Search

OBJECTIVE: We aimed to explore the effectiveness of the modified tubularized incised plate urethroplasty (Snodgrass Technique) in hypospadias surgery. PATIENTS AND METHODS: A study was conducted on 50 pediatric patients with hypospadias treated in our hospital from May 2020 to May 2023. The patients were divided into two groups based on the condition of their urethral plate; 22 patients were included in the study group and 28 patients were included in the control group. The control group underwent the traditional Snodgrass technique, while the study group received the modified Snodgrass technique. The two groups were compared in terms of treatment efficacy, preoperative and postoperative 6-month Hypospadias Objective Scoring Evaluation (HOSE) scores, surgical data, and postoperative complications. RESULTS: The operation time for the study group was longer than that of the control group, and the intraoperative blood loss was less, but the differences were not statistically significant (p > 0.05). The success rate of surgery in the study group was 95.45% (21/22), compared to 71.43% (20/28) in the control group, showing a statistically significant difference (p < 0.05). The maximum urinary flow rate at 3 and 6 months postoperatively was significantly higher in the study group than in the control group (p < 0.05). The time to maximum flow (TQmax) and postvoid residual (PVR) at 3 and 6 months postoperatively were significantly lower in the study group (p < 0.05). A total of 3 patients in the cohort developed urethral fistulas, all between 0.10 cm x 0.10 cm and 0.15 cm x 0.15 cm in size. By instructing the patients to apply pressure to the fistula during urination, all fistulas closed between 3 and 6 months postoperatively. The incidence of postoperative complications was 4.55% in the study group and 28.57% in the control group, a difference that was statistically significant (p < 0.05). CONCLUSIONS: The modified Snodgrass technique shows significant therapeutic effectiveness in hypospadias surgery, substantially increasing the success rate and reducing postoperative complications in pediatric patients, making it suitable for widespread application. [ABSTRACT FROM AUTHOR]

BACKGROUND: The double-J stent (DJS) is a commonly used ureteral stent in urological surgeries, which provides support and drainage. However, the DJS may result in various complications such as infection, hematuria, stone formation, stent occlusion, and migration. Normally, one end of the DJS is located in the renal pelvis, and the other end in the bladder. In this case report, we describe the rare occurrence of a misplaced DJS during laparoscopic pyeloplasty, which was unintentionally placed in the contralateral renal pelvis. CASE REPORT: A 4-month-old male infant was diagnosed with left hydronephrosis. After confirmation of the diagnosis, laparoscopic left pyeloplasty was performed with the placement of a DJS. The patient did not experience any discomfort, such as nausea, vomiting, refusal to feed, crying and restlessness, or fever, after the operation, and was discharged on postoperative day 4. The patient returned to the hospital for DJS removal 6 weeks after the operation. However, the kidneys, ureters, and bladder (KUB) X-ray examination showed that the DJS was unintentionally placed in the contralateral ureter and renal pelvis. The stent was confirmed and removed under cystoscopy. Postoperative examination of the DJS showed that there was a hole in the side of the middle of the stent for urine drainage, with no obstruction or contralateral hydronephrosis. CONCLUSIONS: Misplacement of a DJS in the contralateral renal pelvis during laparoscopic pyeloplasty is a rare but potentially serious complication. Surgeons should be cautious when placing the stent and confirm its placement with imaging studies. Patients should be closely monitored for postoperative complications and prompt intervention should be taken if necessary. