Sleep Loss and Affective Functioning: More Than Just Mood

Empirical evidence supports an intimate link between sleep and affective functioning. While the bidirectional relationship between sleep duration and mood is well documented, limited research targets other aspects of affective functioning, such as emotion and emotion regulation, or considers their interrelationships. The present review summarizes research examining the relationship between sleep and emotion, emotion regulation, and mood, and presents a theoretical model representing the relationships between these constructs. Disruptions to sleep and mood may trigger and maintain a negative cascade, leading to more entrenched sleep problems and psychopathology. Given that insufficient sleep is a widespread phenomenon, understanding the interrelationships between sleep and affective functioning has implications for both public health and clinical practice.     

Detection and reproducibility of mental stress—induced myocardial ischemia with Tc-99m sestamibi SPECT in normal and coronary artery disease populations

BACKGROUND: Mental stress-induced ischemia, as detected by radionuclide studies, has yielded reversible ischemia in only 30% to 60% of patients with exercise-induced ischemia. Little is known about the reproducibility of myocardial perfusion imaging in detecting mental stress-induced ischemia. The purpose of this study was to further evaluate the occurrence and reproducibility of mental stress-induced ischemia in patients with coronary artery disease (CAD) and in normal control subjects with a low likelihood of CAD by using sestamibi single photon emission computed tomography (SPECT) imaging. METHODS AND RESULTS: A total of 40 patients were enrolled in this study: 19 patients with CAD and typical angina or reversible ischemia (positive exercise treadmill study or positive adenosine thallium study) and 21 normal control subjects underwent mental stress testing as well as myocardial perfusion imaging. The subjects were given a speaking task, and SPECT imaging was subsequently performed. Two experienced readers compared mental stress imaging with a resting image using a 20-segment cardiac model. Hemodynamic changes in blood pressure and heart rate with mental stress were also measured in all subjects. Each patient with CAD also underwent repeat mental stress testing and myocardial imaging approximately 2 weeks later. Of the 19 patients with CAD and typical angina or with evidence of reversible ischemia, 16 (84%) demonstrated ischemia with mental stress, as detected by sestamibi SPECT imaging. The mean number of new or worsened perfusion defects attributable to mental stress was 3.5, with a mean severity of 1.7. These results were also reproducible. With repeated mental stress testing and myocardial imaging, 12 of the 16 CAD patients (75%) demonstrated evidence of myocardial ischemia. None of the 21 normal control subjects had evidence of mental stress-induced myocardial ischemia. Mental stress also induced reproducible and significant hemodynamic changes in CAD patients. CONCLUSIONS: In patients with known CAD with typical angina or with evidence of reversible ischemia despite taking medications, mental stress was very effective in inducing myocardial ischemia, as detected by sestamibi SPECT imaging. Mental stress was also found to elicit significant hemodynamic responses. Furthermore, these findings demonstrated good reproducibility.     

Staphylococcus simulans septicemia in a patient with chronic osteomyelitis and pyarthrosis.

Staphylococcus simulans was identified as the etiological agent of osteomyelitis and septic arthritis in an adult male who had sustained a fracture of the fibula and syndesmosis separation which required the installation of orthopedic hardware. Identifying characteristics and antibiograms for this organism, recovered from blood, wound exudate, and deep tissue samples, were determined. Recent evidence has linked slime production (adherence to smooth surfaces) by coagulase-negative staphylococci to infections by these organisms at sites where foreign bodies had been inserted. Tests for adherence showed this S. simulans strain to be a strong slime producer. This is the first reported case of osteomyelitis and septicemia due to S. simulans.     

Plasma concentrations of soluble urokinase-type plasminogen activator receptor are increased in patients with malaria and are associated with a poor clinical or a fatal outcome

BACKGROUND: Blood concentrations of soluble urokinase-type plasminogen activator receptor (suPAR) are increased in conditions with immune activation, and high concentrations of suPAR often predict a poor clinical outcome. This study explored the hypothesis that high plasma concentrations of suPAR are associated with disease severity in malaria. METHODS: At admission to the hospital, plasma concentrations of suPAR were measured by ELISA in samples from 645 African children with clinical symptoms of malaria: 478 had malaria, and 167 had a blood film negative for Plasmodium parasites. Fourteen healthy children were included for comparison. RESULTS: Plasma concentrations of suPAR were higher in patients with malaria (median, 7.90 ng/mL [interquartile range [IQR], 6.56-9.15 ng/mL]), compared with those in plasmodium-negative patients (median, 5.59 ng/mL [IQR, 4.54-8.16 ng/mL]; P < .001) and those in healthy children (3.94 ng/mL [IQR, 3.46-4.82 ng/mL]; P < .001). The highest concentrations were found in patients with malaria who died (P = .008) or had complicated malaria (P < .001). In univariate logistic regression analysis, a 1 ng/mL increase in plasma concentration of suPAR was associated with increased risk of mortality (odds ratio, 1.42 [95% confidence interval, 1.09-1.86]; P = .009). In multivariate linear regression analysis, lower platelet count, lower hemoglobin level, and higher neutrophil count were independently associated with a higher plasma concentration of suPAR. CONCLUSIONS: If the plasma concentration of suPAR reflects the extent of parasite-induced immune activation, this may explain why a high concentration of suPAR is associated with a poor clinical outcome in patients with malaria.     

