CO2-formatics: how do proteins bind carbon dioxide?

The rising atmospheric concentration of CO(2) has motivated researchers to seek routes for improved utilization, increased mitigation, and enhanced sequestration of this greenhouse gas. Through a combination of bioinformatics, molecular modeling, and first-principles quantum mechanics the binding of carbon dioxide to proteins is analyzed. It is concluded that acid/base interactions are the principal chemical force by which CO(2) is bound inside proteins. With respect to regular secondary structural elements, beta-sheets show a marked preference for CO(2) binding compared to alpha-helices. The data also support the inference that while either or both oxygens of CO(2) are generally tightly bound in the protein environment, the carbon is much less "sequestered." First principles and more approximate modeling techniques are assessed for quantifying CO(2) binding thermodynamics.

Palliative care needs of cancer patients in U.S. nursing homes.

BACKGROUND: Increasingly, nursing homes are the place of care for older Americans with cancer. Yet, few studies has characterized the quality of care for this growing population. OBJECTIVE: Characterize the scope and quality of cancer care in U.S. nursing homes. DESIGN: Secondary analysis of the national repository of the Minimum Data Set (MDS) SETTING AND SUBJECTS: Nursing home residents noted to have cancer diagnosis on the MDS. RESULTS: Of the 190,769 New Hampshire residents (8.8%) with a cancer diagnosis, 1 in 4 had weight loss (23.4%), received intravenous medications (27.7%), or used oxygen (25.4%). Overall, 45.3% had a do-not-resuscitate (DNR) order, with state variations ranging from 17.8% (New Jersey) to 70.5% (Wisconsin). More than 1 in 10 (12.0%) were defined as terminally ill, although only 29.3% of these received hospice services. Among patients with pain, half of those who survived to a second assessment had persistent, severe pain (51.3%), which also varied by state, ranging from 43.3% (Iowa) to 65.8% (Nevada). Active treatment was rare; less than 5% received chemotherapy or radiotherapy. However, 15.5% had parenteral and/or tube feedings for nutrition. Approximately, 1 in 10 New Hampshire residents had advanced cancer. CONCLUSION: Our findings suggest important opportunities to improve the quality of cancer care for older adults.

Acute right atrial strain: regression in normal as well as abnormal P-wave amplitudes with treatment of obstructive pulmonary disease.

OBJECTIVE: To evaluate right atrial (RA) "strain" as reflected by changes in P-wave amplitude and vector in patients with COPD immediately before and immediately after beginning treatment of exacerbations. BACKGROUND: P-pulmonale (frequently temporary, reflecting acute RA strain) occurs under a variety of circumstances, including COPD. Emergency room (ED) ECGs in patients with acute exacerbations of COPD have suggested that P-pulmonale (P waves > or = 2.5 in leads II, III, and aVF) tends to resolve subsequent to acute treatment. RA strain is defined as a response to RA stress (probably transient pressure rise and/or acute RA enlargement) in patients with COPD. Since P-pulmonale occurs in a small minority of patients with COPD, we investigated dynamic changes in size and mean vector (axis) of all frontal plane P waves in the ED vs the immediate subsequent ward ECG in patients with acute exacerbations of COPD. METHODS: We prospectively compared P-wave amplitude in the ED with the first in-patient ECG in 50 consecutive patients with acute exacerbations of COPD and in 20 consecutive nonpulmonary control patients, analyzing only ECGs showing sinus rhythm and in which P waves were clearly recorded. Despite using a calibrated magnifying graticule, it was difficult to interpret a dynamic change if the initial ED ECG had P-wave amplitude < 1.5 mm in leads II and aVF. We selected lead II because it usually has the largest frontal plane P waves and also aVF to reflect the relative verticality of the mean P vector (axis). We performed a matched-pair analysis to compare the equality of means. RESULTS: Of the patients with COPD, only seven patients (14%) had classical P-pulmonale on the ED ECG. Forty-eight of 50 consecutive patients (96%) demonstrated a decrease in P-wave amplitude between ED and subsequent ward ECGs. Two patients showed no change. The mean differences of P-wave amplitude between ED and ward ECGs in lead II was 0.78 mm, and that in lead aVF was 0.8 mm. The difference of the mean P-axis between ED and ward ECGs was - 5.24 degrees (p < 0.0001 for all three measurements). There was no P-wave amplitude change in the control group between ED and ward ECGs. CONCLUSIONS: P-wave amplitude in patients with COPD decreases once an acute exacerbation subsides. Thus, P-wave amplitude and vector are dynamic and could reflect reduced RA strain. We question the traditional (1935) absolute cutoff of 2.5 mm for P-pulmonale as of limited value due to insensitivity, hence inappropriate for what this investigation demonstrates to be a continuous variable.