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study was performed to evaluate the clinical efficacy of the modified Brisson+Devine procedure in the management of concealed penis. PATIENTS AND METHODS: In this retrospective study, the medical data of 45 children diagnosed with concealed penis who underwent modified Brisson+Devine procedure in the Department of Urology of Anhui Provincial Children's Hospital between January 2019 and December 2021 were analyzed. Follow-up visits were performed at one, three, and six months postoperatively, and outcome measures included postoperative complications and parental satisfaction. RESULTS: All 45 children completed the surgery uneventfully. At 3-4 days after surgery, the penile dressing and the urinary catheter were removed. The patients were discharged 4-5 days postoperatively without ischemic necrosis of metastatic flaps. The follow-up visits spanned from 7 to 33 months, with a mean of 14.6 months. A statistically significant increase in the penile length after surgery was observed (p<0.05). The postoperative penile appearance was good, and the parents of the children had high treatment satisfaction (p<0.05). 38 children developed postoperative transferred flap edema, and the edema disappeared at 3 months postoperatively. CONCLUSIONS: The modified Brisson+ Devine procedure for concealed penis allows maximum use of the foreskin to improve the appearance of the penis and has a high safety profile by reducing postoperative complications, and provides high treatment satisfaction. [ABSTRACT FROM AUTHOR]

The dry gas seal (DGS) is a non-contacting, gas-lubricated mechanical face seal commonly used in rotating machinery. Traditional analyses of DGSs treat the end face as an independent factor by setting the end-face inlet as boundary conditions, but limited attention is focused on the sealing chamber of the DGS. Using the finite volume method and the shear stress transport (SST) k-ω model, the coupling between the millimeterscale sealing chamber and the micrometer-scale end face are simulated with regard to the real gas effect of CO². The three-dimensional distributions of velocity, pressure and temperature in the cross-scale flow field are investigated under different working conditions. Moreover, the boundary parameters of the end-face inlet are modified by response surface methodology with a central composite rotatable design. The results demonstrate that the real gas effect of CO² leads to an increased total inlet flow. When the pressure reaches 10.3 MPa, the relative difference is 51.90% compared to ideal gas. Minor temperature and pressure changes occur in the sealing chamber when the dry gas seal is in operation. However, the inlet temperature of the end face Tf increases and the inlet pressure of the end face pf decreases. These research results provide a reliable reference for engineering practice. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Long non-coding RNA (lncRNA) has been verified to regulate several cancers, including bladder cancer (BC). Our study aimed to elucidate the expression, function, and mechanism of lncRNA BRE-AS1 in BC. PATIENTS AND METHODS: Relative expression of lncRNA BRE-AS1 in 77 BC tissues and adjacent normal tissues was determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Expression of lncRNA BRE-AS1 in T24 and EJ cells was up-regulated using lentivirus transfection. Cell counting kit-8 (CCK-8) assay and colony formation assay were used to assess the proliferation of T24 and EJ cells influenced by lncRNA BRE-AS1. Also, the influence of lncRNA BRE-AS1 on cell apoptosis and cell cycle was measured using flow cytometry. Western blot was employed to explore the downstream molecules for lncRNA BRE-AS1 in BC. In vivo, xenograft formation experiment was established in nude mice to study the function of lncRNA BRE-AS1 in BC. RESULTS: LncRNA BRE-AS1 showed significantly decreased expression in BC tissues than the paired normal tissues. In vitro experiments demonstrated that over-expression of lncRNA BRE-AS1 inhibited cell proliferation but promoted cell apoptosis of EJ and T24 cells. STAT3 was determined as a target for lncRNA BRE-AS1. In vivo, up-regulation of lncRNA BRE-AS1 reduced cancer growth in nude mice bearing BC via repressing the phosphorylation of STAT3. CONCLUSIONS: LncRNA BRE-AS1 was down-regulated in BC tissues. Over-expression of lncRNA BRE-AS1 inhibited BC cell proliferation in vitro and in vivo via repressing the phosphorylation of STAT3. This might provide a new sight for the understanding of BC progression and biotherapy. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to uncover the expression pattern and biological function of circ_0001982 in the progression of colorectal cancer (CRC). PATIENTS AND METHODS: Relative expression level of circ_0001982 in 66 paired CRC tissues and adjacent normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRTPCR). The association between circ_0001982 level and clinical indexes of CRC patients was assessed. The effect of circ_0001982 on cellular behaviors of HT29 and HCT-116 cells was evaluated in vitro. Dual-Luciferase reporter gene assay was conducted to verify the binding relation between circ_0001982 and microRNA-144. Finally, rescue experiments were performed to assess the role of the circ_0001982/microRNA-144 axis in mediating the progression of CRC. RESULTS: Circ_0001982 was significantly up-regulated in CRC tissues when compared with adjacent normal ones. CRC patients with a high expression level of circ_0001982 showed a significantly higher rate of distant metastasis and worse survival. Knockdown of circ_0001982 remarkably attenuated the proliferative, migratory, and invasive capacities of HCT-116 cells. However, opposite results were observed after the overexpression of circ_0001982 in HT29 cells. MicroRNA-144 was verified as a target gene of circ_0001982, which could be negatively regulated by circ_0001982. Furthermore, microRNA- 144 was capable of reversing the regulatory effect of circ_0001982 on the proliferative, migratory, and invasive capacities of CRC cells. CONCLUSIONS: Up-regulated circ_0001982 was closely related to distant metastasis and poor prognosis of CRC. In addition, circ_0001982 attenuated the progression of CRC by negatively regulating microRNA-144. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Embryonic stem cells (ESCs) mainly originate from totipotent cells in early-stage of mammalian embryo and could proliferate in a manner of un-limitation. This study aimed to investigate roles of Axin2 in proliferation of ESCs and explore the associated mechanisms. MATERIALS AND METHODS: Axis inhibition protein 2 (AXIN2) over-expression (LV5-AXIN2) and AXIN2 RNA interfere (LV3-AXIN2-RNAi) vectors were structured and transfected into H9 cells. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) was used to evaluate cell proliferative activity. Flow cytometry analysis was employed to measure apoptosis of H9 cells. AXIN2, ß-catenin, transcription factor 4 (TCF4), c-myc, c-jun and Cyclin D mRNA levels and protein expressions were determined using quantitative real-time PCR (qRT-PCR) and Western blotting assay. RESULTS: LV5-AXIN2 and LV3-AXIN2-RNAi were successfully structured with higher transfecting efficacy. AXIN2 gene silencing remarkably increased proliferative activity and AXIN2 treatment significantly induced apoptosis of H9 cells, comparing with blank vector group (p<0.05). AXIN2 gene silencing significantly enhanced B-cell lymphoma-2 (Bcl-2) expression and remarkably inhibited cleaved caspase-3 expression comparing to that in blank vector group (p<0.05). AXIN2-RNAi treatment significantly enhanced and AXIN2 over-expression significantly reduced ß-catenin and TCF4 expression, comparing to that in blank vector group (p<0.05). AXIN2 gene silence activated down-stream molecules of Wnt/ß-catenin signaling pathway, including c-jun, c-myc, and Cyclin D1 (p<0.05). CONCLUSIONS: AXIN2 gene silencing reduced apoptosis by regulating mitochondria-associated apoptosis signaling pathway and enhanced proliferation by modulating molecules in Wnt/ß-catenin signaling pathway. Therefore, targeting of aberrant apoptosis and AXIN2 might be a novel clinical strategy to inhibit aging and enhance self-renewal of ESCs. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the expression characteristics of forkhead box K1 (FOXK1) in breast cancer (BCa). Meanwhile, its relationship with clinicopathology and prognosis of patients with BCa was also explored. PATIENTS AND METHODS: The expression level of FOXK1 in 65 paired BCa tissues and paracancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between FOXK1 expression and BCa pathological parameters as well as the prognosis of patients was analyzed. Meanwhile, the expression of FOXK1 in BCa cells was detected by qRT-PCR. Subsequently, FOXK1 knockdown and overexpression models were constructed by lentivirus transfection in BCa cell lines (including MCF-7 and SKBR3). The effect of FOXK1 on the biological functions of BCa cells was analyzed using Cell Counting Kit-8 (CCK-8), cell cloning assay and flow cytometry, respectively. Finally, whether the role of FOXK1 was achieved via the PI3K/AKT/mTOR signaling pathway was explored. RESULTS: The qRT-PCR results showed that FOXK1 expression in BCa tissues was significantly higher than that of adjacent tissues. Compared with patients with low expression of FOXK1, the pathological grading was markedly higher in those with high expression. Meanwhile, the overall survival rate was remarkably lower in patients with high expression. In addition, compared with the negative control group, the proliferation ability of cells in FOXK1 knockdown group was significantly decreased, while cell apoptosis was markedly up-regulated. Besides, Western blot results revealed that silencing FOXK1 could reduce the levels of key proteins in the PI3K/AKT/mTOR signaling pathway, thereby promoting the malignant progression of BCa. Finally, PI3Kα/mTOR-IN-1, which was the inhibitor of the PI3K/AKT/mTOR signaling pathway, significantly reversed the proliferative capacity of cells in FOXK1 overexpression group, as well as enhanced anti-apoptotic ability. CONCLUSIONS: FOXK1 expression was remarkably increased both in BCa tissues and cells. Meanwhile, it was markedly associated with pathological stage and poor prognosis of patients. Besides, FOXK1 might promote the malignant progression of BCa by inhibiting the PI3K/AKT/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the role of NLRP12 in regulating Pseudomonas aeruginosa (P. aeruginosa) keratitis. MATERIALS AND METHODS: Real-Time-PCR and Western blot were performed to measure the NLRP12 level in corneas and bone marrow-derived macrophages (BMDMs) of C57BL/6 (B6) mice. B6 mice received a subconjunctival injection of lentivirus expressing active NLRP12 (NLRP12-lentivirus) or Ctl-lentivirus (as control), followed by infection of P. aeruginosa. The clinical score, slit lamp and bacterial plate count of mice were evaluated. In addition, myeloperoxidase (MPO) was detected to assess the infiltration of polymorphonuclear neutrophil (PMN). Cytokine levels were measured by Real Time-PCR and ELISA. Meanwhile, the bacterial burden was also evaluated. The activation of NF-κB signaling was determined by pIκBα/IκBα levels based on Western blot and NF-κB-dependent Luciferase activity on the basis of Luciferase assays using 293T cells. RESULTS: NLRP12 mRNA and protein levels were decreased in B6 corneas and BMDMs after P. aeruginosa infection. The over-expression of NLRP12 in B6 corneas significantly ameliorated the severity of corneal disease, bacterial burden, PMN infiltration and pro-inflammatory cytokine expression. In vitro analysis demonstrated that the up-regulation of NLRP12 suppressed pro-inflammatory cytokine production and enhanced bacterial clearance in RAW264.7 cells. The protein levels of pIκBα and IκBα were significantly decreased after NLRP12-lentivirus treatment compared with that of Ctl-lentivirus. NF-κB-dependent Luciferase activity was potently inhibited by NLRP12 infected with P. aeruginosa or cotransfected with the downstream signaling molecules including IKKα and IKKβ in 293T cells. CONCLUSIONS: NLRP12 decreases the severity of P. aeruginosa keratitis, reduces corneal inflammation and bacterial burden through the down-regulation of the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Breast cancer cell infiltration, migration, and proliferation significantly affect its curative effect. Stemness gene octamer-binding transcription factor 4 (OCT4) upregulated in breast cancer tissue compared with normal control. MiRNA exhibits regulatory role in gene expression. This study adopted bioinformatics to predict the miRNA to regulate OCT4 gene and investigated its impact on breast cancer cell infiltration, migration, and proliferation. MATERIALS AND METHODS: MirBase database was analyzed to explore the potential miRNA in regulating OCT4 based on human OCT4 gene sequence. MiRNA mimics and inhibitor were synthetized and transfected to BS524 cells. qRT-PCR was applied to test miRNA and OCT4 mRNA expressions in cells at 12 h, 24 h, and 48 h after transfection. Western blot was selected to detect OCT4 protein expression. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was selected to determine cell proliferation. Scratch assay was adopted to evaluate cell migration. Transwell assay was used to analyze cell infiltration. RESULTS: MiR-145 may regulate OCT4 gene with score 82. OCT4 mRNA and protein increased at 12 h after transfection (p > 0.05). OCR4 gene significantly upregulated, cell proliferation, migration, and infiltration enhanced by miR-145 transfection compared with control (p < 0.05). OCT4 gene downregulated, while cell proliferation, infiltration, and migration markedly weakened in miR-145 inhibitor group compared with control (p < 0.05). CONCLUSIONS: M iR-145 a ffects b reast c ancer BS524 cell proliferation, infiltration, and migration via positively regulating OCT4 gene expression. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The present study was designed to investigate the effect of microRNA- 126 (miR-126) on the migration and homing of endothelial progenitor cells (EPCs) within arterial thrombus of cerebral infarction patients. MATERIALS AND METHODS: EPCs from rat bone marrow were isolated, and miR-126 overexpressed EPCs were constructed by lentiviral transfection. Then, the middle cerebral artery occlusion (MCAO) model was established by the method of thread ligation. Successfully established model rats were randomly divided into miR-126 overexpression EPC group, miR-126 wild type EPC group, and normal saline group. One day after the infarction, the miR-126 overexpression EPCs, miR-126 wild type EPCs, and normal saline, were injected into the lateral ventricle of the corresponding groups. Also, the transplanted cells were tracked by cell dye SPDiIC18. The expression of tight junction proteins ZO-1 and Claudin-5 in brain tissue was detected by Western blotting. RESULTS: Transplanted cells were detected in the cerebral infarction area 3 days after transplantation by cell dye SP-DiIC18. The number of homing EPCs in miR-126 overexpression group was significantly higher than that of miR-126 wild type EPC group (p < 0.05). Also, the protein expression of ZO-1 and Claudin-5 in the miR- 126 overexpression EPC group was significantly higher compared with that of the miR-126 wild type EPC group and the normal saline group. CONCLUSIONS: miR-126 overexpression EPCs, which were transplanted in the lateral ventricle, can home to the cerebral infarction areas via increasing increase the expression of ZO-1 and Claudin-5. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the effetcs of autophagy on the proliferation of renal carcinoma (RCCs). MATERIALS AND METHODS: Authophagy related protein 7 (Atg7)-overexpressing and knockdown RCC cell lines were established using lentiviral transfection and shRNA interference, respectively. (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) (MTT) was used to determine the Cell growth rate, and western blot was used to determine the expression of protein. In order to establish xenograft animal models, stable transfected cells were injected into nude mice. After that those mice were used to detect the effect of autophagy on the growth of RCC in vivo. RESULTS: Atg7 overexpression could up-regulate the level of LC3II in RCC cell lines, while Atg7-knockdown suppressed the expression of light chain 3 II (LC3II) in RCC cell lines. Atg7-overexpression cells exhibited a decreased growth profile, while suppressing the expression of Atg7 could accelerate the growth of RCC formed tumors. CONCLUSIONS: Our data indicated that autophagy could suppress the growth of RCC cells in vivo and in vitro, and autophagy appeared to be a new therapeutic target for treating advanced renal cell carcinoma. [ABSTRACT FROM AUTHOR]

A correction is presented to the article "Hyaluronic Acid Accelerates Re-epithelialization and Healing of Acute Cutaneous Wounds," which appeared in the 2023 issue,

A retraction is presented to the article "LncRNA BRE-AS1 Acts As a Tumor Suppressor Factor in Bladder Cancer Via Mediating STAT3," which appeared in the 2020 issue.

