 16.

Jiangsu Key Laboratory of Low Carbon Agriculture and GHGs Mitigation, College of Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing 210095, China. Electronic address:

Biochar application to fertilized paddy soils has been recommended as an effective countermeasure to mitigate methane (CH) emissions, but its mechanism and effective duration has not yet been adequately elucidated. A laboratory incubation experiment was performed to gain insight into the combined effects of fresh and six-year aged biochar on potential methane oxidation (PMO) in paddy soils with ammonium or nitrate-amendment. Results showed that both ammonium and nitrate were essential for CH oxidation though high ammonium (4 mM) inhibited PMO as compared to low ammonium (1 mM and 2 mM), and that nitrate was better in promoting PMO than ammonium. Moreover, ammonium-amendment promoted type I pmoA, and nitrate-amendment enhanced type II pmoA abundance. Both fresh and aged biochar increased PMO as well as nitrification by enhancing the total, type I and type II methanotrophs as compared to the control. Increased soil PMO with mineral N input in both six-year aged biochar and fresh biochar amendment, indicating that biochar mitigated CH by promoting PMO for prolonged period in fertilized paddy soils.
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http://dx.doi.org/10.1016/j.envpol.2019.07.073DOI Listing
October 2019

Ex vivo detection of cadmium-induced renal damage by using confocal Raman spectroscopy.

J Biophotonics 2019 12 2;12(12):e201900157. Epub 2019 Sep 2.

School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu, China.

Cadmium (Cd) is a toxic heavy metal which is harmful to environment and organisms. The reabsorption of Cd in kidney leads it to be the main damaged organ in animals under the Cd exposure. In this work, we applied confocal Raman spectroscopy to map the pathological changes in situ in normal and Cd-exposed mice kidney. The renal tissue from Cd-exposed group displayed a remarkable decreasing in the intensity of typical peaks related to mitochondria, DNA, proteins and lipids. On the contrary, the peaks of collagen in Cd-exposed group elevated significantly. The components in each tissue were identified and distinguished by principal component analysis. Furthermore, all the biological investigations in this study were consistent with the Raman spectrum detection, which revealed the progression and degree of lesion induced by Cd. The confocal Raman spectroscopy provides a new perspective for in situ monitoring of substances changes in tissues, which exhibits more comprehensive understanding of the pathogenic mechanisms of heavy metals in molecular toxicology.
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http://dx.doi.org/10.1002/jbio.201900157DOI Listing
December 2019

Long noncoding RNA GIHCG functions as an oncogene and serves as a serum diagnostic biomarker for cervical cancer.

J Cancer 2019 1;10(3):672-681. Epub 2019 Jan 1.

Fuzong Clinical College of Fujian Medical University, Fuzhou, Fujian 350025, China.

Cervical cancer is the most common and lethal gynaecological tumor. Long noncoding RNAs (lncRNAs) have critical roles in various cancers, including cervical cancer. However, few studies investigated the diagnostic value of lncRNAs for cervical cancer. In this study, we investigated the expression pattern of a recently identified lncRNA GIHCG in cervical cancer tissues, cell lines, and serums by qRT-PCR. Furthermore, we explored the roles of GIHCG in cervical cancer using gain-of-function and loss-of-function assays. Our results revealed that GIHCG is up-regulated in cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cell line, respectively. Furthermore, serum GIHCG is significantly up-regulated in cervical cancer patients compared with healthy controls. ROC curve analysis revealed that serum GIHCG could accurately discriminate cervical cancer patients from healthy controls. Functionally, we found that overexpression of GIHCG promotes cell proliferation, inhibits cell apoptosis, and promotes cell migration of cervical cancer cells. Conversely, depletion of GIHCG inhibits cell proliferation, induces cell apoptosis, and inhibits cell migration of cervical cancer cells. Mechanistically, we found that GIHCG represses the expression of miR-200b. The expression of miR-200b is inversely correlated with the expression of GIHCG in cervical cancer tissues. Moreover, overexpression of miR-200b attenuates the roles of GIHCG in promoting cervical cancer tumor growth . In summary, this study demonstrated that GIHCG functions as an oncogene in cervical cancer via repressing miR-200b. This study also suggested that GIHCG may be a non-invasive diagnostic biomarker and a potential therapeutic target for cervical cancer.
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http://dx.doi.org/10.7150/jca.28525DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6360414PMC
January 2019

A Hypothesis Generating the Mechanical Systems Underlying Posterior Vaginal Prolapse Based on Observed Displacements by Dynamic Magnetic Resonance Imaging.

Female Pelvic Med Reconstr Surg 2020 09;26(9):585-590

From the Department of Obstetrics and Gynecology, Fuzong Clinical College of Fujian Medical University, Fuzhou, China.

Objective: The aim of this study was to analyze quantified displacements of the posterior vaginal wall (PVW) on dynamic magnetic resonance imaging (MRI), which may generate hypotheses for the detailed mechanisms that underlie the development of posterior vaginal prolapse.

