Psychometric evaluation of a quality of recovery score for the postanesthesia care unit-A preliminary validation study.

INTRODUCTION: Patients' perception of postoperative recovery is a key aspect of perioperative care. Self-reported quality of recovery (QoR) has evolved as a relevant endpoint in perioperative research. Several psychometric instruments have been introduced to assess self-reported recovery 24 hours after surgery. However, there is no questionnaire suitable for use in the postanesthesia care unit (PACU). We aimed to develop and psychometrically evaluate a QoR questionnaire for the PACU (QoR-PACU). METHODS: The QoR-PACU was developed in German language based on the 40-item QoR-40 questionnaire. Between March and November 2020, adult patients scheduled for elective urologic surgery completed the QoR-PACU preoperatively and during the PACU stay. We evaluated feasibility, validity, reliability, and responsiveness. RESULTS: We included 375 patients. After two piloting phases including 72 and 48 patients, respectively, we administered the final version of the QoR-PACU to 255 patients, with a completion rate of 96.5%. Patients completed the QoR-PACU at a median of 125.0 (83.0; 156.8) min after arrival in the PACU. Construct validity was good with postoperative QoR-PACU sum scores correlating with age (r = 0.23, 95% CI: 0.11 to 0.35, p < 0.001), length of PACU stay (r = -0.15, 95%CI: -0.27 to -0.03, p = 0.02), pain in the PACU (r = -0.48, 95% CI: -0.57 to -0.37, p < 0.001) and piritramide dose administered (r = -0.29, 95% CI: -0.40 to -0.17, p < 0.001). Cronbach's alpha was 0.67 (95% CI: 0.61-0.73) with moderate test-retest reliability (ICC of 0.67, 95% CI: 0.38 to 0.83). Cohen's effect size was 3.08 and the standardized response mean was 1.65 indicating adequate responsiveness. CONCLUSION: The assessment of QoR in the early postoperative period is feasible. We found high acceptability, good validity, adequate responsiveness, and moderate reliability. Future studies should evaluate the psychometric properties of the QoR-PACU in more heterogeneous patient populations including female and gender-diverse patients with varying degress of perioperative risk.

Unexpected Poor Growth in Pediatric Patients on Food-based Enteral Therapy: Case Series and Suggested Practice Changes.

INTRODUCTION: Enteral feeding pumps at times may deliver different volumes than are prescribed, which can negatively impact growth, nutrition, and well-being. This study sought to assess whether challenges with pump accuracy for patients on food-based formulas contributed to challenges with weight gain. METHODS: Chart review identified complex feeding patients receiving food-based enteral nutrition via feeding pump with unexpected weight loss. Relevant data, such as enteral formula type, and anthropometric information were extracted. RESULTS: Five complex pediatric feeding patients were identified and 2 of these cases were summarized as representative examples, showing weight loss in children following the introduction of enteral food-based formulas because of feeding pump inaccuracy. CONCLUSIONS: Complex pediatric feeding patients may display unexpected and poor weight gain and growth while receiving food-based enteral feeding interventions because of pump errors. It is vital for providers to be aware of these challenges for timely intervention.

α1-antitrypsin mitigates NLRP3-inflammasome activation in amyloid ß1-42-stimulated murine astrocytes.

BACKGROUND: Neuroinflammation has an essential impact on the pathogenesis and progression of Alzheimer's disease (AD). Mostly mediated by microglia and astrocytes, inflammatory processes lead to degeneration of neuronal cells. The NLRP3-inflammasome (NOD-like receptor family, pyrin domain containing 3) is a key component of the innate immune system and its activation results in secretion of the proinflammatory effectors interleukin-1ß (IL-1ß) and interleukin-18 (IL-18). Under physiological conditions, cytosolic NLRP3-inflammsome is maintained in an inactive form, not able to oligomerize. Amyloid ß1-42 (Aß1-42) triggers activation of NLRP3-inflammasome in microglia and astrocytes, inducing oligomerization and thus recruitment of proinflammatory proteases. NLRP3-inflammasome was found highly expressed in human brains diagnosed with AD. Moreover, NLRP3-deficient mice carrying mutations associated with familial AD were partially protected from deficits associated with AD. The endogenous protease inhibitor α1-antitrypsin (A1AT) is known for its anti-inflammatory and anti-apoptotic properties and thus could serve as therapeutic agent for NLRP3-inhibition. A1AT protects neurons from glutamate-induced toxicity and reduces Aß1-42-induced inflammation in microglial cells. In this study, we investigated the effect of Aß1-42-induced NLRP3-inflammasome upregulation in primary murine astrocytes and its regulation by A1AT. METHODS: Primary cortical astrocytes from BALB/c mice were stimulated with Aß1-42 and treated with A1AT. Regulation of NLRP3-inflammasome was examined by immunocytochemistry, PCR, western blot and ELISA. Our studies included an inhibitor of NLRP3 to elucidate direct interactions between A1AT and NLRP3-inflammasome components. RESULTS: Our study revealed that A1AT reduces Aß1-42-dependent upregulation of NLRP3 at the mRNA and protein levels. Furthermore, A1AT time-dependently mitigated the expression of caspase 1 and its cleavage product IL-1ß in Aß1-42-stimulated astrocytes. CONCLUSION: We conclude that Aß1-42-stimulation results in an upregulation of NLRP3, caspase 1, and its cleavage products in astrocytes. A1AT time-dependently hampers neuroinflammation by downregulation of Aß1-42-mediated NLRP3-inflammasome expression and thus may serve as a pharmaceutical opportunity for the treatment of Alzheimer's disease.

