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Predicting survival and disclosing the prediction to patients with advanced disease, particularly cancer, is among the most difficult tasks that physicians face. With the de-emphasis of prognosis in favor of diagnosis and therapeutics in the medical literature, physicians may have difficulty finding the survival information they need to make appropriate estimates of survival for patients who develop cancer. Quite separate from the challenge of estimating survival accurately, physicians may also find the process of disclosing the prognosis to their patients difficult. Using the vignette of a real patient with advanced cancer who far outlived her physician's prognostic estimate, we discuss clinical issues related to the science of prognosis in advanced cancer and the art of its disclosure.
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Recent advances in human immunodeficiency virus (HIV) therapy have significantly reduced HIV-related mortality in the developed world, but mortality rates have plateaued, and AIDS remains a leading cause of serious illness and death for young adults. The chronic nature of the HIV disease course and the increasing burden of cumulative HIV-related morbidity and treatment-related toxic effects pose new challenges to the care of patients over time. Uncertainties about prognosis and the promise and limitations of rapidly evolving therapies have made decision making about advance care planning and end-of-life issues more complex and elusive than when the disease course was more uniform, rapid, and predictable. The emerging biomedical paradigm of highly active antiretroviral therapy (HAART) as the cornerstone of treatment has helped to transform HIV into a manageable chronic disease, yet at the same time has resulted in a more narrow focus and a de facto separation between disease-specific "curative" and symptom-specific "palliative" care for patients with HIV/AIDS. As patients survive longer in the latter stages of progressive HIV disease, they may in fact have increasing need for comprehensive symptom management as well as wide-ranging need for psychosocial, family, and care planning support. In the HAART era, the false dichotomy of curative vs palliative care for patients with HIV/AIDS must be supplanted by a more integrated model to provide comprehensive care for patients with advanced HIV disease and their families.
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Various health, quality, utility and disability adjusted life years or life expectancy (HALY, QALY, DALY; HALE, QALE, DALE) measures have become gold standards for defining outcomes in technology evaluation, population health monitoring, and other evaluative efforts. As such, the analytical framework within which these measures are used for descriptive and evaluative purposes should be theoretically consistent and statistically rigorous. For instance, widely accepted definitions of cost-effectiveness ratios and other technology evaluation criteria that are based on expectations of the respective cost and outcome measures must, as such, be defined in terms of expected HALYs or QALYs. Similarly, measures like HALEs or QALEs used for population health monitoring are typically concerned with population expectations of such measures (or their corresponding totals). This paper demonstrates that estimation of such expectations necessitates consideration of the population variation in, and covariation between, quality and longevity. From the perspective of several different environments characterizing such heterogeneity, quantification or estimation of measures like QALYs is reconsidered. An empirical example of the central issues is provided by means of an analysis of the years of healthy life (YHL) measure drawn from the US National Health Interview Survey.
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Microbial mats are layered communities of bacteria that form cohesive structures, some of which are preserved in sedimentary rocks as stromatolites. Certain rocks, approximately three and a half thousand million years old and representing the oldest known fossils, are interpreted to derive from microbial mats and to contain fossils of microorganisms. Modern microbial mats (such as the one described here from Matanzas, Cuba) and their fossil counterparts are of great interest in the interpretation of early life on Earth. Since examination of microbial mats and stromatolites increases our understanding of long-term stability and change, within the global environment, such structures should be protected wherever possible as natural science preserves. Furthermore, since they have existed virtually from the time of life's origin, microbial mats have developed exemplary mechanisms of local community persistence and may even play roles in the larger global environment that we do not understand.
Proteorhodopsin is a family of over 50 proteins that provide phototrophic capability to marine bacteria by acting as light-powered proton pumps. The potential importance of proteorhodopsin to global ocean ecosystems and the possible applications of proteorhodopsin in optical data storage and optical signal processing have spurred diverse research in this new family of proteins. We show that proteorhodopsin expressed in Escherichia coli is functional and properly inserted in the membrane. At high expression levels, it appears to self-associate. We present a method for determining spectral properties of proteorhodopsin in intact E. coli cells that matches results obtained with detergent-solubilized, purified proteins. Using this method, we observe distinctly different spectra for protonated and deprotonated forms of 21 natural proteorhodopsin proteins in intact E. coli cells. Upon protonation, the wavelength maxima red shifts between 13 and 53 nm. We find that pKa values between 7.1 and 8.5 describe the pH-dependent spectral shift for all of the 21 natural variants of proteorhodopsin. The wavelength maxima of the deprotonated forms of the 21 natural proteorhodopsins cluster in two sequence-related groups: blue proteorhodopsins (B-PR) and green proteorhodopsins (G-PR). The site-directed substitution Leu105Gln in Bac31A8 proteorhodopsin shifts this G-PR's wavelength maximum to a wavelength maximum the same as that of the B-PR Hot75m1 proteorhodopsin. The site-directed substitution Gln107Leu in Hot75m1 proteorhodopsin shifts this B-PR's wavelength maximum to a wavelength maximum as that of Bac31A8 proteorhodopsin.
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