Methods: Pelvic dynamic MRI scans were obtained for 12 women with normal vaginal structure (stage 0) and 62 women with 4 consecutive stages (1-4) of posterior vaginal prolapse. Structural locations (apex vagina, distal vagina, and mid-perineal body [PB]) and equidistant points along the PVW (points 4-6 were considered as midvagina) were identified, and PVW length, straight distance of PVW, levator ani parameters (levator hiatus length [LHL], levator hiatus width [LHW], levator plate angle, anorectal angle, and M line [ML]), urogenital hiatus, and prolapse diameter were measured at rest and maximal Valsalva, respectively. The displacement of these measurements was obtained.

Results: From stage 0 to 2, the variables LHL, LHW, levator plate angle, anorectal angle, and ML increased gradually, but midvagina, distal vagina, and mid-PB were the opposite. From stage 2 to 3, apex vagina, midvagina, distal vaginal, mid-PB, LHL, LHW, and ML raised rapidly and peaked at stage 3, then declined at stage 4. In addition, the correlation coefficients between each measurement from stage 2 to 3 were statistically higher than those from stage 0 to 2.

Conclusions: Quantified displacements of the PVW and its supporting structure were shown on dynamic MRI, and the mechanical mechanisms were hypothesized regarding the interaction between pressure and the support force contributing to the deformation of the PVW and the supporting structures.
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http://dx.doi.org/10.1097/SPV.0000000000000637DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7458084PMC
September 2020

MiR-212 Attenuates MPP⁺-Induced Neuronal Damage by Targeting KLF4 in SH-SY5Y Cells.

Yonsei Med J 2018 May;59(3):416-424

Department of Internal Medicine-Neurology, Hua Mei Branch of the Second People's Hospital of Liaocheng, Linqing, China.

Purpose: Parkinson's disease (PD) is a common age-dependent neurodegenerative disease. MiR-212 has been demonstrated to exert protective effects in several neurological disorders. The present study aimed to investigate the role and underlying molecular mechanism of miR-212 in PD.

Materials And Methods: 1-methyl-4-phenylpyridinium (MPP+)-induced SH-SY5Y cells were applied as a PD model in vitro. RT-qPCR was used to measure the expression of miR-212 and Kruppel-like factor 4 (KLF4) mRNA. Western blot analysis was performed to detect the protein levels of KLF4, Notch1 and Jagged1. Cell viability and apoptosis were determined by the Cell Counting Kit-8 and flow cytometry, respectively. Quantitative analysis of caspase-3 activity, lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), and interleukin-1 beta (IL-1β) was conducted with corresponding ELISA kits. Dual-luciferase reporter assay was employed to evaluate the relationship between miR-212 and KLF4.

Results: MiR-212 was downregulated in MPP⁺-induced SH-SY5Y cells. Also, miR-212 alleviated MPP⁺-induced SH-SY5Y cell damage, embodied by increased cell viability, decreased caspase-3 activity, LDH release, ROS production, TNF-α, and IL-1β expression, as well as elevated SOD levels. KLF4 was a direct target of miR-212, and miR-212 repressed KLF4 expression in a post-transcriptional manner. Moreover, miR-212-mediated protection effects were abated following KLF4 expression restoration in MPP⁺-induced SH-SY5Y cells, represented as lowered cell viability and enhanced apoptotic rate. Furthermore, Notch signaling was involved in the regulation of miR-212/KLF4 axis in MPP⁺-induced SH-SY5Y cells.

Conclusion: miR-212 might attenuate MPP⁺-induced neuronal damage by regulating KLF4/Notch signaling pathway in SH-SY5Y cells, a promising target for PD therapy.
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http://dx.doi.org/10.3349/ymj.2018.59.3.416DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5889994PMC
May 2018

Effects of maternal undernutrition on the growth, development and antioxidant status of ovine placentome subtypes during late pregnancy.

Theriogenology 2018 Apr 11;110:96-102. Epub 2018 Jan 11.

College of Animal Science, Inner Mongolia Agricultural University, Hohhot, 010018, China. Electronic address:

This study investigated the effects of maternal undernutrition on the growth, development and antioxidant status of ovine placentome subtypes during late pregnancy. Eighteen time-mated Mongolian ewes with singleton fetuses were allocated to three groups at d 90 of pregnancy: Restricted Group 1 (RG1, 0.18 MJ ME · kg BW · d, n = 6), Restricted Group 2 (RG2, 0.33 MJ ME · kg BW · d, n = 6) and Control Group (CG, ad libitum, 0.67 MJ ME · kg BW · d , n = 6). All animals were supplied chopped hay during the restriction period. At 140 days of pregnancy, the gravid uterus was removed; then individual fetuses and placentae were weighed. The numbers and weight of the placentome subtypes were examined. The number of vessels of the placentome subtypes were observed in sections stained with hematoxylin-eosin. The indexes of antioxidant capacity and oxidative stress, including total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and mal-ondialdehyde (MDA) concentration, were measured by spectrometric kits. The fetal weights, placental weights and the numbers of Type A placentomes in both restricted groups were reduced (P < .05). Decreased fetal/placental weight ratio and increased total weight of the Type A placentome were found in the RG1 group compared to CG (P < .05). The total weights and the numbers of the Type B, Type C and Type D increased with severe maternal undernutrition in RG1 compared to CG (P < .05), as well as the increased numbers of Type B in the RG2 group compared to the CG group (P < .05). The placentome subtypes in RG1, including Type A, Type B and Type C, exhibited decreased concentrations of T-AOC and SOD activities, but higher MDA concentration and GSH-Px activity than those in CG (P < .05). For the RG2 group, the decreased T-AOC and SOD and increased GSH-Px were found in Type A placentome compared to CG (P < .05). For the same subtype placentome, there were no differences in the number of vessels among CG, RG2 and RG1 (P > .05); however, the number of vessels and MDA concentration of Type C and Type D placentome were higher than those of the Type A and Type B (P < .05). These results indicate that the growth and development of ovine Type A placentome was altered during late pregnancy. More and more Type B, Type C and Type D were formed from the Type A associated with maternal undernutrition. Oxidative stress occurred in all types of placentomes for the RG1 group, and the more flattening placentomes that were converted, the worse the antioxidant/pro-oxidant imbalance that was induced.
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http://dx.doi.org/10.1016/j.theriogenology.2018.01.002DOI Listing
April 2018

