Isolation & identification of bacteria for the treatment of brown crab (Cancer pagurus) waste to produce chitinous material.

AIMS: To isolate bacteria from soil for microbial pretreatment of brown crab (Cancer pagurus) shell waste and the production of chitin. METHODS AND RESULTS: Isolates were screened for protease enzymes and acid production in order to facilitate the removal of protein and calcium carbonate fractions from brown crab shell to yield a chitinous material. Selected isolates were applied in various combinations in successive, two-step fermentations with brown crab shell waste. These isolates were identified as: Exiguobacterium spp. (GenBank accession number: KP050496), Bacillus cereus (GenBank accession number: KP050499), B. subtilis (GenBank accession number: KP050498), Bacillus licheniformis (GenBank accession number: KP050497), Pseudomonas migulae (GenBank accession number: KP050501), Pseudomonas spp. (GenBank accession number: KP050500), Pseudomonas spp. (GenBank accession number: KP050502), Arthrobacter luteolus (GenBank accession number: KP050503), Lactobacillus spp. (GenBank accession number: KP072000) and Enterococcus spp. (GenBank accession number: KP071999). CONCLUSIONS: Successive two-step fermentations with isolates in certain combinations resulted in a demineralization of >94% and the extraction of a crude chitin fraction from brown crab processing waste. The highest demineralization, 98·9% was achieved when isolates identified as B. cereus and Pseudomonas spp. were used in combination. The transfer of fermentations to a larger scale requires further research for optimization. SIGNIFICANCE AND IMPACT OF THE STUDY: The successful application of these isolates in successive two-step fermentation of brown crab shell waste to extract chitin means with further research into optimization and scale up, this chitin extraction process may be applied on an industrial scale and provide further commercial value from brown crab shell waste.

Transesophageal echocardiography: an objective tool in defining maximum ventricular response to intravenous fluid therapy.

Ventricular preload is an important determinant of cardiac function, which is indirectly measured in the clinical setting by the pulmonary capillary wedge pressure (PCWP). Transesophageal echocardiography (TEE) is rapidly gaining acceptance as a monitor of cardiac function. Although it provides high-resolution images of cardiac structures, clinical assessment of ventricular preload using TEE has been subjective, since quantitative measurements have been difficult to perform in a timely fashion. Automated border detection (ABD) is a new technology used in conjunction with TEE that allows quantitative real-time, two-dimensional measurement of cavity areas. To determine whether enddiastolic area (EDA) measured by ABD can be used to determine an appropriate end point for intravenous fluid administration, nine mongrel dogs were studied. Anesthetized animals were hemorrhaged to achieve a central venous pressure of 0-5 mm Hg. Each animal was then given intravenous fluid (autologous blood followed by hetastarch) until a peak in thermodilution cardiac output (CO) was achieved. Measures of PCWP, EDA, CO, and left ventricular stroke work (LVSW) were obtained after each fluid bolus. Bivariate plots displaying administered volume versus CO, LVSW, and EDA revealed parallel curves for each of these variables with peaks evident at cumulative volumes of 50-55 mL/kg. Multiple regression with mixed model analysis of covariance was performed to determine the significance of EDA in relation to changes in CO and LVSW. Analysis was likewise performed comparing the relationship between PCWP and changes in CO or LVSW. A significant relationship was demonstrated when comparing EDA to changes in CO and LVSW (P = 0.03 and P < 0.0001, respectively). Similar analysis comparing PCWP to changes in CO and LVSW failed to demonstrate a significant relationship (P = 0.54 and P = 0.36, respectively). These data suggest that changes in EDA measured using TEE with ABD are related to trends in cardiac function and can suggest an appropriate end point for intravenous fluid administration as defined by maximum CO and LVSW. PCWP did not demonstrate a significant relationship to changes in CO and LVSW.

Levosimendan (OR-1259), a myofilament calcium sensitizer, enhances myocardial contractility but does not alter isovolumic relaxation in conscious and anesthetized dogs.

BACKGROUND: Levosimendan is a myofilament calcium sensitizer with phosphodiesterase III inhibiting properties which increases contractile state in vitro by stabilizing calcium-induced changes in troponin C. This latter effect may produce positive inotropic actions but may also cause deleterious negative lusitropic effects. This investigation examined the effects of levosimendan on systemic and coronary hemodynamics and left ventricular systolic and diastolic function in conscious and anesthetized dogs. METHODS: Because autonomic nervous system activity may influence the actions of levosimendan and volatile anesthetics in vivo, experiments were conducted in the presence of pharmacologic blockade of the autonomic nervous system. A total of 24 experiments were performed in eight dogs chronically instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase and decrease of left ventricular pressure, subendocardial segment length, diastolic coronary blood flow velocity, and cardiac output. The slope of the regional preload recruitable stroke work relation was used to assess myocardial contractility. Diastolic function was evaluated by the peak rate of decrease of left ventricular pressure, a time constant of isovolumic relaxation, maximum segment lengthening velocity during rapid ventricular filling, and a regional chamber stiffness constant. Systemic and coronary hemodynamics and left ventricular pressure-segment length diagrams and waveforms were recorded after 10 min equilibration at each dose of levosimendan (0.5, 1.0, 2.0, and 4.0 micrograms.kg-1.min-1) in the conscious state or during isoflurane or halothane anesthesia (1.0 MAC) on 3 days of experimentation. RESULTS: In conscious dogs, levosimendan increased heart rate, cardiac output, diastolic coronary blood flow velocity, and segment shortening and decreased left ventricular end-diastolic pressure, systemic vascular resistance, and diastolic coronary vascular resistance. Levosimendan caused dose-dependent increases in the slope of the regional preload recruitable stroke work relation (65 +/- 6 during control to 139 +/- 9 mmHg during the high dose), consistent with a direct positive inotropic effect. No changes in the peak rate of decrease of left ventricular pressure or in the time constant of isovolumic relaxation were produced by with levosimendan in conscious dogs, indicating that isovolumic relaxation was unaffected. In contrast, increases in rapid ventricular filling were observed (maximum segment lengthening velocity 34 +/- 3 during control to 47 +/- 5 mm.s-1 at the high dose). In the presence of isoflurane and halothane, levosimendan caused cardiovascular actions which were similar to those observed in the conscious state. Levosimendan increased, in a dose-related manner, the slope of the regional preload recruitable stroke work relation and in the maximum segment lengthening velocity during rapid ventricular filling in anesthetized dogs. However, there were no changes in the time constant of isovolumic relaxation or in the peak rate of decrease of left ventricular pressure. CONCLUSIONS: The results indicate that levosimendan causes systemic and coronary vasodilatation in conscious and anesthetized dogs during blockade of the autonomic nervous system. Levosimendan caused direct positive inotropic effects and improved rapid ventricular filling but did not alter indices of isovolumic relaxation, suggesting that levosimendan may selectively enhance systolic performance and diastolic filling without affecting left ventricular relaxation.