Effect of Kraft Pulping on Oxygen Delignification

The objective of the study reported here was to investigate experimentally the effect of the major Kraft pulping variables on the response of brownstock pulps to medium consistency oxygen delignification. Kraft pulping was performed on mixed Northeastern hardwood chips in a laboratory rocking digester. Kraft pulps of kappa number 16 and 20 mL KMnO4 were produced by pulping under a variety of conditions. The effective alkali (EA) charged to the digester was varied over the range of 12 to 21% while the sodium sulfide content of the pulping liquor was varied between 0 to 30% sulfidity. Cooking temperatures of 160 to 180°C were investigated by varying the time at temperature as measured by the Hfactor. Anthraquinone was used as a pulping catalyst at levels between 0 to 4%. Conditions of low EA charge, low temperature, high sulfidity and high levels of anthraquinone led to pulps with high pulp yield. When the effective alkali charge in the digester was low, cooking at low temperature gave rise to pulps with high viscosity and improved selectivity in the Krafi pulping process. The response variables following oxygen delignification were found to depend upon the cooking conditions applied in the digester. The kappa number versus time data could be fit to a classical power law model, indicative of lignin fiagmentation occurring by an infinite number of parallel first order reactions (Schoon, 1982). There was a systematic increase in the oxygen delignification rate, as measured by a reduction in the kappa number and an increase in the Schoon rate constant, with decreasing brownstock pulp yield in the digester. The pulp selectivity, when measured as the change in pulp viscosity with changes in kappa number, increased with increasing pulp yield until a maximum was reached. Chemical analysis of the carbohydrates in the pulps indicated that the loss in pulp yield in the digester was caused primarily by a reduction in the hemicellulose polymers as additional effective alkali was added or by cooking at higher temperature in the digester. The loss in pulp yield could be roughly correlated to the COD content of the residual spent liquor

Molecular Level Comparison of Water Extractives of Maple and Oak with Negative and Positive Ion ESI FT-ICR Mass Spectrometry

Soluble extractives in wood function to protect living trees from destructive agents and also contribute to wood color and fragrance. Some extractive components have biological activities with medical applications. They also play important roles in wood processing and related applications. To increase the knowledge of wood chemistry, maple and oak were extracted by water. Ultraviolet/visible (UV/vis) spectroscopy indicated the presence of a phenolic compound, resorcinol, in maple extractives having higher molecular mass and more aromatic components than oak extractives. Negative and positive electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry (ESI FT-ICR-MS) identified thousands of formulas in the two samples in the m/z range of 200 to 800. They mainly fall into the lignin-like, carbohydrate-like, and tannin-like compound categories. The top 25 peaks (ie, formulas) with the highest relative magnitude in negative ESI represented nearly 50% of the summed total spectral magnitude of all formulas assigned in the maple and oak extractives. Furthermore, the base peak (ie, most abundant peak) accounted for about 14% of the total abundance in each wood sample. Literature comparisons identified 17 of 20 formulas in the top five peaks of the four spectra as specific bioactive compounds in trees and other plants, implying the potential to explore utilization of maple and oak extractives for functional and medicinal applications. The various profiling of the top 25 peaks from the two samples also suggested the possible application of FT-ICR-MS for detecting chemical markers useful in profiling and identification of wood types and sources

Investigation on the Electrochemical Micromachining of Micro Through-Hole by Using Micro Helical Electrode

The instability of machining process caused by the difficulty of the electrolyte refresh in electrochemical micromachining (EMM) of micro through-hole has been an unsolved problem. Thus, this paper investigates the electrochemical micromachining of micro through-hole by using a micro helical electrode combining with the jetting electrolyte. With the help of high-speed rotation of micro helical electrode and its spiral shape, the internal electrolyte can be stirred while the external jetting electrolyte can flow into the hole along the spiral groove to refresh the electrolyte effectively, thereby, improving the machining stability of EMM. Firstly, the influence of the process parameters on the fabrication of micro through-hole in the EMM by using micro helical electrode without non-conductive mask is investigated. Based on the optimization of the process parameters, a micro through-hole with an inlet dimension of 121.6 μm and an outlet dimension of 114.9 μm is obtained successfully. Furthermore, this paper also tries to use the micro helical electrode coated with the non-conductive mask to decrease the bad influence of the stray corrosion attack. It is found that the non-conductive mask coated on the surface of micro helical electrode can improve the machining accuracy significantly under the condition of low pulse frequency (≤1 KHz). However, its good effect on preventing the stray corrosion decreases along with the increase of the pulse frequency

ISL1 overexpression enhances the survival of transplanted human mesenchymal stem cells in a murine myocardial infarction model