Function of RAD6B and RNF8 in spermatogenesis.

Cell Cycle 2018 19;17(2):162-173. Epub 2018 Jan 19.

a Department of Anatomy and Histology , Lanzhou University , School of Basic Medical Sciences , Lanzhou , China.

Histone ubiquitination regulates sperm formation and is important for nucleosome removal during spermatogenesis. RNF8 is an E3 ubiquitin ligase, and RAD6B is an E2 ubiquitin-conjugating enzyme. Both proteins participate in DNA damage repair processes via histone ubiquitination. Loss of RNF8 or RAD6B can lead to sterility in male mice. However, the specific mechanisms regulating these ubiquitin-mediated processes are unclear. In this study, we found that RNF8 knockout mice were either subfertile or sterile based on the numbers of offspring they produced. We explored the mechanism by which RAD6B and RNF8 knockouts cause infertility in male mice and compared the effects of their loss on spermatogenesis. Our results demonstrate that RAD6B can polyubiquitinate histones H2 A and H2B. In addition, RNF8 was shown to monoubiquitinate histones H2 A and H2B. Furthermore, we observed that absence of histone ubiquitination was not the only reason for infertility. Senescence played a role in intensifying male sterility by affecting the number of germ cells during spermatogenesis. In summary, both histone ubiquitination and senescence play important roles in spermatogenesis.
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http://dx.doi.org/10.1080/15384101.2017.1361066DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884393PMC
August 2019

Primary Blast Causes Delayed Effects without Cell Death in Shell-Encased Brain Cell Aggregates.

J Neurotrauma 2018 01 14;35(1):174-186. Epub 2017 Sep 14.

1 Defence Research and Development Canada, Suffield Research Center , Medicine Hat, Alberta, Canada .

Previous work in this laboratory used underwater explosive exposures to isolate the effects of shock-induced principle stress without shear on rat brain aggregate cultures. The current study has utilized simulated air blast to expose aggregates in suspension and enclosed within a spherical shell, enabling the examination of a much more complex biomechanical insult. Culture medium-filled spheres were exposed to single pulse overpressures of 15-30 psi (∼6-7 msec duration) and measurements within the sphere at defined sites showed complex and spatially dependent pressure changes. When brain aggregates were exposed to similar conditions, no cell death was observed and no changes in several commonly used biomarkers of traumatic brain injury (TBI) were noted. However, similarly to underwater blast, immediate and transient increases in the protein kinase B signaling pathway were observed at early time-points (3 days). In contrast, the oligodendrocyte marker 2',3'-cyclic nucleotide 3'-phosphodiesterase, as well as vascular endothelial growth factor, both displayed markedly delayed (14-28 days) and pressure-dependent responses. The imposition of a spherical shell between the single pulse shock wave and the target brain tissue introduces greatly increased complexity to the insult. This work shows that brain tissue can not only discriminate the nature of the pressure changes it experiences, but that a portion of its response is significantly delayed. These results have mechanistic implications for the study of primary blast-induced TBI and also highlight the importance of rigorously characterizing the actual pressure variations experienced by target tissue in primary blast studies.
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http://dx.doi.org/10.1089/neu.2016.4961DOI Listing
January 2018

MicroRNA-181a Regulates Apoptosis and Autophagy Process in Parkinson's Disease by Inhibiting p38 Mitogen-Activated Protein Kinase (MAPK)/c-Jun N-Terminal Kinases (JNK) Signaling Pathways.

Med Sci Monit 2017 Apr 2;23:1597-1606. Epub 2017 Apr 2.

Department of Internal Medicine Neurology, HuaMei Branch of the 2nd People's Hospital of Liaocheng, Liaocheng, Shandong, China (mainland).

