Temperature-time combination effects on aged beef volatile profiles and their relationship to sensory attributes.

Beef ageing (in vacuo) for tenderisation and flavour development may be accelerated by favourable temperature-time combinations (TTCs), however the effect of such manipulations on volatile organic compounds (VOCs) that are generated during cooking, is unknown. We compared VOCs from grilled beef longissimus lumborum muscle samples which had been subjected to different TTCs. The TTCs consisted of combinations of temperatures (~ 3, 5, or 7 °C) and ageing time periods (6, 8, 10 or 12 d); as well as control samples, which were held at 0-2 °C for a total of 14 d. Sensory quality attributes of these same samples were measured by untrained consumer panellists. Generally, it was found that TTCs had negligible effects on grilled beef VOCs and were comparable to controls. Furthermore, many VOCs were significantly related to flavour intensity, flavour liking and overall liking. These findings support the use of TTCs as a viable means to accelerate the rate of beef ageing without compromising quality.

The effect of different temperature-time combinations when ageing beef: Sensory quality traits and microbial loads.

The ageing of beef is essential to provide a tender product which is deemed acceptable by consumers, with beef processors routinely ageing beef for ~ 14 d at 0-2 °C. The rate of tenderisation is directly affected by temperature, and as such the possibility of decreasing the required ageing time by increasing storage temperature could provide an opportunity to decrease associated costs. To test this, 320 beef M. longissimus lumborum portions were subjected to one of 72temperature-time combinations (TTC) incorporating temperatures of 3, 5 or 7 °C and ageing times of 6, 8, 10 or 12 d, with some temperature changes occurring during ageing. Controls (n = 32) were held at ~ 1 °C for 14 d. The application of TTCs did not affect beef quality, however longer storage at higher temperatures resulted in higher microbial loadings. Therefore, it can be concluded that shorter, cooler TTCs could be implemented to decrease ageing time requirements and maintain beef safety.

Effects of canola proteins and hydrolysates on adipogenic differentiation of C3H10T/2 mesenchymal stem cells.

This study assessed the ability of canola protein isolate (CPI) and enzymatic hydrolysates (CPHs) to inhibit adipogenic differentiation of C3H10T1/2 murine mesenchymal stem cells in vitro. Cell viability was maintained at concentrations of 60 µg/ml of sample. Cells treated with Alcalase hydrolysate demonstrated a higher reduction in anti-adipogenic differentiation through quantitation by oil-red O staining. qPCR analysis showed that CPI and CPH-treated cells significantly inhibited PPARγ expression, a key transcription factor involved in adipocyte differentiation, as evident in an ∼ 60-80% fold reduction of PPARγ mRNA. Immunofluorescence staining for PPARγ protein also showed a reduced expression in some treated cells when compared to differentiated untreated cells. The 50% inhibition concentration (IC50) of CPI, CPHs and their membrane ultrafiltration fractions on pancreatic lipase (PL) activity ranged between 0.75 and 2.5 mg/ml, (p < 0.05) for the hydrolysed and unhydrolysed samples. These findings demonstrate that CPI and CPHs contain bioactive components which can modulate in vitro adipocyte differentiation.

Antioxidant properties of Australian canola meal protein hydrolysates.

Antioxidant activities of canola protein hydrolysates (CPHs) and peptide fractions prepared using five proteases and ultrafiltration membranes (1, 3, 5, and 10kDa) were investigated. CPHs had similar and adequate quantities of essential amino acids. The effective concentration that scavenged 50% (EC50) of the ABTS(+) was greatest for the <1kDa pancreatin fraction at 10.1µg/ml. CPHs and peptide fractions scavenged DPPH(+) with most of the EC50 values being <1.0mg/ml. Scavenging of superoxide radical was generally weak, except for the <1kDa pepsin peptide fraction that had a value of 51%. All CPHs inhibited linoleic acid oxidation with greater efficiency observed for pepsin hydrolysates. The oxygen radical absorbance capacity of Alcalase, chymotrypsin and pepsin hydrolysates was found to be better than that of glutathione (GSH) (p<0.05). These results show that CPHs have the potential to be used as bioactive ingredients in the formulation of functional foods against oxidative stress.

The hands of John Snow: clue to his untimely death?