Abstract Background The LIM-homeobox transcription factor islet-1 (ISL1) has been proposed as a marker for cardiovascular progenitor cells. This study investigated whether forced expression of ISL1 in human mesenchymal stem cells (hMSCs) improves myocardial infarction (MI) treatment outcomes. Methods The lentiviral vector containing the human elongation factor 1α promoter, which drives the expression of ISL1 (EF1α-ISL1), was constructed using the Multisite Gateway System and used to transduce hMSCs. Flow cytometry, immunofluorescence, Western blotting, TUNEL assay, and RNA sequencing were performed to evaluate the function of ISL1-overexpressing hMSCs (ISL1-hMSCs). Results The in vivo results showed that transplantation of ISL1-hMSCs improved cardiac function in a rat model of MI. Left ventricle ejection fraction and fractional shortening were greater in post-MI hearts after 4 weeks of treatment with ISL1-hMSCs compared with control hMSCs or phosphate-buffered saline. We also found that ISL1 overexpression increased angiogenesis and decreased apoptosis and inflammation. The greater potential of ISL1-hMSCs may be attributable to an increased number of surviving cells after transplantation. Conditioned medium from ISL1-hMSCs decreased the apoptotic effect of H2O2 on the cardiomyocyte cell line H9c2. To clarify the molecular basis of this finding, we employed RNA sequencing to compare the apoptotic-related gene expression profiles of control hMSCs and ISL1-hMSCs. The results showed that insulin-like growth factor binding protein 3 (IGFBP3) was the only gene in ISL1-hMSCs with a RPKM value higher than 100 and that the difference fold-change between ISL1-hMSCs and control hMSCs was greater than 3, suggesting that IGFBP3 might play an important role in the anti-apoptosis effect of ISL1-hMSCs through paracrine effects. Furthermore, the expression of IGFBP3 in the conditioned medium from ISL1-hMSCs was almost fourfold greater than that in conditioned medium from control hMSCs. Moreover, the IGFBP3 neutralization antibody reversed the apoptotic effect of ISL1-hMSCs-CM. Conclusions These results suggest that overexpression of ISL1 in hMSCs promotes cell survival in a model of MI and enhances their paracrine function to protect cardiomyocytes, which may be mediated through IGFBP3. ISL1 overexpression in hMSCs may represent a novel strategy for enhancing the effectiveness of stem cell therapy after MI

Additional file 2: of ISL1 overexpression enhances the survival of transplanted human mesenchymal stem cells in a murine myocardial infarction model

Figure S1. Transplantation of ISL1-hMSCs improved cardiac function (LVEDV, LVESV and CO) in amyocardial infarction (MI) model. *p < 0.05 vs. sham; #p < 0.05 vs. MI + PBS; & p < 0.05 vs. MI + ISL1-hMSCs. Figure S2. ISL1 overexpression reduced TUNEL-positive cardiomyocytes in infarct hearts. Scale bar = 50 μm. Figure S3. ISL1 overexpression reduced CD3+ T lymphocytes in infarct hearts. Scale bar = 50 μm. Figure S4. ISL1 overexpression reduced the number of CD68+ T lymphocytes in infarct hearts. Scale bar = 50 μm. Figure S5. ISL1 overexpression reduced inflammation cytokines TNFα, IL-6, and IL-10. Scale bar = 50 μm. Figure S6. ISL1 overexpression downregulated the proliferation and proinflammatory cytokine production of CD3+ T cells in vitro. *p < 0.05 vs. control; #p < 0.05 vs. Ctrl-hMSCs. Figure S7. Representative images and quantification of Bax, Bcl-2, cleaved caspase 3, and full-length caspase 3 in ISL1-hMSCs and Ctrl-hMSCs with or without H2O2. *p < 0.05 vs. H2O2 + Ctrl-hMSCs. Figure S8. Top 10 GO functions of upregulated (a) and downregulated (b) genes in ISL1-MSCs. Figure S9. Heat map display of secreted proteins with RPKM values of more than 100 in ISL1-hMSCs and Ctrl-hMSCs. Figure S10. The IGFBP3 inhibition assay showed a reduction in active IGFBP3 in ISL1-hMSCs-CM. *p < 0.05 vs. control; #p < 0.05 vs. H2O2; &p < 0.05 vs. H2O2 + ISL1-hMSCs. Scale bar = 100 μm. Figure S11. The anti-apoptotic effect of IGFBP3 in ISL1-hMSCs-CM on the human cardiomyocyte cell line AC16 subjected to oxidative injury. Apoptosis rate = (TUNEL positive nuclei / DAPI + nuclei) × 100%. *p < 0.05 vs. control; #p < 0.05 vs. H2O2; &p < 0.05 vs. H2O2 + Ctrl-hMSCs; @p < 0.05 vs. H2O2 + ISL1-hMSCs. Scale bar = 100 μm. DAPI: 4′,6- diamidino-2-phenylindole. (PPT 15681 kb

Additional file 1: of ISL1 overexpression enhances the survival of transplanted human mesenchymal stem cells in a murine myocardial infarction model

Table S1. qPCR primer information. Table S2. Sequencing data statistical results. Table S3. Alignment data statistical results. Table S4. Apoptosis-related secreted factors induced by Ctrl-hMSCs and ISL1-hMSCs. (PPTX 81 kb