Modeling time to inactivation of Listeria monocytogenes in response to high pressure, sodium chloride, and sodium lactate

A mathematical model was developed to predict time to inactivation (TTI) by high pressure processing of Listeria monocytogenes in a broth system (pH 6.3) as a function of pressure (450 to 700 MPa), inoculum level (2 to 6 log CFU/ml), sodium chloride (1 or 2%), and sodium lactate (0 or 2.5%) from a 4°C initial temperature. Ten L. monocytogenes isolates from various sources, including processed meats, were evaluated for pressure resistance. The five most resistant strains were used as a cocktail to determine TTI and for model validation. Complete inactivation of L. monocytogenes in all treatments was demonstrated with an enrichment method. The TTI increased with increasing inoculum level and decreasing pressure magnitude, from 1.5 min at 700 MPa and 2 log CFU/ml, to 15 min at 450 MPa and 6 log CFU/ml. Neither NaCl nor sodium lactate significantly influenced TTI. The model was validated with ready-to-eat, uncured, Australian retail poultry products, and with product specially made at a U.S. Department of Agriculture, Food Safety and Inspection Service (FSIS)-inspected pilot plant in the United States. Data from the 210 individual product samples used for validation indicate that the model gives "fail-safe" predictions (58% with response as expected, 39% with no survivors where survivors expected, and only 3% with survivors where none were expected). This model can help manufacturers of refrigerated ready-to-eat meats establish effective processing criteria for the use of high pressure processing as a postlethality treatment for L. monocytogenes in accordance with FSIS regulations.     

Lipoxygenase activity in wholemeal flours from Triticum monococcum, Triticum turgidum and Triticum aestivum

To minimise lipid oxidation and maintain high carotenoid and tocol concentrations in wheat flours and products, fifty-seven accessions, belonging to different Triticum species (Triticum monococcum, Triticum turgidum and Triticum aestivum), were assessed for lipoxygenase activity. The highest enzymatic activity was observed in T. aestivum (8.02 ± 0.492 μmol/min/g DM), followed by T. turgidum (3.48 ± 0.701) and by T. monococcum (0.45 ± 0.072). While the lipoxygenase was consistently high amongst T. aestivum and steadily low amongst T. monococcum samples, the T. turgidum accessions clustered in three different groups, with low (0.12-0.91 μmol/min/g DM), medium (3.10-4.17) and high (5.57-9.51) activity. Enzymatic activity was maximum in the pH range 5-6. LOX activity was higher in the germ (206 μmol/min/g DM), than in the bran (13.4) or in the endosperm (3.1).The results demonstrate that the selection of genotypes with low LOX, a factor limiting oxidative degradation, is feasible.     

Representative literature on the phytonutrients category: Phenolic acids

Research concerning the benefits derived from dietary polyphenols, a significant class within the family of phytonutrients, has increased considerably in the last decade. Prior to the late 1990s, the nutritional spotlight focused on the antioxidant capabilities of carotenoids, vitamins, and minerals. More recently, however, research has emerged in strong support of the antioxidant capacity of polyphenols and their role in the prevention and/or treatment of certain cancers, diabetes, cardiovascular diseases, and inflammation. Polyphenols are categorized according to the nature of their carbon skeleton, ranging from basic phenolic molecules to highly complex compounds, such as flavonoids, the most common and widely studied of all phenolic compounds. The most prevalent phenolic acids include ellagic acid, gallic acid, tannic acid, and capsaicin.     

Sleep problems in individuals with spinal cord injury: Frequency and age effects.

Objectives: The two objectives of this study were (a) to replicate the previous finding of more severe sleep difficulties in a sample of individuals with spinal cord injury (SCI) compared with normative samples, and (b) to examine the associations between aging variables (specifically, chronological age, duration of SCI, age at SCI onset) and the severity of sleep difficulties. Design: Cross-sectional survey. Research Method: A survey was administered to 620 individuals with SCI that included measures of demographic characteristics and sleep difficulties. Results: The findings indicated that sleep problems are more common in individuals with SCI than in normative samples. In addition, younger participants in our sample reported more sleep problems than did older participants. Duration of SCI and age at onset, however, were not significantly associated with sleep difficulties. Conclusion: The analyses used in this study provide a model for examining age effects using concurrent survey data that may be useful for other investigators interested in studying the associations between age-related variables and important health-related domains. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Pathophysiological Link between Insulin Resistance and Adrenal Incidentalomas

Adrenal incidentalomas are incidentally discovered adrenal masses greater than one centimeter in diameter. An association between insulin resistance and adrenal incidentalomas has been established. However, the pathophysiological link between these two conditions remains incompletely characterized. This review examines the literature on the interrelationship between insulin resistance and adrenal masses, their subtypes, and related pathophysiology. Some studies show that functional and non-functional adrenal masses elicit systemic insulin resistance, whereas others conclude the inverse. Insulin resistance, hyperinsulinemia, and the anabolic effects on adrenal gland tissue, which have insulin and insulin-like growth factor-1 receptors, offer possible pathophysiological links. Conversely, autonomous adrenal cortisol secretion generates visceral fat accumulation and insulin resistance. Further investigation into the mechanisms and timing of these two pathologies as they relate to one another is needed and could be valuable in the prevention, detection, and treatment of both conditions.     