The accomplishments of John Snow (1813-1858), physician-epidemiologist, inventor and anaesthetist to Queen Victoria, are well documented, but the causes of his untimely death at age 45 remain conjectural. Snow suffered a paralysing stroke while working on his magnum opus, On Chloroform and Other Anaesthetics, and died a few days later on 16 June 1858. Snow had a history of renal problems associated with tuberculosis. He also experimented on himself with ether, chloroform and other agents over several years, but whether this prolonged self-experimentation contributed to his early death is uncertain. A photograph of Snow taken in 1857 shows that the fingers of his right hand were swollen. Could this be a clue to the cause of his death? The "modern" view is that Snow's early tuberculosis and associated renal disease led to hypertension, chronic renal failure and stroke. The tuberculosis and renal involvement may have been worsened by vegetarianism and perhaps resulting vitamin D deficiency. However, the renal damage caused by tuberculosis is unlikely to have been progressive. Based on current evidence of renal toxicity associated with exposure to anaesthetic agents, it is perhaps more likely that extensive and prolonged self-experimentation with anaesthetics over a 9-year period led to Snow's renal failure, swollen fingers and early death from stroke.

Antimicrobial activity of cinnamon and clove oils under modified atmosphere conditions.

Mixtures of cinnamon and clove oils were tested for inhibitory activity against important spoilage microorganism of intermediate moisture foods. Four fungal species (Aspergillus flavus, Penicillium roqueforti, Mucor plumbeus and Eurotium sp.), four yeasts species (Debaryomyces hansenii, Pichia membranaefaciens, Zygosaccharomyces rouxii and Candida lipolytica), and two bacteria species (Staphylococcus aureus and Pediococcus halophilus) inoculated separately on agar plates were sealed in a barrier pouch and exposed to essential oil volatiles under a modified atmosphere of low O2 (<0.05-10%) and high CO2 (20% or 40%), with the balance being N2. A. flavus and Eurotium sp. proved to be the most resistant microorganisms. Cinnamon and clove oils added between 1000 and 4000 microL at a ratio of 1:1 were tested for minimum inhibitory volume (MIV) against molds and yeasts. The gas phase above 1000 microL of the oil mixture inhibited growth of C. lipolytica and P. membranaefaciens; 2000 microL inhibited growth of A. flavus, P. roqueforti, M. plumbeus, Eurotium sp., D. hansenii, and Z. rouxii, while inhibition of A. flavus required the addition of 4000 microL. Higher ratios of cinnamon oil/clove oil were more effective for inhibiting the growth of A. flavus.

Membrane cleaning in the dairy industry: a review.

Membrane separation processes have become part of the set of basic unit operations for dairy process design and product development. These processes are employed in a variety of separation and concentration duties, but in all cases, the membranes must be cleaned regularly to remove both organic and inorganic material deposited on the surface from the fluid stream being processed. Cleaning is a vital step in maintaining the permeability and selectivity of the membrane and is necessary to return the plant to its original capacity, to minimize risks of bacteriological contamination, and to produce acceptable products. Caustic-, acidic-, and enzyme-based cleaners may be used for membrane cleaning and are usually formulated with additives to best match the specific cleaning duty. Cleaning generates significant volumes of wastewater and reduces membrane life and plant productivity, so each regime must be optimized with respect to concentration, order and duration of cleaning steps, temperature, pressure, and flow rate. This article reviews the key mechanisms governing cleaning performance and suggests directions by which further optimization may be achieved.

Early asthma control and maintenance with eformoterol following reduction of inhaled corticosteroid dose.

