Evaluation of nail psoriasis with ultrasound enhanced blood flow imaging (eflow) and Power Doppler (PD).

OBJECTIVE: The aim of this study was to assess the discriminative utility of nail features detected by B-mode (BM), enhanced flow (eflow) and power Doppler (PD) in patients with psoriasis or nail psoriasis (NP) and healthy controls. PATIENTS AND METHODS: Ultrasound appearance of nails was investigated in 5 patients with NP, 8 patients with psoriasis and 7 healthy controls. In total, 195 nails were examined. RESULTS: The thickness of the nail bed (TNB), the thickness of the nail plate (TNP) and the thickness of the nail matrix (TNM) did not differentiate between NP and psoriasis in longitudinal and cross-section of nails. Resistance index (RI) in nails was higher in patients with NP than in patients with psoriasis, and significantly higher in patients with psoriasis than in healthy controls. TNP between patients with psoriasis and healthy controls was statistically insignificant in longitudinal section of nails, but higher than that in the cross-section of nails. TNM was higher in patients with psoriasis than in healthy controls. The ultrasound features of NP in longitudinal and cross-section of nails, nail bed (NB) eflow and PD signal were statistically significant among patients with NP or psoriasis and healthy controls. In patients with NP, there was a correlation between the ultrasound features of NP in longitudinal and cross-section of nails and nail psoriasis severity index (NAPSI). CONCLUSIONS: Our study displayed the usefulness of ultrasound nail examinations in psoriatic nails, not only assessing ultrasonic features of nails and proving correlation between ultrasonic features of nails and NAPSI, but also comparing the accuracy of new technology of blood flow signal in nails.

lnc94638 is a testis-specific long non-coding RNA involved in spermatozoa formation in Zeugodacus cucurbitae (Coquillett).

Long non-coding RNAs (lncRNAs) generally display tissue-specific distributions, and testis-specific lncRNAs form the highest proportion of lncRNAs in many species. Here, we presented a detailed analysis of testis-specific lncRNAs in the melon fly, Zeugodacus cucurbitae, a highly destructive insect pest of cucurbitaceous and other related crops. Most testis-specific lncRNAs were found to be long intergenic non-coding RNAs (lincRNA). The size distribution of these lncRNAs ranged between 600 and 1000 nucleotides. Testis-specific lncRNAs that harboured one isoform number and two exons were the most abundant. Compared to other male tissues, the testis had more highly expressed lncRNAs. The quantitative real-time polymerase chain reaction results of 10 randomly selected testis-specific lncRNAs showed expression patterns consistent with RNA-seq data. Further analysis of the most highly expressed testis-specific lncRNA, lnc94638, was undertaken. Fluorescent in situ hybridization assays localized lnc94638 to the apical region of the testis that contains mature spermatozoa. RNA interference-mediated knockdown of lnc94638 expression reduced spermatozoa numbers and impaired the fertility of Z. cucurbitae male. This study provides a catalogue of testis-specific lncRNAs, shows that the testis-specific lnc94638 is involved in spermatogenesis and has the potential to be used for treating male sterility.

Correlations of changes in inflammatory factors, glucose and lipid metabolism indicators and adiponectin with alterations in intestinal flora in rats with coronary heart disease.