BACKGROUND microRNA (miR)-181a has been reported to be downregulated in Parkinson's disease (PD), but the regulatory mechanism of miR-181a on neuron apoptosis and autophagy is still poorly understood. We aimed to investigate the neuroprotective effects of miR-181a on PD in vitro. MATERIAL AND METHODS Human SK-N-SH neuroblastoma cells were incubated with different concentrations of 1-methyl-4-phenylpyridinium ion (MPP+) to induce the PD model. The expression of miR-181a was then analyzed. After transfection with miR-181a mimic or scramble following MPP+ treatment, the expression of autophagy protein markers (LC3II, LC3I, and Beclin 1) and p38 mitogen-activated protein kinase (MAPK)/c-Jun N-terminal kinases (JNK) signaling proteins (p-p38, p38, p-JNK, and JNK) and cell apoptosis were detected. Furthermore, the cells were transfected with miR-181a inhibitor and cultured in the presence or absence of p38 inhibitor SB203582 or JNK inhibitor SP600125, and the cell apoptosis was tested again. RESULTS The expression of miR-181a was gradually decreased with the increase of MPP+ concentration (P<0.05, P<0.01, or P<0.001). Overexpression of miR-181a significantly decreased the LC3II/LC3I ratio, Beclin 1 expression, cell apoptosis, and the expression of p-p38 and p-JNK compared to the MPP+ + miR-181a scramble group (all P<0.05). In addition, we observed that SB203582 or SP600125 showed no effects on cell apoptosis, but the effects of miR-181a inhibitor on cell apoptosis were reversed by administration of SB203582 or SP600125 compared to the scramble group (P<0.05). CONCLUSIONS Our results suggest that miR-181a regulates apoptosis and autophagy in PD by inhibiting the p38 MAPK/JNK pathway.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386441PMC
http://dx.doi.org/10.12659/msm.900218DOI Listing
April 2017

Comparative toxicity of mono- and bifunctional alkylating homologues of sulphur mustard in human skin keratinocytes.

Toxicology 2017 05 8;382:36-46. Epub 2017 Mar 8.

Defence Research & Development Canada, Suffield Research Center, Box 4000, Medicine Hat, Alberta, T1A 8K6, Canada.

Sulphur mustard (bis(2-chloroethyl) sulphide; agent H) is a vesicant chemical warfare (CW) agent whose mechanism of action is not known with any certainty and for which there are no effective antidotes. It has a pronounced latent period before signs and symptoms of poisoning appear which it shares with the nitrogen mustards, and that differentiates it from other classes of vesicant agents. Sulphur mustard, the sulphur mustard CW agents Q (1,2-bis(2-chloroethylthio) ethane) and T (1,1 bis(2-chloroethylthioethyl) ether), the H partial hydrolysis product hemi-sulphur mustard (2-chloroethyl 2-hydroxyethyl sulphide; HSM), and the commercially available 2-chloroethyl ethyl sulphide (CEES) were characterized with respect to their toxicity in first passage cultures of proliferating human skin keratinocytes, the target cell of H-induced skin vesication. Agents H and T were equitoxic and half as toxic as agent Q. Hemi-sulphur mustard and CEES were approximately six times and seventeen times, respectively less cytotoxic than H. 2-Chloroethyl ethyl sulphide was only slightly less toxic in confluent cultures compared to actively proliferating cells. In contrast, the toxicity of H, Q, T and HSM significantly decreased as the cultures became confluent, paralleling the decreasing sensitivity of skin keratinocytes to H as they leave the basement membrane of the skin. The toxicity of CEES was maximal by 24h. In contrast, the maximal toxicity of the other four agents occurred at 48h, mirroring the latent period observed for these agents in vivo. The markedly different characteristics of toxicity between CEES and the other four test compounds indicate that it is likely that different mechanisms of action are operative between them. Caution should therefore be taken when interpreting the results of studies utilizing CEES as a simulant for the mechanistic study of H, or in the elucidation of medical countermeasures against this CW agent. It is also notable that the toxicity characteristics of the mono-alkylating HSM mirrors those of H, Q and T, suggesting that the bi-alkylating characteristics of these latter compounds may not play as large a role in their toxic effects as commonly thought.
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http://dx.doi.org/10.1016/j.tox.2017.03.005DOI Listing
May 2017

Identification of Differentially Expressed Genes in Pelvic Organ Prolapse by RNA-Seq.

Med Sci Monit 2016 Nov 7;22:4218-4225. Epub 2016 Nov 7.

Department of Obstetrics and Gynecology, Fuzhou General Hospital of Nanjing Military Command, Fuzhou, Fujian, China (mainland).

BACKGROUND Pelvic organ prolapse (POP) brings major health issues for women, affecting 40% of postmenopausal women, and directly affects bladder and bowel function, as well as quality of life. In light of the projected growth in demand for care for pelvic floor disorders, determining the etiology and progression of POP has important public health implications. MATERIAL AND METHODS Uterosacral ligaments (USLs) samples of POP patients and normal controls were enrolled for RNA-Seq, and functional annotation analysis and Protein-Protein interaction (PPI) networks construction were performed for differentially expressed genes (DEGs). RESULTS A total of 81 DEGs were identified between POP and normal control, and distinctly classify all samples into normal and POP group by hierarchical clustering. Sixty-six DEGs demonstrated the same expression pattern among the POP samples with different stages. For those DEGs, canonical Wnt receptor signaling pathway was the most significantly enriched GO term (P value=3.33E-07), and neuroactive ligand-receptor interaction was the most significantly enriched pathway (P value=1.24E-03). In The PPI networks of 81 dysregulated genes, significant hub proteins contained TOP2A (Degree=54), KCNA5 (Degree=22) and PLA2G2A (Degree=19), suggesting their important role in the development of POP. CONCLUSIONS This RNA-seq analysis identified a POP signature of 81 genes, and some ECM-related genes, including COMP, NDP, and SNAI2 might participate in the pathology of POP and be applied as potential therapeutic targets.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110227PMC
http://dx.doi.org/10.12659/msm.900224DOI Listing
November 2016

DNA damage preceding dopamine neuron degeneration in A53T human α-synuclein transgenic mice.

