Search

In the present study, the hemicellulose from bamboo sawdust (BSD) was selectively removed in the form of xylose and acetic acid using the wet-torrefaction technique in presence of formic acid and NaCl as catalysts. The best torrefaction activity, with xylose yield 85% and complete removal of hemicellulose, was obtained with formic acid:BSD 1:1 and NaCl:BSD 3:1 w/w. The torrefied BSD (TBSD) was catalytically co-pyrolyzed with linear low-density polyethylene (LLDPE) over HZSM-5. The apparent activation energies (Em) of catalytic pyrolysis (CP) of TBSD, and LLDPE were 187 and 147 kJ mol−1, respectively, from Kissinger–Akahira–Sunose (KAS) model. Those of catalytic co-pyrolysis (CCP) of blends TBP3:1, TBP1:1 and TBP1:3 were 163, 135 and 133 kJ mol−1, respectively. The CCP of TBP1:3 and TBP1:1 showed synergism between TBSD and LLDPE in terms of Em and TBP1:3 (TBSD: LLDPE 1:3 w/w) showed the highest synergism with the least Em. The CCP mechanism of samples with a higher fraction of TBSD was more complex, as depicted from Criado's master plot.

In this study, the bamboo saw dust (BSD) was wet-torrefied (WT) to selectively remove hemicellulose in the form of pentoses (xylose + arabinose) with 85% yield and to produce hydrochar (with the high energy density of 24 MJ/kg, which is similar to that of lignite). Further, the pyrolysis and co-pyrolysis behavior of hydrochar, LLDPE, and their blends were analyzed by thermogravimetric analysis in the temperature range of 30–800°C and under argon atmosphere. The blend with one part hydrochar and three parts LLDPE (TBP1:3) showed the highest positive synergism during co-pyrolysis at a 40 °C min−1 heating rate. The average apparent activation energies (as calculated using isoconversional methods) of co-pyrolysis of blended samples (TBP3:1, TBP1:1, and TBP1:3) were found to be 232, 261, 247 kJ mol−1, respectively. The Criado's master plot showed the reaction mechanism of co-pyrolysis to be multistep. For example, the blend TBP1:3 followed the trend of two-dimensional Avrami-Erofeyev model (A2) at lower conversions, diffusion-reaction model (D2) at high conversions and end with a first-order reaction.

Angiogenesis is a key aspect of the dynamic changes occurring during the normal ovarian cycle. Hyperplasia and hypervascularity of the ovarian theca interna and stroma are also prominent features of the polycystic ovary syndrome (PCOS), a leading cause of infertility. Compelling evidence indicated that vascular endothelial growth factor (VEGF) is a key mediator of the cyclical corpus luteum angiogenesis. However, the nature of the factor(s) that mediate angiogenesis in PCOS is less clearly understood. Endocrine gland-derived (EG)-VEGF has been recently identified as an endothelial cell mitogen with selectivity for the endothelium of steroidogenic glands and is expressed in normal human ovaries. In the present study, we compared the expression of EG-VEGF and VEGF mRNA in a series of 13 human PCOS and 13 normal ovary specimens by in situ hybridization. EG-VEGF expression in normal ovaries is dynamic and generally complementary to VEGF expression in both follicles and corpora lutea. A particularly high expression of EG-VEGF was detected in the Leydig-like hilus cells found in the highly vascularized ovarian hilus. In PCOS ovaries, we found strong expression of EG-VEGF mRNA in theca interna and stroma in most of the specimens examined, thus spatially related to the new blood vessels. In contrast, VEGF mRNA expression was most consistently associated with the granulosa cell layer and sometimes the theca, but rarely with the stroma. These findings indicate that both EG-VEGF and VEGF are expressed in PCOS ovaries, but in different cell types at different stages of differentiation, thus suggesting complementary functions for the two factors in angiogenesis and possibly cyst formation.

Graft-versus-host disease (GVHD) complicating allogeneic bone marrow transplantation (BMT) is often attributed to mismatched minor histocompatibility antigens (mHags), which are poorly defined in humans. CD31 is a candidate human mHag relevant to acute GVHD, but reports disagree about its level of significance, the role of HLA restriction, and the relative importance of different polymorphic codons within the molecule. We therefore examined in greater detail the impact of CD31-matching on BMT outcome in a prospective study from a single institution. Samples of recipient and donor DNA were collected pretransplantation for all patients receiving unmanipulated bone marrow from an HLA-identical sibling over a 45-month period at our institution. CD31 DNA typing of alleles at the 3 polymorphic codons 125 (L or V), 563 (N or S), and 670 (R or G) was performed for 118 patient-donor pairs plus 2 additional pairs who had codon 125 typing only. Donor-recipient CD31 nonidentity was tested for correlation with BMT clinical outcome measures of severe acute GVHD, chronic GVHD, relapse, and survival. Gene frequencies of approximately 0.5 for each allele at all 3 codons were comparable to previous reports. Because complete association was seen for 563N with 670G and for 563S with 670R, nonidentity for those codons was analyzed as a single genetic marker designated codon 563/670. Donor-recipient CD31 nonidentity was a significant risk factor for overall survival, both at codon 563/670 (hazard ratio [hr] = 2.58, P = .005) and at codon 125 (hr = 1.07, P = .036). Similar results held for disease-free survival. Nonidentity at codon 563/670 was also a significant risk factor (odds ratio [OR] = 11.15, P = .011) for severe (grades III, IV) versus no (grade 0) acute GVHD. Nonidentity at codon 125 posed less but still significant risk (OR = 9.30, P = .030). When the comparison group without severe acute GVHD was expanded to include grade I as well as grade 0 patients, the risk from CD31 nonidentity increased for both codon 563/670 (OR = 12.31, P = .010) and codon 125 (OR = 11.24, P = .011). CD31 nonidentity remained a significant independent risk factor for survival and for severe acute GVHD when tested in multivariate analysis with the covariates of adulthood, recipient-donor sex difference, ethnic group, disease, pretransplantation risk category, HLA-A2 type, B44-like types, and GVHD prophylactic regimen. CD31 nonidentity showed a trend but failed to achieve statistical significance as a risk factor for relapse and for chronic GVHD. In conclusion, donor-recipient CD31 nonidentity is a significant risk factor for survival and for severe acute GVHD in HLA-identical sibling BMT. The stronger associations with codon 563/670 suggest that polymorphism may be more important than the linked polymorphism at codon 125.Biol Blood Marrow Transplant 2001;7(9):503-12.