BACKGROUND: Previous studies have indicated the benefits of adding long acting beta(2) agonists to inhaled corticosteroids in the maintenance treatment of moderate to severe asthma. The effects of adding eformoterol to corticosteroids on asthma control and exacerbations in patients with mild to moderate asthma were studied. METHODS: After a run in period of 7-14 days on existing medication, 663 symptomatic patients were randomised to receive budesonide Turbohaler 400 microg twice daily together with either eformoterol Turbohaler 9 micro g (delivered dose) or placebo twice daily. After 4 weeks patients whose asthma was well controlled (n=505) were re-randomised to receive budesonide 400 microg daily and either eformoterol 9 micro g or placebo twice daily for a further 6 months. RESULTS: Patients receiving eformoterol achieved asthma control 10 days sooner than those receiving budesonide alone, and improvements in lung function, symptoms, quality of life, and relief beta(2) agonist use were significantly greater with eformoterol. During the 6 month follow up the frequency of mild exacerbations was significantly lower in the eformoterol group than in those receiving budesonide alone (7.2 versus 10.5 per patient, 95% confidence interval for ratio 0.49 to 0.96, p=0.03). The time to first day of poorly controlled asthma was 97 days in the eformoterol group compared with 42 days in the placebo group (p=0.003). CONCLUSIONS: Adding eformoterol to a low or moderate dose of budesonide in mild asthma resulted in faster and more effective control than treatment with budesonide alone. Eformoterol allowed the corticosteroid dose to be reduced while also decreasing the rate of mild exacerbations compared with budesonide alone. These data suggest a therapeutic advantage of adding eformoterol to inhaled corticosteroids in patients with mild to moderate asthma.

Could bronchial asthma be an endogenous, pulmonary expression of retinoid intoxication?

Asthma has become a major public health problem, affecting about 17 million people in the United States, including 4.8 million children. A striking increase in asthma and other forms of atopy has occurred in children in the U.S. and other western countries during the past 30 years. Several studies have reported an inverse association between childhood infectious illness and the development of atopy, suggesting that certain forms of infection protect against and even inhibit asthma. This may involve a shift in the balance of CD4 T lymphocyte helper cells from a Th2 to a Th1-type cytokine profile. However, the underlying mechanisms remain uncertain. Based on a review of the literature, it is conjectured that in the absence of certain types of childhood infection, retinoids (vitamin A and its congeners) accumulate in the lung. Later, upon exposure to known triggers for asthma, retinoid metabolites may be produced in such high concentration that they produce an acute, localized form of retinoid intoxication, recognized as status asthmaticus.

Possible role of retinoids in hepatitis B virus-associated liver damage.

Liver damage following hepatitis B virus (HBV) infection may be due to the action of retinoids as modulators of viral replication. The reduced rate of survival of liver grafts in patients with HBV infection could also be due to the continued presence of the virus, stimulated by retinoids in the graft tissue. Subject to obtaining empirical support for this hypothesis, the use of retinoid-blocking agents could be explored to reduce the risk of liver damage in HBV infection and to enhance the survival of liver grafts. Continued use of such agents may need to be used in conjunction with anti-viral modalities such as HBV hyperimmune globulin and lamivudine to prevent recurrent liver damage and to increase the long-term viability of the graft.

SET-related cell division autoantigen-1 (CDA1) arrests cell growth.

We used an autoimmune serum from a patient with discoid lupus erythematosus to clone a cDNA of 2808 base pairs. Its open reading frame of 2079 base pairs encodes a predicted polypeptide of 693 amino acids named CDA1 (cell division autoantigen-1). CDA1 has a predicted molecular mass of 79,430 Daltons and a pI of 4.26. The size of the cDNA is consistent with its estimated mRNA size. CDA1 comprises an N-terminal proline-rich domain, a central basic domain, and a C-terminal bipartite acidic domain. It has four putative nuclear localization signals and potential sites for phosphorylation by cAMP and cGMP-dependent kinases, protein kinase C, thymidine kinase, casein kinase II, and cyclin-dependent kinases (CDKs). CDA1 is phosphorylated in HeLa cells and by cyclin D1/CDK4, cyclin A/CDK2, and cyclin B/CDK1 in vitro. Its basic and acidic domains contain regions homologous to almost the entire human leukemia-associated SET protein. The same basic region is also homologous to nucleosome assembly proteins, testis TSPY protein, and an uncharacterized brain protein. CDA1 is present in the nuclear fraction of HeLa cells and localizes to the nucleus and nucleolus in HeLa cells transfected with CDA1 or its N terminus containing all four nuclear localization signals. Its acidic C terminus localizes mainly to the cytoplasm. CDA1 levels are low in serum-starved cells, increasing dramatically with serum stimulation. Expression of the CDA1 transgene, but not its N terminus, arrests HeLa cell growth, colony numbers, cell density, and bromodeoxyuridine uptake in a dose-dependent manner. The ability of CDA1 to arrest cell growth is abolished by mutation of the two CDK consensus phosphorylation sites. We propose that CDA1 is a negative regulator of cell growth and that its activity is regulated by its expression level and phosphorylation.