Biochem Biophys Res Commun 2016 Dec 3;481(1-2):104-110. Epub 2016 Nov 3.

Department of Internal Medicine, Gansu Academic Institute for Medical Research, Lanzhou, China. Electronic address:

Defective DNA repair has been linked with age-associated neurodegenerative disorders. Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by genetic and environmental factors. Whether damages to nuclear DNA contribute to neurodegeneration of PD still remain obscure. in this study we aim to explore whether nuclear DNA damage induce dopamine neuron degeneration in A53T human α-Synuclein over expressed mouse model. We investigated the effects of X-ray irradiation on A53T-α-Syn MEFs and A53T-α-Syn transgene mice. Our results indicate that A53T-α-Syn MEFs show a prolonged DNA damage repair process and senescense phenotype. DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice and decrease the number of nigrostriatal dopaminergic neurons. Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.
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http://dx.doi.org/10.1016/j.bbrc.2016.11.008DOI Listing
December 2016

The Effect of Underwater Blast on Aggregating Brain Cell Cultures.

J Neurotrauma 2017 01 8;34(2):517-528. Epub 2016 Jul 8.

1 Defence Research and Development Canada, Suffield Research Center , Medicine Hat, Alberta, Canada .

Although the deleterious effects of primary blast on gas-filled organs are well accepted, the effect of blast-induced shock waves on the brain is less clear because of factors that complicate the interpretation of clinical and experimental data. Brain cell aggregate cultures are comprised of multiple differentiated brain cell types and were used to examine the effects of underwater blast. Suspensions of these cultures encased in dialysis tubing were exposed to explosive-generated underwater blasts of low (∼300 kPa), medium (∼2,700 kPa), or high (∼14,000 kPa) intensities and harvested at 1-28 days post-exposure. No changes in gross morphology were noted immediately or weeks after blast wave exposure, and no increases in either apoptotic (caspase-3) or necrotic (lactate dehydrogenase) cell death were observed. Changes in neuronal (neurofilament H, acetylcholinesterase, and choline acetyltransferase) and glial (glial fibrillary acidic protein, glutamine synthetase) endpoints did not occur. However, significant time- and pressure-related increases in Akt (protein kinase B) phosphorylation were noted, as well as declines in vascular endothelial growth factor levels, implicating pathways involved in cellular survival mechanisms. The free-floating nature of the aggregates during blast wave exposure, coupled with their highly hydrolyzed dialysis tubing containment, results in minimized boundary effects, thus enabling accurate assessment of brain cell response to a simplified shock-induced stress wave. This work shows that, at its simplest, blast-induced shock waves produce subtle changes in brain tissue. This study has mechanistic implications for the study of primary blast-induced traumatic brain injury and supports the thesis that underwater blast may cause subtle changes in the brains of submerged individuals.
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http://dx.doi.org/10.1089/neu.2016.4430DOI Listing
January 2017

DNA Damage-Induced Foci of E2 Ubiquitin-Conjugating Enzyme are Detectable upon Co-transfection with an Interacting E3 Ubiquitin Ligase.

Biochem Genet 2016 Apr 30;54(2):147-57. Epub 2015 Dec 30.

Department of Anatomy and Histology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.

DNA damage repair elements accumulate at DNA damage sites to form ionizing radiation-induced foci (IRIF) for damage repair. IRIF, which represent direct evidence of DNA damage response activity, which are conveniently to be observed via immunofluorescence staining. Protein ubiquitination plays an important role in initiating the DNA damage response. Following DNA damage, the substrate binding protein E3 ubiquitin-ligases enzymes are recruited to DNA damage sites, then the E2 ubiquitin-conjugating enzymes are recruited to these sites by the E3 where they catalyze protein ubiquitination. However, IRIF of E2 enzymes are relatively transient and unstable in vivo and difficult to detect. Here, we present a new method for the observation of E2 IRIF. This method is based on the co-transfection of interacting E2 and E3 enzymes into cells and identifies IRIF via immunofluorescence following DNA damage.
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http://dx.doi.org/10.1007/s10528-015-9707-8DOI Listing
April 2016

RNF8 deficiency results in neurodegeneration in mice.

Neurobiol Aging 2015 Oct 11;36(10):2850-2860. Epub 2015 Jul 11.

Department of Anatomy and Histology, Lanzhou University School of Basic Medical Sciences, Lanzhou, 730000, China.

