/fiber Ratios (fiber + ratio)

Distribution by Scientific Domains


Selected Abstracts


Thermal properties of extruded/injection-molded poly(lactic acid) and biobased composites,,

JOURNAL OF APPLIED POLYMER SCIENCE, Issue 2 2008
Abdellatif A. Mohamed
Abstract To determine the degree of compatibility between poly(lactic acid) and different biomaterials (fibers), poly(lactic acid) was compounded with sugar beet pulp and apple fibers. The fibers were added in 85 : 15 and 70 : 30 poly(lactic acid)/fiber ratios. The composites were blended by extrusion followed by injection molding. Differential scanning calorimetry and thermogravimetric analysis were used to analyze the extruded and extruded/injection-molded composites. After melting in sealed differential scanning calorimetry pans, the composites were cooled through immersion in liquid nitrogen and aged (stored) at room temperature for 0, 7, 15, and 30 days. After storage, the samples were heated from 25 to 180°C at 10°C/min. The neat poly(lactic acid) showed a glass-transition transition at 59°C with a change in heat capacity (,Cp) value of 0.464. The glass transition was followed by crystallization and melting transitions. The enthalpic relaxation of the poly(lactic acid) and composites steadily increased as a function of the storage time. Although the presence of fibers had little effect on the enthalpic relaxation, injection molding reduced the enthalpic relaxation. The crystallinity percentage of the unprocessed neat poly(lactic acid) dropped by 95% after extrusion and by 80% for the extruded/injection-molded composites. The degradation was performed in air and nitrogen environments. The degradation activation energy of neat poly(lactic acid) exhibited a significant drop in the nitrogen environment, although it increased in air. This meant that the poly(lactic acid) was more resistant to degradation in the presence of oxygen. Overall, injection molding appeared to reduce the activation energy for all the composites. Sugar beet pulp significantly reduced the activation energy in a nitrogen environment. In an air environment, both sugar beet pulp and apple fibers increased the activation energy. The enzymatic degradation of the composites showed a higher degradation rate for the extruded samples versus the extruded/injection-molded composites, whereas the apple composites exhibited higher weight loss. The thermogravimetric analysis data showed that the degradation of unprocessed and extruded neat poly(lactic acid) followed a one-step mechanism, whereas extruded/injection-molded composites showed two-step degradation. A higher fiber content resulted in up to three-step degradation mechanisms. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci 2008 [source]


G-CSF-mobilized peripheral blood mononuclear cells from diabetic patients augment neovascularization in ischemic limbs but with impaired capability

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2006
B. ZHOU
Summary.,Background: Autologous transplantation of mobilized peripheral blood mononuclear cells (M-PBMNCs) is a novel approach to improve critical limb ischemia (CLI) in diabetes. However, endothelial progenitor cells (EPCs) from diabetes are dysfunctional and impaired in ischemia-induced neovascularization. Objective: This study aimed to confirm the compromised efficiency of diabetic M-PBMNCs in therapeutic neovascularization, and to determine the underlying mechanisms of this impairment. Methods: Diabetic M-PBMNCs from 17 diabetic patients or healthy controls, or phosphate-buffered saline (PBS) were injected into the ischemic limbs of streptozotocin-induced diabetic nude mice. The limb blood perfusion, ambulatory score, ischemia damage, capillary/fiber ratio, arteriole density, collateral vessel formation, and pericytes recruitment were evaluated between these three groups. Non-invasive real time image and histopathology were used to detect the in vivo role of transplanted M-PBMNCs. Proliferation and adhesion of EPCs were assayed. In vitro vascular network incorporation and matrigel plug assay were used to test the pro-neovascularization role of M-PBMNCs. Results: Transplantation of diabetic M-PBMNCs also improved neovascularization, but to a lesser extent from that observed with non-diabetic ones. This was associated with the impairment of diabetic M-PBMNCs capacity to differentiate into EPCs, to incorporate into vessel-like tubules in vitro, to participate in vascular-like structure formation in a subcutaneous matrigel plug, and to stimulate the recruitment of pericytes/smooth muscle cells. In addition, there was impairment in vasculogenesis, which was related to the reduced adhesion ability of EPCs from diabetic M-PBMNCs. Conclusions: Diabetes reduced the capacity of M-PBMNCs to augment neovascularization in ischemia. [source]


Clenbuterol increases muscle fiber size and GATA-2 protein in rat skeletal muscle in utero

MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 5 2008
Diane Downie
Abstract Certain ,2 -adrenoceptor agonists, such as clenbuterol, are known to elicit a muscle-specific anabolism or hypertrophy in both normal and catabolic muscle in a wide variety of species. However, the underlying mechanism(s) of the ,2 -agonist-induced anabolism remains unclear. This study aimed to determine the effects of clenbuterol administration in utero on skeletal muscle and to examine the underlying molecular mechanisms. Pregnant rats were fed clenbuterol (2 mg/kg diet) from Day 4 of gestation (4 dg) until weanling and fetal samples were taken from 13.5, 15.5, 17.5, and 19.5 dg and from 1d neonatal pups. Muscles were analyzed for total DNA, RNA and protein and sections examined morphologically for changes in muscle development. Western and immunohistochemical analyses were performed to identify changes in known myogenic signaling proteins. Clenbuterol increased the size of both fast and slow fibers in utero which was associated with a decreased DNA:protein ratio (28%) and an increased RNA:DNA ratio (36%). Additionally, drug treatment in utero induced a decrease in the fast:slow fiber ratio (38%). These myogenic changes were correlated with an increase in the GATA-2 hypertrophic transcription factor at both 17.5 dg (by 250%) and 19.5 dg (by 40%) in fetuses from clenbuterol treated dams. In addition, drug treatment resulted in increased membrane association of PKC-µ at 17.5 dg (325%) and increased PKC-, cytosolic abundance (40%) and PKC-, membrane abundance at 19.5 dg (250%). These results are the first demonstration that ,2 -agonists such as clenbuterol may act through upregulating the GATA-2 transcription factor and implicate certain PKC isoforms in the drug-induced regulation of skeletal muscle development. Mol. Reprod. Dev. 75: 785,794, 2008. © 2007 Wiley-Liss, Inc. [source]


ORIGINAL RESEARCH,BASIC SCIENCE: Cavernous Neurotomy in the Rat is Associated with the Onset of an Overt Condition of Hypogonadism

THE JOURNAL OF SEXUAL MEDICINE, Issue 5 2009
Linda Vignozzi MD
ABSTRACT Background., Most men following radical retropubic prostatectomy (RRP) are afflicted by erectile dysfunction (ED). RRP-related ED occurs as a result of surgically elicited neuropraxia, leading to histological changes in the penis, including collagenization of smooth muscle and endothelial damage. Aim., To verify whether hypogonadism could contribute to the pathogenesis of RRP-ED. Methods., Effects of testosterone (T), alone or in association with long-term tadalafil (Tad) treatment in a rat model of bilateral cavernous neurotomy (BCN). Main Outcome Measures., Penile tissues from rats were harvested for vasoreactivity studies 3 months post-BCN. Penile oxygenation was evaluated by hypoxyprobe immunostaining. Phosphodiesterase type 5 (PDE5), endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) mRNA expression were quantified by Real Time quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results., In BCN rats, we observed the onset of an overt condition of hypogonadism, characterized by reduced T plasma level, reduced ventral prostate weight, reduced testis function (including testis weight and number of Leydig cells), with an inadequate compensatory increase of luteinizing hormone. BCN induced massive penile hypoxia, decreased muscle/fiber ratio, nNOS, eNOS, PDE5 expression, increased sensitivity to the nitric oxide donor, sodium nitroprusside (SNP), and reduced the relaxant response to acetylcholine (Ach), as well as unresponsiveness to acute Tad dosing. In BCN rats, chronic Tad-administration normalizes penile oxygenation, smooth muscle loss, PDE5 expression, SNP sensitivity, and the responsiveness to the acute Tad administration. Chronic Tad treatment was ineffective in counteracting the reduction of nNOS and eNOS expression, along with Ach responsiveness. T supplementation, in combination with Tad, reverted some of the aforementioned alterations, restoring smooth muscle content, eNOS expression, as well as the relaxant response of penile strips to Ach, but not nNOS expression. Conclusion., BCN was associated with hypogonadism, probably of central origin. T supplementation in hypogonadal BCN rats ameliorates some aspects of BCN-induced ED, including collagenization of penile smooth muscle and endothelial dysfunction, except surgically induced altered nNOS expression.Vignozzi L, Filippi S, Morelli A, Marini M, Chavalmane A, Fibbi B, Silvestrini E, Mancina R, Carini M, Vannelli GB, Forti G, and Maggi M. Cavernous neurotomy in the rat is associated with the onset of an overt condition of hypogonadism. J Sex Med 2009;6:1270,1283. [source]