Systemic activation of the transient receptor potential vanilloid subtype 4 channel causes endothelial failure and circulatory collapse: Part 2

The transient receptor potential (TRP) vanilloid subtype 4 (V4) is a nonselective cation channel that exhibits polymodal activation and is expressed in the endothelium, where it contributes to intracellular Ca2+ homeostasis and regulation of cell volume. The purpose of the present study was to evaluate the systemic cardiovascular effects of GSK1016790A, a novel TRPV4 activator, and to examine its mechanism of action. In three species (mouse, rat, and dog), the i.v. administration of GSK1016790A induced a dose-dependent reduction in blood pressure, followed by profound circulatory collapse. In contrast, GSK1016790A had no acute cardiovascular effects in the TRPV4-/- null mouse. Hemodynamic analyses in the dog and rat demonstrate a profound reduction in cardiac output. However, GSK1016790A had no effect on rate or contractility in the isolated, buffer-perfused rat heart, and it produced potent endothelial-dependent relaxation of rodent-isolated vascular ring segments that were abolished by nitric-oxide synthase (NOS) inhibition (N-nitro-L-arginine methyl ester; L-NAME), ruthenium red, and endothelial NOS (eNOS) gene deletion. However, the in vivo circulatory collapse was not altered by NOS inhibition (L-NAME) or eNOS gene deletion but was associated with (concentration and time appropriate) profound vascular leakage and tissue hemorrhage in the lung, intestine, and kidney. TRPV4 immunoreactivity was localized in the endothelium and epithelium in the affected organs. GSK1016790A potently induced rapid electrophysiological and morphological changes (retraction/condensation) in cultured endothelial cells. In summary, inappropriate activation of TRPV4 produces acute circulatory collapse associated with endothelial activation/injury and failure of the pulmonary microvascular permeability barrier. It will be important to determine the role of TRPV4 in disorders associated with edema and microvascular congestion.     

Severe isolated aortic stenosis with normal left ventricular systolic function and low transvalvular gradients: pathophysiologic and prognostic insights

BACKGROUND AND AIM OF THE STUDY: A significant proportion of patients with severe valvular aortic stenosis (AS) and preserved left ventricular (LV) systolic function have low transvalvular gradients. The study aim was to determine the mechanisms and outcome of patients with this hemodynamic profile of AS. METHODS: Among 1,679 patients who underwent transthoracic echocardiography for the evaluation of AS at the authors' institution, 215 (105 females, 110 males; mean age: 77 +/- 10 years) had isolated AS (mean aortic valve area index 0.39 +/- 0.1 cm2/m2), normal sinus rhythm and normal LV ejection fraction. The mean follow up was 23 +/- 12 months, and the end-points were mortality, aortic valve replacement (AVR), or mortality or AVR. RESULTS: Forty-seven patients had a transvalvular mean gradient (MG) <30 mmHg (MG(low)) and 168 had MG > or = 30 mmHg (MG(high)). Compared to MG(high), the MG(low) group had a higher prevalence of hypertension, lower LV end-diastolic volume index (47 +/- 9 versus 56 +/- 12 ml/m2, p <0.0001), lower LV stroke vol-ume index (37 +/- 12 versus 41 +/- 11 ml/beat, p <0.0002), a lesser severity of stenosis (aortic valve area index 0.37 +/- 0.09 versus 0.46 +/- 0.09 cm2/m2, p <0.0001) and a higher systemic vascular resistance (2163 +/- 754 versus 1879 +/- 528 dyne cm s(-5). The LV end-diastolic volume index, systemic vascular resistance and energy loss index were predictors of MG <30 mmHg (OR = 0.30, 95% CI, 0.12, 0.62; OR = 3.05, 95% CI, 1.71, 6.26; and OR = 6.76, 95% CI, 3.44,15.38, respectively). MG <30 mmHg (MGhigh) was associated with almost 50% lower referral to surgery and a two-fold increase in preoperative mortality. CONCLUSION: In severe AS with a normal LV ejection fraction, MG <30 mmHg is related to a lesser severity of stenosis, a smaller LV volume, a lower flow rate and a higher systemic vascular resistance. Compared to the MG(high) group, these patients were less frequently referred to surgery and had a higher mortality.