Introduction The laminin α4 subunit (LAMA4) has been shown to promote migration, proliferation, and survival of various cell types. This study investigated LAMA4's role in trophoblast cells during placental development. Methods LAMA4 expression was immunohistochemically assessed in the first trimester and term human placentas. LAMA4 siRNA was applied to silence LAMA4 expression in extravillous explants and HTR8/SVneo cells. Hypoxia–reoxygenation (H/R) conditions were applied to mimic preeclampsia. LAMA4 expression and trophoblast cell invasion, migration, and tube formation (a measure of angiogenesis) were assessed in HTR8/SVneo cells. The p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 was used to study the mechanism underlying LAMA4 activity. LAMA4 promoter methylation was assessed by bisulfite-sequencing polymerase chain reaction (PCR) or methylation-specific PCR. Results LAMA4 levels in preeclamptic placentas were significantly lower than those in controls. LAMA4 silencing significantly inhibited extravillous explant outgrowth as well as HTR8/SVneo cell invasion and migration. H/R conditions significantly lowered LAMA4 expression. Application of either H/R conditions or LAMA4 silencing both significantly decreased HTR8/SVneo cell invasion, migration, and tube formation, decreased MMP2 and MMP9 expression, and increased TIMP2 expression. SB203580 significantly reduced LAMA4 expression. LAMA4 silencing significantly decreased p-p38, p-c-Jun N-terminal kinase (JNK), and p-extracellular signal-regulated kinase (ERK) expressions; by contrast, H/R conditions induced significant upregulation of p-p38 and p-ERK but decreased p-JNK. LAMA4 promoter methylation was not significantly altered in preeclamptic placentas compared to controls. Conclusions LAMA4 expression is lowered in preeclamptic placentas and promotes trophoblast cell invasion, migration, and angiogenesis. H/R conditions decrease LAMA4 expression and appear to decouple the positive relationship between LAMA4 expression and p38 and ERK activation. [ABSTRACT FROM AUTHOR]

Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

AIM: TO investigate the mechanism of melatonin (MT) protection of adult rate myocardial ischemia-reperfusion injury and its influence on rat's hemodynamic recovery. MATERIALS AND METHODS: 48 rats were randomly divided into MT group (n=36) and the control group (n=12), MT group was divided into three sub-groups according to different dosages: Group I (n=12) was administered with 2.5 mg/kg MT; Group II (n=12) was administered with 5 mg/kg MT; Group III (n=12) was administered with 10 mg/kg MT. The electrocardiogram of four groups was observed with the left coronary artery blocked for 10min at first and then reperfused for 15min. Hemodynamic evolving was observed and changes in energy metabolism of rat myocardium were monitored. TUNEL and immunohistochemistry were applied to detect the cell apoptosis index, protein expression of Bcl-2 and Bax. RESULTS: LVDP (left ventricular developed pressure) and ± dp/dt in MT group presented better recovery at various time points than the control group. Among them, Group III had the optimal recovery degree (p < 0.05). After MT administration, ATP content in myocardial cells in MT group was significantly higher than the control group. Compared with the control group, the concentration of mitochondrial MDA and Ca2+ in myocardial cells in MT group showed a downward trend. But its GSH concentration was significantly higher than the control group (p < 0.05). The improvement degree of ATP, MDA, GSH and Ca2+ concentration in Group II over-performed Group I (p < 0.05). MT-inter-vened myocardial apoptosis index (AI) and Bax positive expression index declined while Bcl-2 positive expression index increased (p < 0.01). CONCLUSIONS: MT effectively inhibited myocardial apoptosis during the myocardial ischemia-reperfusion of rats, protected the structural integrity of mitochondria in myocardial cells, promoted ATP synthesis, and avoided heart damage in many ways. This protection mechanism was related with anti-oxidative damage. Meanwhile, MT could promote the hemodynamic recovery after myocardial ischemia-reperfusion in rats. [ABSTRACT FROM AUTHOR]

