Application of electron‐beam irradiation pasteurization of ground beef,from steers fed vitamin E fortified diets: microbial and chemical effects

The effects of vitamin E supplementation of diets and electron‐beam irradiation (EBI) processing of ground beef patties on microbial and chemical qualities were investigated during 21 days of storage at 4 °C. Oxidative damage to lipids induced by EBI in ground beef patties containing different fat contents was first determined at 3 day intervals throughout a 7 day storage period at 4 °C. Significantly (P ≤ 0.05) higher values for thiobarbituric acid reactive substances (TBARS) were detected in beef patties of higher fat content (ie at 17 and 30%), which was further enhanced by irradiation at 5 kGy. Since lipid oxidation proceeded to a greater extent in beef patties with higher fat levels, ground beef patties of 30% fat were prepared from steers fed basal (diet I) or basal + 500 IU (diet II) of the antioxidant (vitamin E) supplemented diets. Plasma vitamin E concentrations in cattle fed diets I and II were 1.58 ± 0.42 µg ml^?1 and 2.49 ± 0.40 µg ml^?1 respectively. Patties were processed with three doses (2, 5, or 10 kGy) of EBI and compared with non‐irradiated patties. Microbial indices monitored at 3 day intervals included total aerobic plate count, psychrotrophic counts, and total coliform and Escherichia coli counts. Bacterial growth in ground beef patties stored at 4 °C was significantly (P ≤ 0.05) reduced by EBI at 2 kGy dose. Complete inhibition of bacteria occurred at 5 kGy or higher (P ≤ 0.05) dosage of EBI over 21 days of storage at 4 °C. Quality indices monitored at 3 day intervals throughout a 21 day storage (4 °C) study involving 30% fat ground beef patties made from steers fed vitamin E supplemented diets I and II included TBARS and colour. Results indicated that irradiation at the highest dosages was associated with higher (P ≤ 0.05) TBARS values, which in turn corresponded to lower linoleic acid content. With all three levels of irradiation, Hunter a values of beef patties decreased (P ≤ 0.05) significantly. Lipid oxidation was significantly (P ≤ 0.05) retarded in stored beef patties derived from cattle fed vitamin E (diet II). Copyright © 2003 Society of Chemical Industry     

Planning and assessment system for light rail transit construction in Taiwan

Microsystem Technologies - The development of public transportation systems is emphasized worldwide. Energy conservation and carbon reduction are necessary and constitute a constraint for the...     

TGF‐β1 Conjugated to Gold Nanoparticles Results in Protein Conformational Changes and Attenuates the Biological Function

Gold nanoparticles (AuNPs) are widely used as carriers or therapeutic agents due to their great biocompatibility and unique physical properties. Transforming growth factor‐beta 1 (TGF‐β1), a member of the cysteine‐knot structural superfamily, plays a pivotal role in many diseases and is known as an immunosuppressive agent that attenuates immune response resulting in tumor growth. The results reported herein reflect strong interactions between TGF‐β1 and the surface of AuNPs when incubated with serum‐containing medium, and demonstrate a time‐ and dose‐dependent pattern. Compared with other serum proteins that can also bind to the AuNP surface, AuNP–TGFβ1 conjugate is a thermodynamically favored compound. Epithelial cells undergo epithelial–mesenchymal transition (EMT) upon treatment with TGF‐β1; however, treatment with AuNPs reverses this effect, as detected by cell morphology and expression levels of EMT markers. TGF‐β1 is found to bind to AuNPs through S–Au bonds by X‐ray photoelectron spectroscopy. Fourier transform infrared spectroscopy is employed to analyze the conformational changes of TGF‐β1 on the surface of AuNPs. The results indicate that TGF‐β1 undergoes significant conformational changes at both secondary and tertiary structural levels after conjugation to the AuNP surface, which results in the deactivation of TGF‐β1 protein. An in vivo experiment also shows that addition of AuNPs attenuates the growth of TGF‐β1‐secreting murine bladder tumor 2 cells in syngeneic C3H/HeN mice, but not in immunocompromised NOD‐SCID mice, and this is associated with an increase in the number of tumor‐infiltrating CD4⁺ and CD8⁺ T lymphocytes and a decrease in the number of intrasplenic Foxp3(+) lymphocytes. The findings demonstrate that AuNPs may be a promising agent for modulating tumor immunity through inhibiting immunosuppressive TGF‐β1 signaling.     

