Water properties in cream cheeses with variations in pH, fat, and salt content and correlation to microbial survival

Water mobility and distribution in cream cheeses with variations in fat (4, 15, and 26%), added salt (0, 0.625, and 1.25%), and pH (4.2, 4.7, and 5.2) were studied using (1)H NMR relaxometry. The cheese samples were inoculated with a mixture of Listeria innocua, Escherichia coli O157 and Staphylococcus aureus, and partial least-squares regression revealed that (1)H T(2) relaxation decay data were able to explain a large part of the variation in the survival of E. coli O157 (64-83%). However, the predictions of L. innocua and S. aureus survival were strongly dependent on the fat/water content of the samples. Consequently, the present results indicate that NMR relaxometry is a promising technique for predicting the survival of these bacteria; however, the characteristics of the sample matrix are substantial.     

Comparative effects of cut and treated seed tubers vs untreated whole seed tubers on seed decay, Rhizoctonia stem canker, growth, and yield of Russet Burbank Potatoes

Whole seed tubers have been reported to have performance advantages over seed tubers that have been cut, even if the cut tuber pieces are treated with a fungicide dust. For this study, whole seed tubers were compared to cut seedpieces and to cut seedpieces treated with four different commercial fungicide dusts for five consecutive seasons. A new field generation 3 Russet Burbank seed lot was used for each of the five years of this study. Both whole tubers and cut seedpieces were inoculated withFusarium spp., and the seedpieces were then treated with a fungicide dust. Inoculated and uninoculated untreated controls were also included. Emergence,Fusarium seed decay,Rhizoctonia stem canker, stem numbers, and vigor, as well as yield and grade data were obtained.Rhizoctonia stem canker in stems grown from whole seed tubers was significantly higher than in stems from seedpieces receiving fungicide treatment in several of the study years. Predicting whole seed tuber performance is difficult because performance varies more from year to year than performance of cut and treated seedpieces. Yield performance of whole seed tubers was not significantly better than cut and fungicide-treated seedpieces in any experimental year, and yield of large (over 280 g) tubers was significantly less than that recorded for two of the treatments when data from all five years were combined. This study demonstrated that untreated whole seed did not outperform cut and treated seedpieces for vigor, stem numbers, disease ratings, or yield in small plot comparisons for five consecutive seasons.     

Favism-inducing toxins in broad beans (Vicia faba) biological activities of broad beans extracts in favism — Sensitive subjects

Ingestion of broad bean seeds will precipitate an acute haemolytic anaemia (favism) in certain sensitive subjects. Aqueous extracts from both fresh and dried mature broad bean seeds, obtained from a favism-endemic area in Iran, were incubated with blood from favism-sensitive and control subjects. Changes in the reduced glutathione content of red blood cells were determined as an index of toxicity. The results showed that:

1. The toxic principles in broad beans were at least partially water soluble.
2. The seed coats of dry mature seeds and the flesh from fresh seeds had low toxicity.
3. The immature whole seeds and the seed coats of fresh mature seeds were toxic.

     

The nutritional quality of Lupinseed

Mature seeds of four Lupinus species,L. albus, L. angustifolius, L. luteus andL. mutabilis, have been analysed comprehensively to evaluate their potential for nutrition. Particular interest attaches to the comparison betweenlupinus species and soyabeans. All species are rich in high-quality protein, as judged from amino-acid profiles,In vitro studies indicate high levels of digestibility and imply the presence of few interfering factors. In contrast to many other legumes, lupinseeds are free of both protease inhibitors and haemagglutinins. Only one factor, a C-glycosyl poly-hydroxy flavone, which could conceivably interfere with protein absorption, has been identified. Lupinseed could possibly be developed as an oilseed crop, though oil contents are currently somewhat lower than those of soyabeans. The composition of lupinseed oil is similar to that of soyabean oil, both being limited in quality by the presence of linolenic acid. The bright yellow colour of the partially refined oil is due to the presence of the two carotenoids, β-carotene and zeaxanthin. Lupinseed is well-known to contain toxic alkaloids of the quinolizidine group. However, intensive breeding programmes involving all four named species have been in progress for many years. At least in the cases of the first three species, cultivars have been developed that are virtually alkaloid-free. Alkaloid profiles are of interest in being decisive chemotaxonomic indicators of species. The pyrimidine bases responsible for inducing favism through the consumption ofVicia faba are absent from lupinseed. Like soyabeans, lupinseed invariably contains a range of chemically complex saponins. Concentrations in the seed are of a similar order, but it is doubtful whether these should be considered significant anti-nutritional factors for Man. Lupinseeds contain a range of oligosaccharides—raffinose, stachyose and verbascose —which correspond with the flatus factors present in soyabeans and many other legumes. Levels, however, are no higher than those found in soyabeans.     

Quantitative morphology of peracute pulmonary lesions in swine induced by Haemophilus pleuropneumoniae

Twenty-seven six-week-old cesarean-derived, colostrum-deprived pigs were inoculated intratracheally with an isolate of Haemophilus pleuropneumoniae serotype 5 (principles) of high virulence (I-200) or low virulence (B-8) or phosphate buffered saline (controls). Pigs given I-200 had severe serofibrinous pleuropneumonia at three hours after inoculation; two of three pigs were dead by 24 hours after inoculation. Interalveolar septa in the caudal lung lobes were 41% thicker than septa from control pigs at three hours after inoculation and 79% thicker by 24 hours after inoculation. Interalveolar septal capillaries in caudal lung lobes were 10.2% larger than control capillaries at three hours after inoculation and 25.6% larger by 24 hours after inoculation. Interalveolar septal capillary platelet volume was greater than the platelet volume of controls; 70% of these platelets were aggregated. There was severe diffuse alveolar, interalveolar septal, and interlobular septal edema at three hours after inoculation with fibrin, neutrophils, and macrophages present in later samples. Thirty-three percent of the lung parenchyma was necrotic at 24 hours after inoculation. Endothelial cell degeneration was generally mild, but necrotic in regions of pulmonary infarction. Pigs inoculated with the B-8 isolate did not develop marked macroscopic lesions at any sampling time. Interalveolar septa were 18% thicker than controls nine hours after inoculation and 5% thicker at six and 24 hours after inoculation. Capillary platelet volume was greatest at nine hours after inoculation with 50% of these platelets aggregated; 30% of the platelet volume was aggregated at the 24-hour sample period. Moderate diffuse pulmonary and interlobular septal edema was present at three, six, and nine hours after inoculation, but absent 24 hours after inoculation. Intravascular macrophages were present in the six, nine, and 24-hour lung samples in both B-8 and I-200 inoculated pigs. These cells were adherent to interalveolar septal capillary endothelial cells and contained phagocytized cellular debris and fibrin. These results indicate the early effects of H. pleuropneumoniae infection involve macrophage and platelet activation, and a marked increase in interalveolar septal capillary permeability.     

The renin‐angiotensin‐aldosterone system and its suppression

Chronic activation of the renin‐angiotensin‐aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro‐fibrotic, ‐inflammatory, and ‐hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.