The progressive loss of neurons causes neurodegenerative diseases. Because the accumulation of DNA breaks results in neuronal apoptosis, the lack of a variety of DNA damage repair-related proteins contributes to neurodegeneration. The ubiquitin ligase RNF8 plays an important role in DNA double-strand break repair via histone ubiquitination. However, the function of RNF8 in terminally differentiated neurons remains unknown. This study aimed to determine whether RNF8 is involved in the DNA damage response in neurons and contributes to neurodegeneration. Here, we present evidence suggesting that RNF8 deficiency results in DNA damage accumulation and neuronal apoptosis. RNF8(-/-) mice exhibit neuronal degeneration and reactive astrocytosis. Neurons from RNF8(-/-) mice appear to be more susceptible to X-ray-induced DNA damage. These changes were consistent with the behavioral performances of the RNF8-deficient mice, which included impaired performances in the open-field test and step-down avoidance task. Overall, these findings show that RNF8 is required for DNA damage repair in neurons. RNF8 deficiency is sufficient to cause neuronal pathology and cognitive decline, and the loss of RNF8 results in neuron degeneration.
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http://dx.doi.org/10.1016/j.neurobiolaging.2015.07.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851709PMC
October 2015

Relationship between levator ani and bony pelvis morphology and clinical grade of prolapse in women.

Clin Anat 2015 Sep 10;28(6):813-9. Epub 2015 Apr 10.

Department of Radiology, Fuzhou General Hospital, Fuzhou, Fujian, 350025, China.

The aim of this study was to assess the morphological features of the levator ani and bony pelvis in women with different grades of prolapse. Ninety Chinese women with different grades of uterine prolapse were studied, 18 in each stage of prolapse from I to IV, and 18 asymptomatic nulliparous volunteers as normal controls. Three-dimensional (3D) models that included the pelvic bones, levator ani, pubic symphysis, sacrum, and coccyx were generated from magnetic resonance (MR) images. The width and length of the levator hiatus and levator symphysis gap, the width of the iliococcygeus, and the iliococcygeal angle were measured to quantify levator ani morphology; the intertuberous diameter, interspinous diameter, subpubic angle, and pubococcygeal line were measured to characterize the morphology of the bony pelvis. Four patterns of levator ani morphology among women with and without prolapse were distinguished. Among the bony pelvis parameters, no measurement differed significantly between the subjects with prolapse and normal controls, or among subjects with different grades of prolapse. There were significant differences in the width and length of the levator hiatus and levator symphysis gap between women with prolapse and normal controls. Our pilot data help to elucidate bony pelvis and levator ani morphology in women with and without pelvic organ prolapse. In contrast to the iliococcygeus muscle, changes in the morphological features of the pubovisceral muscle are more likely to accompany prolapse.
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http://dx.doi.org/10.1002/ca.22536DOI Listing
September 2015

Significance of preoperative calculation of uterine weight as an indicator for preserving the uterus in pelvic reconstructive surgery.

Int J Clin Exp Pathol 2015 1;8(1):900-5. Epub 2015 Jan 1.

Department of Obstetrics and Gynecology, Fuzhou General Hospital/Dongfang Hospital, Xiamen University Fuzhou 350025, China.

Recently, increasing evidence has shown that uterus preservation is beneficial for pelvic organ prolapse (POP) patients, both physiologically and psychologically. However, the preoperative indicators for uterus preservation have rarely been examined. The current study was designed to determine the relationship between the preoperative evaluated uterus weight and the operation selection (preserving the uterus or not) in pelvic reconstructive surgery (PRS) using vaginal meshes. First, in a series of 96 patients undergoing hysterectomy, the uterine weight was calculated by preoperative ultrasound measurements, and was then compared with the postoperative actual weight of the uterus. Subsequently, in a series of 65 patients undergone PRS using vaginal meshes and preserving the uterus, the uterine weight was calculated by preoperative ultrasound measurements. Lastly, in a series of 43 patients with a uterine weight > 56.12 g who had undergone PRS using vaginal meshes, the operation success rate in patients with a preserved uterus was compared to patients for whom the uterus was not preserved. The results showed that uterus weight can be evaluated by ultrasound and used as a preoperative indicator for whether the uterus should be preserved or not in PRS when using vaginal meshes. It was indicated that preoperative evaluation of uterine weight is beneficial for surgical planning and guidance.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348811PMC
November 2015

[Method and significance of ultrasonographic assessment of the uterine weight before pelvic floor reconstruction].

Zhonghua Fu Chan Ke Za Zhi 2014 Jun;49(6):437-40

Department of Obstetrics and Gynecology, Fuzhou General Hospital of Nanjing Military Command, Fuzhou 350025, China. Email:

Objective: To investigate the accuracy of ultrasonographic assessment of the total uterine weight and the feasibility of using this method in the pelvic floor reconstruction.

Methods: Firstly, 81 cases with hysterectomy due to benign uterine diseases or uterine prolapse were studied. The preoperative dimensions and gravities of corpus uteri and cervix were calculated by formulas, and were then compared with the postoperative measurements. Subsequently, 46 cases with pelvic floor reconstruction and preserved the uterus were subjected to retrospectively analysis of uterine measurement parameters.