OBJECTIVE: The aim of this study was to explore the correlations of changes in inflammatory factors, glucose and lipid metabolism indicators and adiponectin with alterations in intestinal flora in rats with coronary heart disease. MATERIALS AND METHODS: A total of 30 male specific pathogen-free rats were randomly assigned into two groups, including: blank group (n=15) and coronary heart disease group (n=15). The rats in the coronary heart disease group were given high-fat diets and pituitrin to establish the model of coronary heart disease. Meanwhile, rats in the blank group were administered with an equal volume of double-distilled water. The alterations in the intestinal flora of rats were detected in the two groups, respectively. In addition, the changes in the levels of inflammatory factors, glucose and lipid metabolism indicators, adiponectin, creatine kinase (CK) and its isoenzyme, as well as troponin, were also examined. RESULTS: Statistically, significant differences in the levels of glucose and lipid metabolism indicators low-density lipoprotein (LDL) (p=0.040), total cholesterol (TC) (p=0.039), high-density lipoprotein (HDL) (p=0.044), triglyceride (TG) (p=0.000) and blood glucose (p=0.046) were observed between the rats in the coronary heart disease group and blank group. The content of all the glucose and lipid metabolism indicators (except HDL) in coronary heart disease group was significantly higher than the blank group (p<0.05). The rats in the coronary heart disease group had evidently higher levels of CK (p=0.000) and its isoenzyme (p=0.019), as well as troponin (p=0.021), than those in the blank group. The level of serum adiponectin in rats in coronary heart disease group was distinctly lower than that in the blank group, showing statistically significant differences (p<0.05). Besides, the levels of the inflammatory factors interleukin (IL)-2 (p=0.011), transforming growth factor (TGF)-ß (p=0.048), tumor necrosis factor-α (TNF-α) (p=0.025) and IL-6 (p=0.038) in rats in the coronary heart disease group were dramatically higher than those in blank group. Rats in coronary heart disease group had remarkably more Actinobacteria, Desulfovibrio, Aristipus and Escherichia coli in the intestine. Meanwhile, the abundance of Flavobacterium, Burkhofer and some probiotics increased significantly in the intestine of rats in blank group (p<0.05). The changes in the abundance of Actinobacteria, Desulfovibrio, Aristipus and Escherichia coli in the intestine of rats were probably correlated with increased levels of glucose and lipid metabolism indicators, inflammatory factors and adiponectin in coronary heart disease group. Moreover, the abundance of intestinal probiotics such as Bifidobacterium and Lactobacillus in rats in coronary heart disease group was notably lower than that in blank group (p<0.05). The decline in the abundance of such intestinal probiotics as Bifidobacterium and Lactobacillus was correlated with the changes in the levels of glucose and lipid metabolism indicators, inflammatory factors and adiponectin. In addition, decreased levels of probiotics weakened normal physiological functions of the intestine and promoted disease progression. CONCLUSIONS: Inflammatory factors, glucose and lipid metabolism indicators and adiponectin have evident changes in rats with coronary heart disease, which may be correlated with the alterations in the intestinal flora.

MiRNA-203a-5p alleviates the malignant progression of Wilms' tumor via targeting JAG1.

OBJECTIVE: To uncover the potential influence of microRNA-203a-5p (miRNA-203a-5p) on the malignant progression of Wilms' tumor (WT). PATIENTS AND METHODS: MiRNA-203a-5p levels in 49 paired WT and paracancerous tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Prognostic value of miRNA-203a-5p in WT was assessed by the Kaplan-Meier method. Correlation between miRNA-203a-5p level and clinical data of WT patients was analyzed. In G401 and SK-NEP-1 cells, in vitro functions of miRNA-203a-5p in regulating metastatic abilities were explored. The interaction between miRNA-203a-5p and JAG1, and their regulatory role in the malignant progression of WT were evaluated by Dual-Luciferase reporter gene assay and rescue experiments. RESULTS: MiRNA-203a-5p was downregulated in WT tissues than that of paracancerous ones. WT patients expressing low level of miRNA-203a-5p had higher risk of lymphatic metastasis and worse prognosis. Overexpression of miRNA-203a-5p attenuated migratory and invasive abilities in G401 cells. On the contrary, knockdown of miRNA-203a-5p yielded the opposite trends in SK-NEP-1 cells. JAG1 was verified to be the direct gene binding miRNA-203a-5p, which was negatively regulated by miRNA-203a-5p in WT cells. Rescue experiments finally uncovered that miRNA-203a-5p alleviated the malignant progression of WT via negatively regulating JAG1. CONCLUSIONS: MiRNA-203a-5p is downregulated in WT and closely linked to lymphatic metastasis of WT patients. By negatively regulating JAG1, miRNA-203a-5p alleviates the malignant progression of WT.