OBJECTIVES: The multipotent mesenchymal stem cells (MSCs) were distributed in the bone marrow stroma, and could generate all of the different skeletal cell lineages. The osteogenic differentiation of MSCs, which is indicated by the increased alkaline phosphatase (ALP) activity and the enhanced accumulation of collagen, could be induced by a tetradecapeptide termed osteogenic growth peptide (OGP). It has been hypothesized that the OGP induces the osteogenic differentiation of MSCs probably through regulating the fibroblast growth factor signaling pathways. Although the chemically synthesized OGP was widely applied to study the osteogenic differentiation of MSCs, transferring and expressing OGP gene in target cells is more desirable, especially for gene therapy, given the advantages and convenience on the stable expression of OGP. MATERIALS AND METHODS: In this study, we attempt to test the effect of OGP gene transfection; we constructed a eukaryotic expression vector, pcDNA3.1-OGP, which contained the OGP-coding DNA fragment. Subsequently, the vector was transfected into the rabbit MSCs. RESULTS: A significant increase of ALP activity was detected in the supernatant of pcDNA3.1-OGP transfected MSCs, and the enhanced collagen accumulation, which was inferred by the increased hydroxyproline content and RT-PCR. CONCLUSIONS: These results implied that transfecting the OGP-expressing vectors into MSCs might induce the osteogenic differentiation of MSCs. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Well-controlled trophoblast migration and invasion at the maternal–foetal interface are crucial events for normal placentation and successful pregnancy. Growing evidence has revealed that growth arrest and DNA damage-inducible 45 alpha (Gadd45α) participates in tumour migration and invasion as a tumour suppressor. However, the expression and function of Gadd45α in trophoblasts is unknown. This study aimed to determine the Gadd45α expression and function in the human first trimester placenta and identify the underlying mechanisms. Methods: The expression of Gadd45α in human first trimester placenta was determined using immunohistochemistry. HTR8/SVneo cell line was used to investigate the effects of Gadd45α on proliferation, apoptosis, migration/invasion, matrix metalloproteinase (MMP)2/9 activities, and tissue inhibitor of metalloproteinase (TIMP)1/2 expression using cell proliferation assays, flow cytometric analysis, transwell migration/invasion assays, gelatin gel zymography, and western blotting, respectively. Moreover, a placental villous explant model was employed to verify its functions in placentation. Results: Gadd45α was strongly expressed in syncytiotrophoblasts and trophoblast columns of human placental villi, extravillous trophoblast cells and glandular epithelium within the maternal decidua. Gadd45α knockdown significantly promoted migration and invasion of HTR8/SVneo cells, whereas it did not affect cell proliferation or apoptosis. Silencing Gadd45α also enhanced trophoblast outgrowth and migration in placental explants. These effects were related to increased activities of MMP2/9 and the decreased expression of TIMP1/2. Discussion and conclusion: Gadd45α may be involved in human trophoblast migration and invasion and may function as an important negative regulator at the foetal–maternal interface during early pregnancy by directly or indirectly regulating MMP2/9 activities. [Copyright &y& Elsevier]

Field and laboratory experiments were conducted to study if rain could wash-off pollen grains from the surface of the stigma and consequently affect the efficiency of fertilisation in loquat (Eriobotrya japonica Lindl.). Flowers of the loquat cultivar, 'Dawuxing', growing in the field, were emasculated, pollinated by hand with pollen of the cultivar 'Longquan No.5', then sprayed with water to simulate the effect of rain at -8, -4, -2 h before, -0 h (immediately before hand-pollination), +0 h (immediately after hand-pollination), and 2,4,8, or 12 h after pollination. A control to which no water treatment was applied was also included in the assay. Meanwhile, additional assays were performed in the laboratory to improve the resolution of the field study by using earlier treatments. Here, treatments were performed by pollinating, immersing, and shaking a branch with flowers in a container of water in the laboratory -120, -60, -30, -0, +0, 30,60, or 120 min before or after hand-pollination. One additional sample was immersed, shaken, then hand-pollinated, and immersed and shaken (ISPIS) again. The results showed that the numbers of pollen grains that germinated, and the percentages of fruit set, differed significantly between the -4, -2, -0, or +0 h treatments and the non-water-treated control in the fleld assays, especially in the case of the -0 h and +0 h treatments in which the stigmas were washed immediately before or after hand-pollination. However, the -8,2,4,8, and 12 h treatments did not show significant differences from the non-treated control. On the other hand, the laboratory experiments showed that all washing treatments reduced the number of germinated pollen grains retained on the stigma, and the immersion treatments at -30, -0, +0, or 30 min as well as the additional ISPIS treatment, showed significant differences from the non-treated controls in the numbers of pollen grains retained on the stigmas. In conclusion, the results showed that adhesion of pollen grains to the stigmas in loquat was rapid and strong, and that the simulated rain treatment was not able to wash-off pollen grains completely from the stigma surface, except in the -0 h and +0 h treatments. [ABSTRACT FROM AUTHOR]