The transition to agricultural sustainability. (49/14889)

The transition to sustainable growth in agricultural production during the 21st century will take place within the context of a transition to a stable population and a possible transition to a stable level of material consumption. If the world fails to successfully navigate a transition to sustainable growth in agricultural production, the failure will be due more to a failure in the area of institutional innovation than to resource and environmental constraints.  (+info)

Gardenification of tropical conserved wildlands: multitasking, multicropping, and multiusers. (50/14889)

Tropical wildlands and their biodiversity will survive in perpetuity only through their integration into human society. One protocol for integration is to explicitly recognize conserved tropical wildlands as wildland gardens. A major way to facilitate the generation of goods and services by a wildland garden is to generate a public-domain Yellow Pages for its organisms. Such a Yellow Pages is part and parcel of high-quality search-and-delivery from wildland gardens. And, as they and their organisms become better understood, they become higher quality biodiversity storage devices than are large freezers. One obstacle to wildland garden survival is that specific goods and services, such as biodiversity prospecting, lack development protocols that automatically shunt the profits back to the source. Other obstacles are that environmental services contracts have the unappealing trait of asking for the payment of environmental credit card bills and implying delegation of centralized governmental authority to decentralized social structures. Many of the potential conflicts associated with wildland gardens may be reduced by recognizing two sets of social rules for perpetuating biodiversity and ecosystems, one set for the wildland garden and one set for the agroscape. In the former, maintaining wildland biodiversity and ecosystem survival in perpetuity through minimally damaging use is paramount, while in the agroscape, wild biodiversity and ecosystems are tools for a healthy and productive agroecosystem, and the loss of much of the original is acceptable.  (+info)

Validity of the uniform mixing assumption: determining human exposure to environmental tobacco smoke. (51/14889)

When using the mass balance equation to model indoor air quality, the primary assumption is that of uniform mixing. Different points in a single compartment are assumed to have the same instantaneous pollutant concentrations as all other points. Although such an assumption may be unrealistic, under certain conditions predictions (or measurements) of exposures at single points in a room are still within acceptable limits of error (e.g., 10%). In this article, three studies of the mixing of environmental tobacco smoke (ETS) pollutants are reviewed, and data from several other ETS field studies are presented. Under typical conditions for both short sources (e.g., 10 min) and the continuous sources of ETS in smoking lounges, I find that average exposure concentrations for a single point in a room represent the average exposure across all points in the room within 10% for averaging times ranging from 12 to 80 min. I present a method for determining theoretical estimates of acceptable averaging times for a continuous point source.  (+info)

Thermodynamics of nucleotide binding to the chaperonin GroEL studied by isothermal titration calorimetry: evidence for noncooperative nucleotide binding. (52/14889)

We characterized the thermodynamics of binding reactions of nucleotides ADP and ATPgammaS (a nonhydrolyzable analog of ATP) to GroEL in a temperature range of 5 degrees C to 35 degrees C by isothermal titration calorimetry. Analysis with a noncooperative binding model has shown that the bindings of nucleotides are driven enthalpically with binding constants of 7x103 M-1 and 4x104 M-1 for ADP and ATPgammaS, respectively, at 26 degrees C and that the heat capacity change DeltaCp is about 100 cal/mol.K for both the nucleotides. The stoichiometries of binding were about 8 and 9 molecules for ADP and ATPgammaS, respectively, per GroEL tetradecamer at 5 degrees C, and both increased with temperature to reach about 14 (ADP) and 12 (ATPgammaS) for both nucleotides at 35 degrees C. The absence of initial increase of binding heat as well as Hill coefficient less than 1.2, which were obtained from the fitting to the model curve by assuming positive cooperativity, showed that there was virtually no positive cooperativity in the nucleotide bindings. Incorporating a difference in affinity for the nucleotide (ADP and ATPgammaS) between the two rings of GroEL into the noncooperative binding model improved the goodness of fitting and the difference in the affinity increased with decreasing temperature.  (+info)

Multiple organ failure. How valid is the "two hit" model? (53/14889)

Inflammatory "one hit" and "two hit" models have recently been proposed to account for the development of multiple organ failure (MOF) in trauma and critically ill surgical patients when no source of infection can be found. In the "one hit" model, the initial insult is so massive that a systemic inflammatory response syndrome is triggered and leads rapidly to MOF. In the "two hit" scenario, initially less severely injured patients eventually develop MOF as a result of a reactivation of their inflammatory response caused by an adverse and often minor intercurrent event. At first sight, the theory is attractive because it seems to fit commonly observed clinical patterns. Indeed, injured patients often respond to initial resuscitation but, after an insult of some sort, develop organ dysfunction and die. The "two hit" model is furthermore mirrored at the cellular level. Inflammatory cells are indeed susceptible of being primed by an initial stimulus and reactivated subsequently by a relatively innocuous insult. However, in the absence of clinical and biological corroboration based on cytokine secretion patterns, these models should not be accepted uncritically.  (+info)