LncRNA HCG11 suppresses laryngeal carcinoma cells progression via sponging miR-4469/APOM axis.

OBJECTIVE: Longnon-coding RNAs (lncRNAs) have been reported to participate in the regulatory mechanisms of various cancers. Therefore, the aim of this study was to investigate the functional role of lncRNA HLA complex group 11 (HCG11) in laryngeal carcinoma. MATERIALS AND METHODS: The laryngeal carcinoma cell lines SNU46, SNU899, AMC-HN-8, and normal human nasopharyngeal epithelial cells NP69 were purchased. The expression of HCG11, miR-4469, and apolipoprotein M (APOM) was detected by quantitative Real Time-PCR (qRT-PCR) in tissues and cells. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay and colony formation assays. The protein expression of Bax and Bcl-2 was detected by Western blot. Besides, the mechanism assays were conducted to observe the interaction between miR-449 and HCG11 or APOM. The apoptosis in each group was detected by TUNEL assay. RESULTS: In this research, low expression of HCG11 was discovered in laryngeal carcinoma tissues and cells. Overexpression of HCG11 retarded cell proliferation and enhanced cell apoptosis. Later, we found that APOM was also downregulated in laryngeal carcinoma tissues and cell lines, and inhibited laryngeal carcinoma progression. HCG11 positively regulated APOM at the post-transcriptional level. MiR-4469 was predicted to have the binding sites of HCG11 and APOM. Furthermore, it was demonstrated that HCG11 absorbed miR-4469 to upregulate APOM expression. Finally, it was indicated that the repression of APOM rescued the effects of HCG11 overexpression on cell proliferation and cell apoptosis. CONCLUSIONS: This study uncovered that HCG11 sponged miR-4469 to suppress laryngeal carcinoma progression by upregulating APOM expression.

LncRNA AK024094 aggravates the progression of breast cancer through regulating miRNA-181a.

OBJECTIVE: The aim of this study was to investigate the role of long noncoding ribonucleic acids (lncRNAs) AK024094 in regulating the progression of breast cancer (BCa) and the potential mechanism. Our findings might help to provide a theoretical basis for the targeted therapy of BCa. PATIENTS AND METHODS: The relative expression level of lncRNA AK024094 in BCa and adjacent normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The prognostic potential of AK024094 in BCa was assessed by the Kaplan-Meier method. Meanwhile, AK024094 level in BCa cell lines was detected by qRT-PCR as well. The regulatory effects of AK024094 on the proliferative, migratory, and invasive abilities of MDA-MB-468 and MCF-7 cells were evaluated by functional assays. The Dual-Luciferase Reporter Gene Assay was applied to verify the binding between AK024094 and miRNA-181a. In addition, the rescue experiments were conducted to uncover the role of AK024094/miRNA-181a in the progression of BCa. RESULTS: AK024094 was significantly upregulated in BCa tissues and cell lines. Compared with BCa patients with low expression of AK024094, the tumor staging of those with a high level of AK024094 was remarkably worse. Meanwhile, the rate of distant metastasis was significantly higher, and the overall survival was shorter in BCa patients with high expression of AK024094. The knockdown of AK024094 significantly attenuated the proliferative, migratory, and invasive abilities of MDA-MB-468 and MCF-7 cells. Subsequently, miRNA-181a was predicted and verified as the target of AK024094. A negative correlation was identified between the expression levels of AK024094 and miRNA-181a in BCa. Furthermore, the knockdown of miRNA-181a partially reversed the effect of AK024094 on cellular behaviors of BCa cells. CONCLUSIONS: AK024094 aggravates the malignant progression of BCa, and is closely related to tumor staging, distant metastasis, and poor prognosis of BCa. In addition, AK024094 accelerates the proliferation and metastasis of BCa cells by targeting miRNA-181a.

LncRNA DLEU1/microRNA-300/RAB22A axis regulates migration and invasion of breast cancer cells.

