Prevalence and Predictors of Quality of Recovery at Home After Day Surgery

Traditionally, major complications and unanticipated admission/readmission rates were used to assess outcome after day surgery. However, in view of the relative absence of major complications the quality of recovery (QOR) should be considered one of the principal endpoints after day surgery. In our study, the level of QOR is defined by a combination of the Global Surgical Recovery (GSR) Index and the Quality of Life (QOL).The aim of this study was to analyze prevalence and predictors of QOR after day surgery on the fourth postoperative day.Elective patients scheduled for day surgery from November 2008 to April 2010 were enrolled in a prospective cohort study. Outcome parameters were measured by using questionnaire packages at 2 time points: 1 week preoperatively and 4 days postoperatively. Primary outcome parameter is the QOR and is defined as good if the GSR index >80% as well as the postoperative QOL is unchanged or improved as compared with baseline. QOR is defined as poor if both the GSR index ≤80% and if the postoperative QOL is decreased as compared with baseline. QOR is defined as intermediate in all other cases. Three logistic regression analyses were performed to determine predictors for poor QOR after day surgery.A total of 1118 patients were included. A good QOR was noted in 17.3% of patients, an intermediate QOR in 34.8%, and a poor QOR in 47.8% 4 days after day surgery. The best predictor for poor QOR after day surgery was type of surgery. Other predictors were younger age, work status, and longer duration of surgery. A history of previous surgery, expected pain (by the patient) and high long-term surgical fear were significant predictors of poor QOR in only 1 of 3 prediction models.The QOR at home 4 days after day surgery was poor in the majority of patients and showed a significant procedure-specific variation. Patients at risk for poor QOR can be identified during the preoperative period based on type of surgery, age, work status, and the duration of the surgery.     

Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats.

Cerebral ischemic preconditioning protects against stroke, but is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role in cerebral injury after stroke; we tested the hypothesis that interrupting reperfusion lessens ischemic injury. We found for the first time that such postconditioning with a series of mechanical interruptions of reperfusion significantly reduces ischemic damage. Focal ischemia was generated by permanent distal middle cerebral artery (MCA) occlusion plus transient bilateral common carotid artery (CCA) occlusion. After 30 secs of CCA reperfusion, ischemic postconditioning was performed by occluding CCAs for 10 secs, and then allowing for another two cycles of 30 secs of reperfusion and 10 secs of CCA occlusion. Infarct size was measured 2 days later. Cerebral blood flow (CBF) was measured in animals subjected to permanent MCA occlusion plus 15 mins of bilateral CCA occlusion, which demonstrates that postconditioning disturbed the early hyperemia immediately after reperfusion. Postconditioning dose dependently reduced infarct size in animals subjected to permanent MCA occlusion combined with 15, 30, and 60 mins of bilateral CCA occlusion, by reducing infarct size approximately 80%, 51%, and 17%, respectively. In addition, postconditioning blocked terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling-positive staining, a marker of apoptosis, in the penumbra 2 days after stroke. Furthermore, in situ superoxide detection using hydroethidine suggested that postconditioning attenuated superoxide products during early reperfusion after stroke. In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment.     

Branches of the splenic artery and splenic arterial segments

In 200 adult autopsy specimens, the arterial supply to the pancreas and spleen was studied radiologically and by manual dissection. The splenic artery divided into two or three lobar arteries, which supplied its corresponding lobe; each lobar artery subsequently divided into two to four lobular branches. Six to twelve lobular branches were observed entering the splenic substance at the hilum. Lobar arteries did not anastomose with each other, hence, the lobes of the spleen are also termed segments. The lobules, however, were not found to be independent segments and the arteries of one lobule anastomosed with those of other lobules. The branching pattern of the splenic artery varied from one specimen to another, so much so that a prevailing pattern could not be identified. Polar arteries, particularly to the superior pole, arose quite proximal to the hilum in 51% of cases and were occasionally missed. In 45% of males and 40% of females, the posterior gastric artery arose from about the middle of the splenic artery. The splenic artery was not found to be tortuous in fetuses, newborns, and young children. Tortuosity was seen in only 10% of adults; thus, the characteristic tortuosity of the splenic artery appears to develop with age.     