Joint anatomy, design, and arthroses: insights of the Utah paradigm. (54/14889)

This model of joint design argues 1) that excessive fatigue damage (MDx) in articular cartilage collagen can be the "final cause" of an arthrosis; 2) that known responses of a growing joint's anatomy and geometry, and modeling and maintenance activities, to mechanical loads minimize that cause and thus arthroses; 3) and many biomechanical, biochemical, cell-biologic, genetic and traumatic "first causes" of arthroses could lead to that final cause. The model depends partly on the following facts (marked by a single asterisk) and ideas (marked by a double asterisk). A) During growth a joint's total loads can increase over 20 times without causing an arthrosis, yet in adults an equal loading increase would cause one. B) Fatigue damage (MDx) occurs in joint tissues, larger strains increase it, and minimizing strains reduces it. C) Bone can repair amounts of MDx below an "MDx threshold," but larger amounts can escape repair and accumulate. The model assumes articular cartilage has similar features. D) Bone modeling makes bones strong enough to keep their strains below bone's MDx threshold and minimize MDx. Chondral modeling shapes and sizes joints during growth; that would keep articular cartilage strains below the chondral MDx threshold to minimize chondral MDx and arthroses. Normal chondral modeling nearly stops in adults, which might explain point A above. E) Throughout life maintenance activities preserve optimal physical, chemical and biologic properties of a joint's tissues. To past emphases on the biochemical, genetic, cellular and molecular biologic features of adult joint physiology, this model adds organ-level, tissue-level and vital-biomechanical features of growing joints that invite study and understanding at lower levels of biologic organization.  (+info)

Vancomycin-resistant enterococci in intensive-care hospital settings: transmission dynamics, persistence, and the impact of infection control programs. (55/14889)

Vancomycin-resistant enterococci (VRE) recently have emerged as a nosocomial pathogen especially in intensive-care units (ICUs) worldwide. Transmission via the hands of health-care workers is an important determinant of spread and persistence in a VRE-endemic ICU. We describe the transmission of nosocomial pathogens by using a micro-epidemiological framework based on the transmission dynamics of vector-borne diseases. By using the concept of a basic reproductive number, R0, defined as the average number of secondary cases generated by one primary case, we show quantitatively how infection control measures such as hand washing, cohorting, and antibiotic restriction affect nosocomial cross-transmission. By using detailed molecular epidemiological surveillance and compliance monitoring, we found that the estimated basic reproductive number for VRE during a study at the Cook County Hospital, Chicago, was approximately 3-4 without infection control and 0.7 when infection control measures were included. The impact of infection control was to reduce the prevalence from a predicted 79% to an observed 36%. Hand washing and staff cohorting are the most powerful control measures although their efficacy depends on the magnitude of R0. Under the circumstances tested, endemicity of VRE was stabilized despite infection control measures, by the constant introduction of colonized patients. Multiple stochastic simulations of the model revealed excellent agreement with observed pattern. In conjunction with detailed microbiological surveillance, a mathematical framework provides a precise template to describe the colonization dynamics of VRE in ICUs and impact of infection control measures. Our analyses suggest that compliance for hand washing significantly in excess of reported levels, or the cohorting of nursing staff, are needed to prevent nosocomial transmission of VRE in endemic settings.  (+info)

Look before you leap: stratify before you standardize. (56/14889)

This paper presents a mathematical model to show the conditions in which age standardization can be used to summarize age-specific rates for comparison purposes over calendar time. It shows that the conditions for valid comparison depend on the type of measure used for comparison, that is, difference, ratio, or percent change. If the measure for comparison is a difference of the standardized rates at two time points, then the age-specific rates need to maintain a constant rate difference over time for the comparison to be valid. If the measure for comparison is a ratio or percent change of the standardized rates at two time points, then the age-specific rates need to maintain a constant rate ratio over time for the comparison to be valid. Since in reality, as shown by our Canadian empirical data, age-specific rates do not always maintain a consistent pattern over time, it is recommended that one should always stratify the data to look at patterns of age-specific rates before applying age standardization.  (+info)