OBJECTIVE: To explore the possible role of deleted in lymphocytic leukemia 1 (DLEU1) in regulating the metastasis of breast cancer and its underlying mechanism. PATIENTS AND METHODS: The expression levels of DLEU1 in 60 cases of breast cancer tissues and adjacent normal tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Survival analysis and receiver operating characteristic (ROC) curves were introduced to analyze the correlation between DLEU1 expression and the clinical features of enrolled breast cancer patients. After altering expressions of DLEU1, RAB22A or microRNA-300 by plasmid transfection, the abilities of breast cancer cells to migrate and invade were evaluated by transwell assay. Western blot was conducted to detect protein level changes of epithelial-mesenchymal transition (EMT)-related genes regulated by DLEU1, RAB22A or microRNA-300. Dual-luciferase reporter gene assay was performed to detect the binding relation between microRNA-300 with DLEU1 and RAB22A. RESULTS: DLEU1 expression remains higher in breast cancer tissues than in normal adjacent tissues, and has a certain diagnostic value. The overall survival of breast cancer patients was negatively correlated with DLEU1 expression. Overexpression of DLEU1 or RAB22A, or microRNA-300 knockdown could enhance the migratory and invasive capacities, as well as increase EMT ofBT549 cells. On the contrary, knockdown of DLEU1 or RAB22A, or microRNA-300 overexpression in MCF-7 cells obtained the opposite trends of cellular behaviors. Dual-luciferase reporter gene assay confirmed that DLEU1 and RAB22A could bind to microRNA-300. Further verification showed that RAB22A expression was positively regulated by DLEU1, but negatively regulated by microRNA-300. Finally, we found that DLEU1 overexpression could reverse the inhibitory effects of microRNA-300 on proliferation, migration, and EMT of breast cancer cells. CONCLUSIONS: DLEU1 is highly expressed in breast cancer, which promotes migration, invasion, and EMT of breast cancer cells by targeting microRNA-300 to mediate RAB22A.

Long noncoding RNA LINC00473 indicates a poor prognosis of breast cancer and accelerates tumor carcinogenesis by competing endogenous sponging miR-497.

OBJECTIVE: Long noncoding RNA LINC00473 (LINC00473) has been reported to be involved in the progression of several tumors. Our present study was conducted to study the potential roles and mechanism of long noncoding RNA LINC00473 (LINC00473) on cells proliferation, migration, invasion, and apoptosis of breast cancer (BC). PATIENTS AND METHODS: RT-PCR was applied for the analysis of LINC00473 in BC cell lines and tissues samples. The correlations between the LINC00473 levels and clinicopathological parameters were investigated. Kaplan-Meier methods and Cox proportional hazards regression models were explored to reveal potential associations of LINC00473 levels with overall survival of BC patients. The effect of LINC00473 on tumor behavior was evaluated by colony formation, Cell Counting Kit-8, EdU assays, flow-cytometric analysis, wound healing assays and transwell assays. Interactions between LINC00473 and miR-497 were determined using a luciferase reporter assay and RT-PCR assays. RESULTS: Upregulation of the expression of LINC00473 was found in BC samples and cell lines, in comparison with non-tumor breast tissues and human breast epithelial cells. High expression of LINC00473 was correlated with lymph node metastasis, clinical stage, and poorer outcome in BC patients. Multivariate logistic regression assays further showed LINC00473 as an independent prognostic factor in BC. Lost-of-function assays revealed that knockdown of LINC00473 resulted in the suppression of tumor cell proliferation, promotion of cells apoptosis, inhibition of cells metastasis. Bioinformatics analysis and luciferase reporter assays revealed LINC00473 bonds to miR-497. Further RT-PCR revealed that knockdown of LINC00473 suppressed the expressions of miR-497 in BC cells. CONCLUSIONS: Our data revealed that LINC00473 acted as a tumor promoter in BC and LINC00473/miR-497 axis may be a novel therapeutic strategy for this tumor.