Administration of 17ß-Estradiol Improves Motoneuron Survival and Down-regulates Inflammasome Activation in Male SOD1(G93A) ALS Mice.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease manifested by the progressive loss of upper and lower motoneurons. The pathomechanism of ALS is complex and not yet fully understood. Neuroinflammation is believed to significantly contribute to disease progression. Inflammasome activation was recently shown in the spinal cord of human sporadic ALS patients and in the SOD1(G93A) mouse model for ALS. In the present study, we investigated the neuroprotective and anti-inflammatory effects of 17ß-estradiol (E2) treatment in pre-symptomatic and symptomatic male SOD1(G93A) mice. Symptomatic mice with E2 substitution exhibited improved motor performance correlating with an increased survival of motoneurons in the lumbar spinal cord. Expression of NLRP3 inflammasome proteins and levels of activated caspase 1 and mature interleukin 1 beta were significantly reduced in SOD1(G93A) mice supplemented with E2.

Free-space quantum key distribution to a moving receiver.

Technological realities limit terrestrial quantum key distribution (QKD) to single-link distances of a few hundred kilometers. One promising avenue for global-scale quantum communication networks is to use low-Earth-orbit satellites. Here we report the first demonstration of QKD from a stationary transmitter to a receiver platform traveling at an angular speed equivalent to a 600 km altitude satellite, located on a moving truck. We overcome the challenges of actively correcting beam pointing, photon polarization and time-of-flight. Our system generates an asymptotic secure key at 40 bits/s.

Large-scale surveillance of Plasmodium falciparum crt(K76T) in northern Ghana.

Surveillance of Plasmodium falciparum crt(K76T) [Pfcrt(K76T)], a resistance marker of chloroquine and, limitedly, amodiaquine, in >4,000 children in northern Ghana revealed a prevalence of 79%. Pfcrt(K76T) was heterogeneously distributed and associated with chloroquine use, low parasitemia, and the dry season. Widespread chloroquine resistance challenges the regional life span of amodiaquine as a partner drug in artemisinin combination therapy.

Malaria, anemia, and malnutrition in african children--defining intervention priorities.

BACKGROUND: Malaria, anemia, and malnutrition contribute substantially to childhood morbidity in sub-Saharan Africa, but their respective roles and interactions in conferring disease are complex. We aimed to investigate these interactions. METHODS: In 2002, we assessed plasmodial infection, anemia, and nutritional indices in 2 representative surveys comprising >4000 children in northern Ghana. RESULTS: Infection with Plasmodium species was observed in 82% and 75% of children in the rainy and dry season, respectively. The fraction of fever attributable to malaria was 77% in the rainy season and 48% in the dry season and peaked in children of rural residence. Anemia (hemoglobin level, <11 g/dL) was seen in 64% of children and was, in multivariate analysis, associated with young age, season, residence, parasitemia, P. malariae coinfection, and malnutrition (odds ratio [OR], 1.68 [95% confidence interval [CI], 1.38-2.04]). In addition, malnutrition was independently associated with fever (axillary temperature, > or = 37.5 degrees C; OR, 1.59 [95% CI, 1.13-2.23]) and clinical malaria (OR, 1.67 [95% CI, 1.10-2.50]). CONCLUSIONS: Malnutrition is a fundamental factor contributing to malaria-associated morbidity and anemia, even if the latter exhibits multifactorial patterns. Our data demonstrate that malaria-control programs alone may not have the desired impact on childhood morbidity on a large scale without concomitant nutrition programs.