Results: There were no statistically differences between the preoperative and postoperative diameters of corpus uteri and cervix (P > 0.05), and no statistically differences between the weight of corpus uteri and cervix estimated by the formulas [(87 ± 55), (32 ± 6) g] and the true weight [(88 ± 57), (33 ± 6) g; P > 0.05]. In 46 cases that underwent the pelvic floor reconstruction by transvaginal mesh repair and preserved the uterus, 42 cases were successful treated and the average weight of total uterus was (49 ± 13) g (95%CI: 39.90-49.88 g); the 4 relapsed cases were treated with hysterectomy and the weight of total uterus were 85.24, 82.69, 92.67 and 120.06 g which were consistent with the weights estimated by the formulas (87.36, 82.00, 90.88, 123.12 g; all P > 0.05).

Conclusions: The uterine weight might be a significant factor for uterus preservation in pelvic floor reconstruction, while ultrasonographic assessment can accurately estimate the uterine weight preoperatively. All these raised the feasibility of assessing uterine weight preoperatively in pelvic floor reconstruction.
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June 2014

[Study on risk factors with the occurrence of the mesh exposure after pelvic floor reconstruction].

Zhonghua Fu Chan Ke Za Zhi 2014 Jan;49(1):26-9

Department of Obstetrics and Gynecology, Fuzhou General Hospital of Nanjing Military Command of People's Liberation Army, Fuzhou 350025, China.

Objective: To study risk factors with the occurrence of the mesh exposure after pelvic floor reconstruction.

Methods: From Mar.2007 to Mar.2011, a retrospective study was made on the clinical data of 353 patients undergoing vaginal mesh pelvic floor reconstruction. The related complications of the mesh were surveyed, and risk factors associated with the mesh's exposure were studied by single factor and multiple factors logistic regression.

Results: It was found that the exposure rate was 9.6% (34/353) after 1 year postoperative follow-up.Single factor analysis showed that patients who were not less than 70 years old, patients who were on their menopause stage, the occurrence of not less than three parturition, history of pelvic surgery, diabetes and smoking had a significant correlation (all P < 0.05) with the occurrence of the mesh exposure after pelvic floor reconstruction. Multiple factors logistic regression analysis showed that patients who were not less than 70 years of age (OR = 2.389), the occurrence of not less than three parturition (OR = 2.688), the history of diabetes (OR = 3.545), the history of pelvic surgery (OR = 5.385) were the independent risk factors, and the operation experience was the protection factors (OR = 0.134).

Conclusions: Mesh exposure is a common complication after pelvic floor reconstruction.Old age, multiple delivery, history of diabetes and history of pelvic surgery are the risk factors of mesh exposure. Preoperative full assessment and the quality of training contribute to reduce the incidence.
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January 2014

IGF-1 gene-modified muscle-derived stem cells are resistant to oxidative stress via enhanced activation of IGF-1R/PI3K/AKT signaling and secretion of VEGF.

Mol Cell Biochem 2014 Jan 15;386(1-2):167-75. Epub 2013 Oct 15.

Fuzong Clinical College, Fujian Medical University, Fuzhou, 350025, Fujian, China.

Reactive oxygen species (ROS)-induced oxidative stress increases in skeletal muscle with aging and decreases the viability of implanted cells. Type 1 insulin-like growth factor (IGF-1) promotes the survival of skeletal muscle cells under oxidative stress. It is unknown whether IGF-1 protects muscle-derived stem cells (MDSCs) from oxidative stress. In this study, we genetically engineered rat MDSCs to overexpress IGF-1 and determined cell viability, apoptosis, and VEGF secretion under oxidative stress. Overexpression of IGF-1 prevented MDSCs from H2O2-induced caspase-dependent apoptotic cell death by upregulating the PI3K/AKT pathway, accompanied with an increase of NF-κB, p-NF-κB, Bcl-2, and VEGF, as well as a decrease of Bax. In contrast, pre-administration of picropodophyllinb, wortmannin, 1L-6-hydroxymethyl-chiro-inositol-2-((R)-2-O-methyl-3-O-octadecylcarbonate), or pyrrolidine-dithiocarbamate, specific inhibitors of IGF-1R, PI3K, AKT, and NF-κB, respectively, followed by treatment with H2O2, resulted in cell death of MDSCs. Our data indicated that IGF-1 suppresses apoptosis and enhances the paracrine function of MDSCs under oxidative stress via enhancing IGF-1R/PI3K/AKT signaling. Thus, IGF-1 gene-modified MDSCs present a potential application in the treatment of muscle wasting, such as urethra intrinsic sphincter deficiency.
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http://dx.doi.org/10.1007/s11010-013-1855-8DOI Listing
January 2014

Identification of pathology from diesel exhaust particles in the bladder in a rat model by aspiration of particles from the pharynx.

Environ Toxicol Pharmacol 2013 May 14;35(3):380-7. Epub 2013 Feb 14.

Fuzong Clinical College of Fujian Medical University, Fuzhou, China.

To determine whether diesel exhaust particles (DEPs) could be a toxic agent to the bladder, rats were exposed to different concentrations of DEPs for one month or three months. When the rats were sacrificed, morphologic changes of the urothelium were investigated. The antioxidase activity and the levels of lipid peroxidation in the bladder were assayed. In the three-month group, DEPs at doses of 21.03 μg/μl insulted the structural integrity of surface glycosaminoglycans, widened the gap between urothelial cells, increased levels of lipid peroxidation, and decreased antioxidase activities in the urinary bladder (p<0.05). Furthermore, DEPs at a dose of 5.61 μg/μl decreased glutathione, catalase, and glutathione peroxidase activities (p<0.05). These results led to the conclusion that DEPs were a toxic agent in the bladder. The toxic effects might be attributed to oxidative damage mediated by pro-oxidant/antioxidant imbalance or excessive free radicals.
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http://dx.doi.org/10.1016/j.etap.2013.01.014DOI Listing
May 2013

Maternal exposure to airborne particulate matter causes postnatal immunological dysfunction in mice offspring.