Increased expression of miR-1179 inhibits breast cancer cell metastasis by modulating Notch signaling pathway and correlates with favorable prognosis.

OBJECTIVE: MicroRNAs (miRNAs) play a key role in the regulation of gene expression. In this study, we aimed to identify the clinical values of miR-1179 and to investigate the potential molecular mechanisms in breast cancer (BC). MATERIALS AND METHODS: RT-PCR was used to detect the expression levels of miR-1179 in both BC tissues and cell lines. We analyzed the association between the miR-1179 levels and clinicopathological factors and patient prognosis. The proliferation ability of miR-1179 on BC cells was assessed by MTT and colony formation assay. The role of miR-1179 in BC cells migration and invasion was measured by transwell assays. Western blot analysis was used to quantify the expression of the molecular biomarkers of the Notch signaling pathway. RESULTS: Our results showed that miR-1179 expression was frequently downregulated in BC tissues and cell lines. Clinicopathologic analysis revealed that low miR-1179 expression is correlated with lymph node metastasis, advanced clinical stage and shorter overall survival. Multivariable Cox proportional hazards regression analysis suggested that increased miR-1179 expression was an independent prognostic factor of overall survival in BC patients. Gain-of-function assay indicated that the overexpression of miR-1179 significantly suppressed BC cells proliferation, migration and invasion. Mechanistically, miR-1179 up-regulation inhibited the expression of Notch 1, Notch 4 and Hes1, indicating that miR-1179 could suppress the activation of the Notch signaling pathway. CONCLUSIONS: We showed that miR-1179 was a tumor suppressor that may serve as a novel potential prognostic biomarker or molecular therapeutic target for BC.

GLI-1 facilitates the EMT induced by TGF-ß1 in gastric cancer.

OBJECTIVE: To explore how GLI-1 affects the EMT induced by TGF-ß1 in gastric cancer. MATERIALS AND METHODS: Following 24 hours of culture of SGC-7901 cells in presence of TGF-ß1, we observed the changes in morphology as well as mRNA and protein expressions of GLI-1, E-cadherin and Vimentin by RT-PCR and Western blot. Transwell assay was conducted to evaluate the changes in invasion ability of SGC-7901 cells. Then, SGC-7901 cells were co-treated with TGF-ß1 and GANT 61, and changes of the above indexes were also detected using the corresponding methods. RESULTS: In presence of TGF-ß1, EMT was initiated in SGC-7901 cells EMT with increased cell invasion ability, and the mRNA and protein expressions of E-cadherin were downregulated, while those of the GLI-1 and Vimentin were upregulated. Conversely, the co-treatment of TGF-ß1 and GANT 61 suppressed the increased cell invasion ability induced only by TGF-ß1, and the changes in mRNA and protein expressions of these factors were abolished. CONCLUSIONS: We found that GLI-1 facilitates the EMT induced by TGF-ß1 in SGC-7901 cells, which may serve as a potential target in developing the clinical treatment of gastric cancer.

HMGB1 affects the development of pulmonary arterial hypertension via RAGE.

OBJECTIVE: To investigate the effect of high-mobility group box 1 (HMGB1) on the proliferation, migration and inflammatory response of human pulmonary artery smooth muscle cells (HPASMCs) and human pulmonary artery endothelial cells (HPAECs) through the receptor for advanced glycation end products (RAGE) and to investigate the mechanism of action underlying the effect of HMGB1 on pulmonary arterial hypertension. MATERIALS AND METHODS: The effect of HMGB1 on the proliferation of the two cell types was examined using the MTT assay under environmental hypoxia (incubation with 1.5% oxygen) to simulate the condition of pulmonary arterial hypertension in the body. The effect of HMGB1 on HPAEC migration was observed using the scratch assay. The effect of HMGB1 on the inflammatory mediators IL-6 and CXCL8 in the two cell types was assessed using qPCR (Real-time Quantitative PCR) and ELISA, and the RAGE mRNA and protein expression levels were also examined. RESULTS: Hypoxia promoted the proliferation of both cell types but inhibited the migration of HPAECs. HMGB1 had no obvious effect on the proliferation and migration of the cells. Both hypoxia and HMGB1 promoted the expression of the pro-inflammatory factors IL-6 and CXCL8. HMGB1 significantly promoted RAGE expression compared to the normal control group. CONCLUSIONS: HMGB1 affects the functions of HPASMCs and HPAECs through RAGE and may affect the course of pulmonary arterial hypertension.