DNA damage in cytologically normal urothelial cells of patients with a history of urothelial cell carcinoma

In order to determine if patients with a history of previous urothelial cell carcinoma (UCC) but with current normal urinary cytology have DNA damage in urothelial cells, the single-cell gel electrophoresis (comet) assay was conducted with cells obtained by urinary bladder washings from 44 patients (28 with a history of previous UCC). Increased DNA damage was observed in cytologically "normal" urothelial cells of patients with a history of UCC when compared with referents with no similar history and after correcting the data for smoking status and age (P < 0.018). Increased DNA damage also correlated with the highest tumor grade, irrespective of time or course of the disease after clinical intervention (Kendall tau correlation, 0.37, P = 0.016). Moreover, aneuploidy, as assessed by DNA content ratio (DCR; 75th/25th percentile of total DNA fluorescence of 50 comets/patient) was unaltered by smoking status, but increased with UCC grade: 1.39 +/- 0.12 (median +/- 95% confidence interval; referents); 1.43 +/- 0.11 (Grade I UCC; P = 0.264, against referents); 1.49 +/- 0.16 (Grade II UCC; P = 0.057); 1.57 +/- 0.16 (Grade III UCC; P = 0.003). Micronucleated urothelial cells (MNC) were also scored on Giemsa-stained routine cytological smears and were found not to correlate with DNA damage or DCR. MNC frequencies were higher for patients with a history of UCC and/or smoking than referents with neither history, but there was no statistical difference between groups. Taken together, these results suggest that the normal-appearing urothelium of patients resected for UCC still harbor genetically unstable cells.     

Sleep deprivation effects on growth factor expression in neonatal rats: a potential role for BDNF in the mediation of delta power

The sleeping brain differs from the waking brain in its electrophysiological and molecular properties, including the expression of growth factors and immediate early genes (IEG). Sleep architecture and homeostatic regulation of sleep in neonates is distinct from that of adults. Hence, the present study addressed the question whether the unique homeostatic response to sleep deprivation in neonates is reflected in mRNA expression of the IEG cFos, brain-derived nerve growth factor (BDNF), and basic fibroblast growth factor (FGF2) in the cortex. As sleep deprivation is stressful to developing rats, we also investigated whether the increased levels of corticosterone would affect the expression of growth factors in the hippocampus, known to be sensitive to glucocorticoid levels. At postnatal days 16, 20, and 24, rats were subjected to sleep deprivation, maternal separation without sleep deprivation, sleep deprivation with 2 h recovery sleep, or no intervention. mRNA expression was quantified in the cortex and hippocampus. cFos was increased after sleep deprivation and was similar to control level after 2 h recovery sleep irrespective of age or brain region. BDNF was increased by sleep deprivation in the cortex at P20 and P24 and only at P24 in the hippocampus. FGF2 increased during recovery sleep at all ages in both brain regions. We conclude that cortical BDNF expression reflects the onset of adult sleep-homeostatic response, whereas the profile of expression of both growth factors suggests a trophic effect of mild sleep deprivation.     

Electrodermal Responsivity in Young Hypotensive and Hypertensive Men

Electrodermal responses were recorded during the presentation of 16 moderately intense (1000 Hz, 90dB) tones in three groups of young men: borderline hypertensives (138/79 mmHg), normotensives (112/65 mmHg), and hypotensives (104/63 mmHg). Electrodermal response habituation was measured as a decline in response over trials, number of trials to a response criterion of three successive nonresponses, and number of inversions of response amplitude (larger responses following smaller responses) in the stimulus sequence. Habituation was fastest in hypotensives. Nonspecific electrodermal responses at rest and during tone presentations were most frequent in borderline hypertensives, least frequent in the hypotensive group, with the normotensive group falling in between. There were no significant differences in electrodermal level. The rapid habituation rate in hypotensives is discussed in terms of cursory information processing associated with impulsive behaviour. The higher nonspecific electrodermal activity in borderline hypertensives is interpreted to indicate increased sympathetic nervous system activity.     