A Novel Loss-of-Function SEMA3E Mutation in a Patient with Severe Intellectual Disability and Cognitive Regression

Intellectual disability (ID) is a neurological disorder arising from early neurodevelopmental defects. The underlying genetic and molecular mechanisms are complex, but are thought to involve, among others, alterations in genes implicated in axon guidance and/or neural circuit formation as demonstrated by studies on mouse models. Here, by combining exome sequencing with in silico analyses, we identified a patient affected by severe ID and cognitive regression, carrying a novel loss-of-function variant in the semaphorin 3E (SEMA3E) gene, which encodes for a key secreted cue that controls mouse brain development. By performing ad hoc in vitro and ex vivo experiments, we found that the identified variant impairs protein secretion and hampers the binding to both embryonic mouse neuronal cells and tissues. Further, we revealed SEMA3E expression during human brain development. Overall, our findings demonstrate the pathogenic impact of the identified SEMA3E variant and provide evidence that clinical neurological features of the patient might be due to a defective SEMA3E signaling in the brain.     

Bacteria-Derived Protein Aggregates Contribute to the Disruption of Host Proteostasis

Neurodegenerative protein conformational diseases are characterized by the misfolding and aggregation of metastable proteins encoded within the host genome. The host is also home to thousands of proteins encoded within exogenous genomes harbored by bacteria, fungi, and viruses. Yet, their contributions to host protein-folding homeostasis, or proteostasis, remain elusive. Recent studies, including our previous work, suggest that bacterial products contribute to the toxic aggregation of endogenous host proteins. We refer to these products as bacteria-derived protein aggregates (BDPAs). Furthermore, antibiotics were recently associated with an increased risk for neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis—possibly by virtue of altering the composition of the human gut microbiota. Other studies have shown a negative correlation between disease progression and antibiotic administration, supporting their protective effect against neurodegenerative diseases. These contradicting studies emphasize the complexity of the human gut microbiota, the gut–brain axis, and the effect of antibiotics. Here, we further our understanding of bacteria’s effect on host protein folding using the model Caenorhabditis elegans. We employed genetic and chemical methods to demonstrate that the proteotoxic effect of bacteria on host protein folding correlates with the presence of BDPAs. Furthermore, the abundance and proteotoxicity of BDPAs are influenced by gentamicin, an aminoglycoside antibiotic that induces protein misfolding, and by butyrate, a short-chain fatty acid that we previously found to affect host protein aggregation and the associated toxicity. Collectively, these results increase our understanding of host–bacteria interactions in the context of protein conformational diseases.     

Targeted and Non-Targeted Mechanisms for Killing Hypoxic Tumour Cells—Are There New Avenues for Treatment?

Purpose: A major issue in radiotherapy is the relative resistance of hypoxic cells to radiation. Historic approaches to this problem include the use of oxygen mimetic compounds to sensitize tumour cells, which were unsuccessful. This review looks at modern approaches aimed at increasing the efficacy of targeting and radiosensitizing hypoxic tumour microenvironments relative to normal tissues and asks the question of whether non-targeted effects in radiobiology may provide a new “target”. Novel techniques involve the integration of recent technological advancements such as nanotechnology, cell manipulation, and medical imaging. Particularly, the major areas of research discussed in this review include tumour hypoxia imaging through PET imaging to guide carbogen breathing, gold nanoparticles, macrophage-mediated drug delivery systems used for hypoxia-activate prodrugs, and autophagy inhibitors. Furthermore, this review outlines several features of these methods, including the mechanisms of action to induce radiosensitization, the increased accuracy in targeting hypoxic tumour microenvironments relative to normal tissue, preclinical/clinical trials, and future considerations. Conclusions: This review suggests that the four novel tumour hypoxia therapeutics demonstrate compelling evidence that these techniques can serve as powerful tools to increase targeting efficacy and radiosensitizing hypoxic tumour microenvironments relative to normal tissue. Each technique uses a different way to manipulate the therapeutic ratio, which we have labelled “oxygenate, target, use, and digest”. In addition, by focusing on emerging non-targeted and out-of-field effects, new umbrella targets are identified, which instead of sensitizing hypoxic cells, seek to reduce the radiosensitivity of normal tissues.     

Interaction of silver nanoparticles with an environmentally beneficial bacterium, Pseudomonas chlororaphis

This study explores the potential antimicrobial mechanisms of commercial silver nanoparticles (Ag NPs) in the environmental bacterium, Pseudomonas chlororaphis O6. The 10nm size NPs aggregated in water, as demonstrated by atomic force microscopy. Solubility of the NPs at 10mg/L was 0.28 mg/L (pH 6) and 2.3mg/L (pH 7); release from 10mg/L bulk Ag was below detection. The NPs eliminated cell culturability at 3mg/L, whereas no effect was observed at 10mg/L bulk Ag. Zeta potential measurements revealed that the NPs were negatively charged; unlike Ag ions, their addition to the negatively charged cells did not change cell charge at pH 6, but showed a trend to reduce cell charge at pH 7. Isolated extracellular polymeric substances (EPS) from PcO6 was polydisperse, with negative charge that was neutralized by Ag ions, but not by the NPs. Addition of EPS eliminated Ag NP's toxicity in cells lacking EPS. Intracellular accumulation of OH was not detected in NP-treated cells; however, the use of scavengers suggested the NPs caused extracellular H(2)O(2) production. No evidence was found for loss of membrane integrity upon treatment with the NPs. Our findings indicate that growth of environmental bacteria could be impaired by Ag NPs, depending on the extent of EPS production.