Effect of adenovirus-mediated RNA interference of IL-1ß expression on spinal cord injury in rats.

STUDY DESIGN: We introduced an adenoviral vector expressing interleukin-1ß (IL-1ß) small-hairpin RNA (shRNA) into the injured spinal cords to evaluate the therapeutic potential of IL-1ß downregulation in a rat model of spinal cord injury (SCI). OBJECTIVES: The purpose of this study was to investigate the possible protective effects of the IL-1ß downregulation on traumatic SCI in rats. SETTING: Department of Orthopedic Surgery, The Second Affiliated Hospital, Fujian Medical University, Quanzhou, People's Republic of China. METHODS: An adenoviral shRNA targeting IL-1ß was constructed and injected at the T12 section 7 days before SCI. The rats' motor functions were evaluated by the Basso-Beattie-Bresnahan (BBB) rating scale. Immunofluorescence, enzyme-linked immunosorbent assay, flow-cytometric analysis and western blots were also performed. RESULTS: Animals downregulating IL-1ß had significantly better recovery of locomotor function and less neuronal loss after SCI. In addition, IL-1ß downregulation significantly decreased tumor necrosis factor-alpha (TNF-α) level and Bax expression, reduced the activity of caspase-3 and increased Bcl-2 expression after SCI. CONCLUSION: This study demonstrated that the IL-1ß downregulation may have potential therapeutic benefits for both reducing secondary damages and improving the outcomes after traumatic SCI.

Early diagnostic and prognostic utility of high-sensitive troponin assays in acute myocardial infarction: a meta-analysis.

BACKGROUND/AIM: To determine the diagnostic and prognostic utility of high-sensitive troponin assays in the very early phase of acute myocardial infarction (AMI) (less than 3 h since symptoms onset) by performing a meta-analysis of prospective studies. METHODS: Relevant studies were identified by searches of MEDLINE and Elsevier Sciencedirect until 31 January 2014 and by reviewing the reference lists from retrieved articles. Prospective studies that reported diagnostic utility in AMI using both high-sensitive troponin assays and conventional cardiac troponin, and reported the estimates of hazard ratio (HR) with 95% confidence intervals (CI) for prognostic utility were included. Data were extracted independently by two authors and summary estimates of association were obtained using a random effects model. RESULTS: Of the seven studies included, four studies reported the diagnostic utility of high-sensitive troponin assays (2863 patients) and three reported the prognostic utility in AMI (2329 patients). Within 12 h of symptoms onset, the pooled sensitivity and specificity of high-sensitive troponin assays were 0.89 (95% CI 0.85-0.91) and 0.89 (95% CI 0.85-0.92), respectively, and within 3 h, the pooled sensitivity and specificity of high-sensitive troponin assays were 0.79 (95% CI 0.71-0.85) and 0.92 (95% CI 0.88-0.96) respectively. Compared with conventional cardiac troponin assays, the high-sensitive troponin assays had higher sensitivity (0.89 vs 0.72) but lower specificity (0.89 vs 0.95) in diagnosing AMI within 12 h of symptoms onset. Within 3 h, the sensitivity of high-sensitive troponin assays was still higher (0.79 vs 0.59), but the specificity was almost the same (0.92 vs 0.95) as that of conventional troponin assays. The elevated high-sensitive troponin assays had an overall pooled HR of 2.66 (95% CI 1.31-5.44) and 2.14 (95% CI 1.15-3.98) for the end-points of death and non-fatal AMI respectively. CONCLUSIONS: These findings provide quantitative data supporting high-sensitive troponin assays having early diagnostic and prognostic utility in AMI.