Possible role of endogenous retinoid (Vitamin A) toxicity in the pathophysiology of primary biliary cirrhosis.

Primary biliary cirrhosis (PBC) is a chronic, cholestatic disease of unknown etiology commonly affecting women. It is characterized by progressive destruction of the small intrahepatic bile ducts and portal inflammation, leading to fibrosis and cirrhosis. The major signs and symptoms of PBC, which include pruritus, lethargy, the sicca syndrome, and osteoporosis, closely resemble the manifestations of hypervitaminosis A. Based on a review of the literature and other observations connecting PBC with retinoid metabolism (vitamin A and its derivatives), the hypothesis is proposed that exposure to excess endogenous retinoids contributes to the pathogenesis of PBC and may be to the cause of some of the signs and symptoms associated with the disease.

Stimulation-induced behavioral inhibition: a new model for understanding physical violence.

Physical violence is widely considered to result from action carried out with the intention of causing injury; that is, from aggression. However, the "hypothesis" of aggression is inapplicable in all but a few instances as well as inappropriate for many destructive, rage-associated responses directed at inanimate objects. This paper outlines a new perspective on physical violence, reinterpreting many behaviors hitherto labeled aggressive as stimulation-seeking behaviors (SSBs) above an arbitrary level of intensity. It is further proposed that: 1) physical violence is a by-product of SSB, driven in part by brain catecholaminergic (CA) systems, and the direct result of exchanges of energy that exceed the body's tolerance threshold; 2) allegedly discrete categories of motor-motivational behavior represent overlapping bands of intensity on a continuous spectrum of SSB; and 3) the sensory input derived from SSB is fed back into the central nervous system where it activates brain serotonergic and/or cholinergic systems, which in turn inhibit CA systems, resulting in a general state of behavioral quiescence. In addition to accounting for a number of previously unexplained observations, the model suggests that physical violence could be prevented by providing groups at high risk with extensive opportunities for therapeutic sensory stimulation to substitute for that derived from excessive SSB. For people at especially high risk, portable devices could be developed that would allow the user to self-administer desired levels of sensory stimulation at moments of intense anger, thereby preventing potentially dangerous outbursts of SSB prior to the onset of the behavior.

Sensation-seeking, criminality, and spinal cord injury: a case-control study.

A retrospective case-control study was performed in New Orleans, Louisiana, in 1985-1986 to test the hypotheses that 1) criminality is a risk factor for severe injury, and 2) the association between criminality and injury can be explained in terms of a common underlying factor--increased sensation-seeking tendencies. A total of 140 males with spinal cord injury were individually matched with 140 driver's license holders on age, race, sex, educational attainment, and zip code of residence and were interviewed by telephone. Criminality prior to spinal cord injury was measured by self-report and police records, and sensation seeking was measured by the Disinhibition and Boredom Susceptibility subscales of Zuckerman's Sensation-Seeking Scale (Form V). Those with spinal cord injuries were significantly more likely than controls to report a history of juvenile delinquency, adult criminality, and incarceration prior to the time of spinal cord injury. Statistically significant but modest difference were also found between cases and controls with respect to Disinhibition, Boredom Susceptibility, and the combined Sensation-Seeking Scale score. Matched-pairs logistic regression analysis indicated that the association between sensation seeking and spinal cord injury remained significant after controlling for criminality, with an estimated relative risk of 2.05 (95% confidence interval 1.67-2.53). However, the association between criminality and spinal cord injury also remained significant after controlling for sensation seeking (estimated relative risk = 2.04, 95% confidence interval 1.09-3.82). On the basis of these results, criminality and sensation seeking may be statistically significant but independent predictors of spinal cord injury.

The place of hysterectomy in the management of benign uterine disease.

The wide variation in hysterectomy rates may reflect professional uncertainty as to the appropriateness of the procedure for managing benign uterine disease. This is thought to be due to diagnostic difficulties and especially to a lack of outcomes data. Many patients experience symptomatic relief after hysterectomy, but the long-term costs and benefits remain uncertain. Alternative treatments are available that spare the uterus and/or ovaries and appear to be as effective as hysterectomy. Vaginal hysterectomy is also associated with significantly reduced hospitalization and convalescent time and a lower rate of post-operative complications compared to abdominal hysterectomy, yet most hysterectomies continue to be performed abdominally. Based on the review, a number of steps are proposed for dealing with the problem of excess hysterectomy rates within a managed care setting.