Community violence exposure and delinquent behaviors among youth: The moderating role of coping

This study examines the moderating roles of guardian and peer support and behavioral coping strategies on the relations between youths' community violence exposure and their delinquent behavior. A sample of 667 public school sixth‐graders in a large inner‐city school district, and their parents or guardians, were interviewed to assess youths' recent exposure to community violence, their delinquent behavior, and proposed moderating variables. Support from guardians buffered the relation between girls' victimization by community violence and delinquency. Support from peers buffered the effects of witnessing community violence on delinquent behavior of boys, but it amplified the effects of victimization for both girls and boys. Avoidant coping behavior buffered the effect of victimization on delinquency for boys but unexpectedly amplified the effect of witnessing violence on delinquency for girls. For both genders, confrontational coping strategies amplified the impact of victimization on delinquency and, for boys only, amplified the impact of witnessing violence as well. Controls were imposed for variables expected to influence the relation between exposure and delinquency, such as ethnicity, family violence, delinquent behavior of friends, and recruitment cohort. Suggestions for future research and implications for intervention are discussed. © 2003 Wiley Periodicals, Inc. J Comm Psychol 31: 489–512, 2003.     

Predictors of Caregiver Participation in an Engagement Strategy to Increase Initiation into a Family-Based Preventive Intervention

Previous studies have shown that engagement strategies can help increase enrollment and initiation of families in evidence-based preventive programs under natural service delivery settings. However, little is known about factors that predict completion of these engagement strategies. This study aimed to examine predictors (i.e., perceived need, perceived barriers, and sociocultural context) of caregiver participation in an evidence-based engagement call strategy. This call was expected to increase initiation into a school-based, family-focused prevention program. In addition, this study examined engagement call completion as a predictor of program initiation among already enrolled families. Participants included ethnically diverse families recruited from three Title I schools (n = 413) who were randomized to receive the prevention program. Results showed that interparental conflict—an indicator of perceived need—was associated with an increased likelihood of completing the engagement call. Furthermore, caregivers from low-socioeconomic status (SES), foreign-born, Spanish-speaking, Hispanic families were more likely to complete the call relative to those from low- and mid-SES, US born, English-speaking, ethnically diverse families. Importantly, engagement call completion was associated with an increased likelihood of program initiation. These findings provide limited support that families with higher perceived needs are more likely to participate in an evidence-based engagement call strategy. Results suggested that the call strategy provides a promising way to reduce attrition from family prevention programs, which is commonly observed between enrollment and initiation. Project Number: R01 DA035855; Date of Registration: 06/15/2014.

     

Gene therapy using viral vectors for acute neurologic insults

Enormous knowledge has emerged concerning the cellular and molecular events underlying necrotic neuron death after seizure, hypoxia-ischemia, or hypoglycemia. This has allowed the design of rational therapies to protect neurons at such times. One of the most exciting arenas of such interventions is the use of viral vectors to deliver neuroprotective genes. This review considers the progress in this nascent discipline. Neuroprotection has been demonstrated against a variety of in vitro and in vivo rodent models of necrotic insults with vectors overexpressing genes that target various facets of injury. These have included the energetic components, calcium excess, accumulation of reactive oxygen species, protein malfolding, inflammation, and triggering of apoptosis (i.e., programmed cell death) in a subset of cells. A number of caveats, subtleties, and pressing questions concerning this literature then are considered. These include whether these gene therapy interventions actually prevent, rather than merely delay, neuron death; the extent to which the effects of such vectors on neuronal cell biology is actually understood; the potential adverse effects of the use of such vectors; and whether sparing a neuron from death with one of these interventions spares function as well. Finally, we consider the likelihood of such gene therapy becoming relevant to clinical neurology in the near future.