Treatment with UDP-glucose, GDNF, and memantine promotes SVZ and white matter self-repair by endogenous glial progenitor cells in neonatal rats with ischemic PVL.

Periventricular leukomalacia (PVL) is one of the foremost neurological conditions leading to long-term abnormalities in premature infants. Since it is difficult to prevent initiation of this damage in utero, promoting the innate regenerative potential of the brain after birth may provide a more feasible, prospective therapy for PVL. Treatment with UDP-glucose (UDPG), an endogenous agonist of G protein-coupled receptor 17 (GPR17) that may enhance endogenous self-repair potentiality, glial cell line-derived neurotrophic factor (GDNF), a neurotrophic factor associated with the growth and survival of nerve cells, and memantine, a noncompetitive antagonist of N-methyl-d-aspartate (NMDA) receptors that block ischemia-induced glutamate signal transduction, has been reported to achieve functional, neurological improvement in neonatal rats with PVL. The aim of the present study was to further explore whether UDPG, GDNF and/or memantine could promote corresponding self-repair of the subventricular zone (SVZ) and white matter (WM) in neonatal rats with ischemia-induced PVL. SVZ or WM tissue samples and cultured glial progenitor cells derived from a 5 day-old neonatal rat model of PVL were utilized for studying response to UDPG, GDNF and memantine in vivo and in vitro, respectively. Labeling with 5'-bromo-2'-deoxyuridine and immunofluorescent cell lineage markers after hypoxia-ischemia or oxygen-glucose deprivation (OGD) revealed that UDPG, GDNF and memantine each significantly increased glial progenitor cells and preoligodendrocytes (preOLs), as well as more differentiated immature and mature oligodendrocyte (OL), in both the SVZ and WM in vivo or in vitro. SVZ and WM glial cell apoptosis was also significantly reduced by UDPG, GDNF or memantine, both in vivo and in vitro. These results indicated that UDPG, GDNF or memantine may promote endogenous self-repair by stimulating proliferation of glial progenitor cells derived from both the SVZ and WM, activating their differentiation into more mature OLs, and raising the survival rate of these newly generated glial cells in neonatal rats with ischemic PVL.

Effects of metoprolol and small intestine RNA on marrow-derived endothelial progenitor cells applied for autograft transplantation in heart disease.

AIMS: The objective of this project was to improve the effect of EPC autograft transplantation and observe the tolerance of EPCs to I/R injury affected by metoprolol and small intestine RNA. MATERIALS AND METHODS: We isolated bone marrow-derived EPCs and examined the effects of metoprolol and small intestine RNA on EPCs to ischemia at different time points after reperfusion. EPCs growth curve, secretion, apoptosis and mortality were also analyzed. RESULTS: EPCs will be better protected if the blood can be recovered within 4 hours after ischemia for cardiac muscle cells and pretreatment of EPCs with metoprolol or small intestine RNA could protect and promote EPCs proliferation. CONCLUSIONS: Our study demonstated that pretreatment of EPCs with metoprolol or small intestine RNA will increase the EPCs proliferation and may improve the EPCs autograft transplantation ability.

Biochemical parameters of Saccharopolyspora erythraea during feeding ammonium sulphate in erythromycin biosynthesis phase.

The physiology of feeding ammonium sulphate in erythromycin biosynthesis phase of Saccharopolyspora erythraea on the regulation of erythromycin A (Er-A) biosynthesis was investigated in 50 L fermenter. At an optimal feeding ammonium sulphate rate of 0.03 g/L per h, the maximal Er-A production was 8281 U/mL at 174 h of growth, which was increased by 26.3% in comparison with the control (6557 U/mL at 173 h). Changes in cell metabolic response of actinomycete were observed, i.e. there was a drastic increase in the level of carbon dioxide evolution rate and oxygen consumption. Assays of the key enzyme activities and organic acids of S. erythraea and amino acids in culture broth revealed that cell metabolism was enhanced by ammonium assimilation, which might depend on the glutamate transamination pathway. The enhancement of cell metabolism induced an increase of the pool of TCA cycle and the metabolic flux of erythromycin biosynthesis. In general, ammonium assimilation in the erythromycin biosynthesis phase of S. erythraea exerted a significant impact on the carbon metabolism and formation of precursors of the process for dramatic regulation of secondary metabolites biosynthesis.