Crossflow microfiltration of cell suspensions.

The application of crossflow microfiltration (CFMF) to processing cell suspensions was proposed in the 1970s. The intervening years have seen the scaling up of the technology to commercial operation and have been a period of intense research interest in the physics of the process. Flaschel et al. (1983) noted that the recovery of biomass (by ultrafiltration) appeared still to be in the phase of development. Later reviews particularly commented on the proprietary nature of much of the useful information required to assess the feasibility of CFMF (Hanisch, 1986; Brown & Kavanagh, 1987), but while the need for further publication of some information is still being stressed (e.g. Heath and Belfort, 1992), detailed reports from biotechnology companies of lab-, pilot- and full-scale applications are now appearing in the literature (Bailey et al., 1990, Sheehan et al, 1990; van Reis et al., 1991). The objective of this review is to describe the major factors influencing CFMF of cell suspensions with particular reference to the recent literature.

Sacral transcutaneous oxygen tension levels in the spinal cord injured: risk factors for pressure ulcers?

Evidence is mounting that susceptibility to pressure ulcers in the spinal cord injured is due to the interactive effects of prolonged immobilization and injury-related autonomic dysfunction associated with reduced tissue perfusion. To determine whether tissue oxygenation at the sacrum is reduced in spinal cord injury, we compared transcutaneous oxygen tension (PtcO2) levels in 21 subjects with spinal cord injury and 11 able-bodied controls lying prone and supine on egg-crate mattresses. Spinal cord injured subjects above and below the median supine PtcO2 value were also compared in terms of the presence or absence of pressure ulcers. The PtcO2 level of the spinal cord injured (mean +/- SD) was lower than that of the controls in the prone position (65.3 +/- 16mmHg vs 76.4 +/- 13mmHg; F = 3.9, df = 1, p = .053), and markedly lower in the supine position (49.1 +/- 26mmHg versus 74.2 +/- 10mmHg; F = 9.7, df = 1, p = .004). Examination of mean PtcO2 levels over time showed that those of the controls fell slightly following supination but returned to the previous level within 15 minutes. In contrast, those of the spinal cord injured fell rapidly by 18mmHg and stabilized after 15 minutes at a level 27mmHg below that of the controls. Five of the 10 (50%) spinal cord injured subjects with PtcO2 levels below the median supine PtcO2 level had a pressure ulcer compared to one among the 11 (9%) spinal cord injured subjects with PtcO2 levels above the median (p = .055, by Fisher's exact test). These results suggest the need for further studies on the role of reduced tissue oxygenation in the etiology of pressure ulcers.

Effect of high voltage pulsed galvanic stimulation on sacral transcutaneous oxygen tension levels in the spinal cord injured.

Evidence is mounting that spinal cord injured (SCI) persons may be at increased risk of pressure ulcers due to prolonged immobilization together with the injury-induced loss of sympathetic tone and decreased vascular resistance. With a view to developing a new method of preventing pressure ulcers, the objective of this study was to determine whether high voltage pulsed galvanic stimulation (HVPGS) could increase sacral transcutaneous oxygen tension (PtcO2) in SCI persons lying prone and supine. In experiment 1, HVPGS applied to the back at spinal level T6 led to a sustained, dose-related increase in sacral PtcO2 in 3 subjects lying prone. In experiment 2, carried out on 29 subjects lying supine on egg-crate mattresses, HVPGS (75 volts, 10 Hz) produced a 35% increase in sacral PtcO2, from a baseline level (Mean +/- SD) of 49 +/- 21 mmHg to 66 +/- 18 mmHg after 30 minutes of stimulation (F = 39.4, p < .00001). In experiment 3, simulated HVPGS was found to have no effect on sacral PtcO2 in 5 subjects lying supine. In experiment 4, HVPGS was repeated on 10 subjects and its effects found to be highly reproducible. It is hypothesized that HVPGS restores sympathetic tone and vascular resistance below the level of the spinal cord lesion, thereby increasing the perfusion pressure gradient in the capillary beds. Randomized controlled trials are now indicated to determine the efficacy of HVPGS for preventing pressure ulcers.