Upregulation of pleiotrophin gene expression in developing microvasculature, macrophages, and astrocytes after acute ischemic brain injury

Pleiotrophin (PTN) is a heparin-binding, 18 kDa secretory protein that functions to induce mitogenesis, angiogenesis, differentiation, and transformation in vitro. PTN gene (Ptn) expression is highly regulated during development and is highest at sites in which mitogenesis, angiogenesis, and differentiation are active. In striking contrast, with the exception of the neuron, the Ptn gene is only minimally expressed in adults. We now demonstrate that Ptn gene expression is strikingly upregulated within 3 d in OX42-positive macrophages, astrocytes, and endothelial cells in areas of developing neovasculature after focal cerebral ischemia in adult rat. Ptn gene expression remains upregulated in these same cells and sites 7 and 14 d after ischemic injury. However, expression of the Ptn gene is significantly decreased in cortical neurons 6 and 24 hr after injury and is undetectable in degenerating neurons at day 3. Neurons in contralateral cortex continue to express Ptn in levels equal to control, uninjured brain. It is suggested that PTN may have a vital role in neovascular formation in postischemic brain and that postischemic brain is an important model in which to analyze sequential gene expression in developing neovasculature. In contrast, Ptn gene expression in injured neurons destined not to recover is strikingly reduced, and potentially its absence may contribute to the failure of the neuron to survive.     

Nf1 regulates hematopoietic progenitor cell growth and ras signaling in response to multiple cytokines

Neurofibromin, the protein encoded by the NF1 tumor-suppressor gene, negatively regulates the output of p21(ras) (Ras) proteins by accelerating the hydrolysis of active Ras-guanosine triphosphate to inactive Ras-guanosine diphosphate. Children with neurofibromatosis type 1 (NF1) are predisposed to juvenile chronic myelogenous leukemia (JCML) and other malignant myeloid disorders, and heterozygous Nf1 knockout mice spontaneously develop a myeloid disorder that resembles JCML. Both human and murine leukemias show loss of the normal allele. JCML cells and Nf1-/- hematopoietic cells isolated from fetal livers selectively form abnormally high numbers of colonies derived from granulocyte-macrophage progenitors in cultures supplemented with low concentrations of granulocyte-macrophage colony stimulating factor (GM-CSF). Taken together, these data suggest that neurofibromin is required to downregulate Ras activation in myeloid cells exposed to GM-CSF. We have investigated the growth and proliferation of purified populations of hematopoietic progenitor cells isolated from Nf1 knockout mice in response to the cytokines interleukin (IL)-3 and stem cell factor (SCF), as well as to GM-CSF. We found abnormal proliferation of both immature and lineage-restricted progenitor populations, and we observed increased synergy between SCF and either IL-3 or GM-CSF in Nf1-/- progenitors. Nf1-/- fetal livers also showed an absolute increase in the numbers of immature progenitors. We further demonstrate constitutive activation of the Ras-Raf-MAP (mitogen-activated protein) kinase signaling pathway in primary c-kit+ Nf1-/- progenitors and hyperactivation of MAP kinase after growth factor stimulation. The results of these experiments in primary hematopoietic cells implicate Nf1 as playing a central role in regulating the proliferation and survival of primitive and lineage-restricted myeloid progenitors in response to multiple cytokines by modulating Ras output.     

Diagnosing and monitoring the clinical course of chronic obstructive pulmonary disease

COPD is an extremely common, chronic disorder characterized by a reduction in airflow after the administration of an inhaled bronchodilator as measured by the FEV1. The diagnosis is suspected in patients with a history of several decades of cigarette smoking who present with nonspecific respiratory symptoms. The diagnosis is established by simple forced expiratory spirometry. Baseline evaluation usually includes a chest radiograph and some assessment of functional capacity, either by history or with some form of exercise testing. In patients whose initial FEV1 is more severely reduced or who have significant dyspnea, an arterial blood gas is indicated at baseline. Dyspnea, hypoxemia, or hypercarbia that is out of proportion to the measured FEV1, at either presentation or follow-up, should prompt a thorough evaluation for complicating conditions. There are important roles in health care delivery and chronic disease management strategies for RCPs, primary care providers, and specialty trained pulmonary physicians. The need for repeated, extensive, or expensive testing will be largely driven by patients symptoms but disease monitoring with periodic assessments of dyspnea, functional capacity, and spirometry can be performed without great expense.