Regulation of mesenchymal stem cell chondrogenesis by glucose through protein kinase C/transforming growth factor signaling.

OBJECTIVE: Effective induction of human mesenchymal stem cell (hMSC) differentiation for regenerative medicine applications remains a great challenge. While much research has studied hMSC activity during differentiation, it is unclear whether pre-differentiation culture can modulate differentiation capacity. We investigate the effect of glucose concentration in pre-differentiation/expansion culture on modulating chondrogenic capacity of hMSCs, and explore the underlying molecular mechanism. DESIGN: The extent of chondrogenesis of hMSCs previously cultured with different concentrations of glucose was evaluated. Transforming growth factor-beta (TGF-ß) signaling molecules and protein kinase C (PKC) were analyzed to identify the role of these molecules in the regulation of glucose on chondrogenesis. In addition, hMSCs in high-glucose expansion culture were treated with the PKC inhibitor to modulate the activity of PKC and TGF-ß signaling molecules. RESULTS: High-glucose maintained hMSCs were less chondrogenic than low-glucose maintained cells upon receiving differentiation signals. Interestingly, we found that high-glucose culture increased the phosphorylation of PKC and expression of type II TGF-ß receptor (TGFßRII) in pre-differentiation hMSCs. However, low-glucose maintained hMSCs became more responsive to chondrogenic induction with increased PKC activation and TGFßRII expression than high-glucose maintained hMSCs during differentiation. Inhibiting the PKC activity of high-glucose maintained hMSCs during expansion culture upregulated the TGFßRII expression of chondrogenic cell pellets, and enhanced chondrogenesis. CONCLUSION: Our findings demonstrate the effect of glucose concentration on regulating the chondrogenic capability of pre-differentiation hMSCs, and provide insight into the mechanism of how glucose concentration regulates PKC and TGF-ß signaling molecules to prime pre-differentiation hMSCs for subsequent chondrogenesis.

Reassessment of the systematics of the suborder Pseudonocardineae: transfer of the genera within the family Actinosynnemataceae Labeda and Kroppenstedt 2000 emend. Zhi et al. 2009 into an emended family Pseudonocardiaceae Embley et al. 1989 emend. Zhi et al. 2009.

The taxonomic status of the families Actinosynnemataceae and Pseudonocardiaceae was assessed based on 16S rRNA gene sequence data available for the 151 taxa with validly published names, as well as chemotaxonomic and morphological properties available from the literature. 16S rRNA gene sequences for the type strains of all taxa within the suborder Pseudonocardineae were subjected to phylogenetic analyses using different algorithms in arb and phylip. The description of many new genera and species within the suborder Pseudonocardineae since the family Actinosynnemataceae was proposed in 2000 has resulted in a markedly different distribution of chemotaxonomic markers within the suborder from that observed at that time. For instance, it is noted that species of the genera Actinokineospora and Allokutzneria contain arabinose in whole-cell hydrolysates, which is not observed in the other genera within the Actinosynnemataceae, and that there are many genera within the family Pseudonocardiaceae as currently described that do not contain arabinose. Phylogenetic analyses of 16S rRNA gene sequences for all taxa within the suborder do not provide any statistical support for the family Actinosynnemataceae, nor are signature nucleotides found that support its continued differentiation from the family Pseudonocardiaceae. The description of the family Pseudonocardiaceae is therefore emended to include the genera previously classified within the family Actinosynnemataceae and the description of the suborder Pseudonocardineae is also emended to reflect this reclassification.