Toxicology 2013 Apr 14;306:59-67. Epub 2013 Feb 14.

Department of Obstetrics and Gynecology, Fuzhou General Hospital, Fujian, China.

Evidence suggests that prenatal exposure to air pollution affects the ontogeny and development of the fetal immune system. The aim of this study was to investigate the effect of maternal exposure to airborne particulate matter (PM) on immune function in postnatal offspring. Pregnant female ICR mice were intralaryngopharyngeally administered with 30 μl of phosphate buffered solution (the control group) or resuspended PM of Standard Reference Material 1649a at 0.09 (low), 0.28 (medium), 1.85 (high) or 6.92 (overdose) μg/μl once every three days from day 0 to 18 of pregnancy (n=8-10). Offspring were sacrificed on postnatal day 30. Interleukin-4 and interferon-γ levels in plasma and splenocytes, splenic lymphocyte proliferation, and expressions of GATA-3 and T-bet mRNA in the spleen were tested. The spleen and thymus were histopathologically examined. The offspring of the medium, high and overdose PM-exposed dams showed significantly suppressed splenocyte proliferation. Decreased interferon-γ and increased interleukin-4 levels in the blood and splenocytes, and lowered T-bet and elevated GATA-3 mRNA expressions were found in the spleen in the medium, high and overdose groups when compared with the control or low dose group (P<0.05). Histopathology revealed prominent tissue damage in the spleen and thymus in the overdose group. These results suggest that exposure of pregnant mice to PM modulates the fetal immune system, resulting in postnatal immune dysfunction by exacerbation of Thl/Th2 deviation. This deviation is associated with altered T-bet and GATA-3 gene expressions.
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http://dx.doi.org/10.1016/j.tox.2013.02.004DOI Listing
April 2013

Adipose-derived stromal cell transplantation for treatment of stress urinary incontinence.

Tissue Cell 2011 Aug 24;43(4):246-53. Epub 2011 Jun 24.

Department of Obstetrics and Gynecology, First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China.

We aimed to investigate the application of adipose-derived stromal cells in the treatment of stress urinary incontinence (SUI). Animal models of stress urinary incontinence were established with Sprague-Dawley female rats by complete cutting of the pudendal nerve. Rat adipose-derived stromal cells were isolated, cultured and successfully transplanted into animal models. Effects of stem cell transplantation were evaluated through urodynamic testing and morphologic changes of the urethra and surrounding tissues before and after transplantation. Main urodynamic outcome measures were measured. Intra-bladder pressure and leak point pressure were measured during filling phase. Morphologic examinations were performed. Transplantation of adipose-derived stem cells significantly strengthened local urethral muscle layers and significantly improved the morphology and function of sphincters. Urodynamic testing showed significant improvements in maximum bladder capacity, abdominal leak point pressure, maximum urethral closure pressure, and functional urethral length. Morphologic changes and significant improvement in urination control were consistent over time. It was concluded that periurethral injection of adipose-derived stromal cells improves function of the striated urethral sphincter, resulting in therapeutic effects on SUI. Reconstruction of the pelvic floor through transplantation of adipose-derived cells is a minimally invasive and effective treatment for SUI.
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http://dx.doi.org/10.1016/j.tice.2011.04.003DOI Listing
August 2011

Impact of the tension-free vaginal tape obturator procedure on sexual function in women with stress urinary incontinence.

Int J Gynaecol Obstet 2011 Mar 15;112(3):187-9. Epub 2011 Jan 15.

476th Clinical Department of Fuzhou General Hospital, Fuzhou, China.

Objective: To evaluate prospectively the impact of the tension-free vaginal tape obturator (TVT-O) procedure on sexual function in women with stress urinary incontinence (SUI).

Methods: The present prospective study included women with SUI and no concomitant prolapse who underwent a TVT-O procedure at Fuzhou General Hospital in Fuzhou, Fujian, China. Before and 6 months after surgery, the patients had their sexual function evaluated using the Female Sexual Function Index (FSFI) questionnaire. Only sexually active women were included in the final analysis.

Results: Among the 55 sexually active patients, 21.8% had coital incontinence, which was cured in 11 of 12 patients (91.7%). More than half (54.5%) the women reported an improvement in sexual function after surgery and 45.5% reported no change. No statistically significant difference was found between preoperative and postoperative total or domain (desire, arousal, lubrication, orgasm, satisfaction, and pain) scores on the FSFI.

Conclusion: The TVT-O procedure in women with SUI did not significantly affect sexual function. Further studies are needed to verify the findings and compare the impact of TVT-O on sexual function with that of other anti-incontinence procedures.
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http://dx.doi.org/10.1016/j.ijgo.2010.09.014DOI Listing
March 2011
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