3.2.2. Cumulative AUC Results of cumulative area under the curve (AUC) for the active moiety were calculated by the trapezoidal method (1), are shown in Table 2: AUC(t1−t2)=[(C1+C2)2]×(t2−  t1). (1) Table

2 AUC for Risperidone PLGA microspheres. In (1) “t” represents time in hours while “C” denotes serum concentration of Risperidone (ng/mL). Results from AUC calculations indicate that the cumulative AUC values through 15 days for Formulations A and B were remarkably similar (1110 and 1159ng×mL/day, respectively). Both formulations, administered at 20mg/kg dose, were prepared using the fast degrading 50:50 PLGA copolymer had a small particle size and high loading but a difference Inhibitors,research,lifescience,medical of ~ 10kDa in molecular weight. In vivo, they exhibited similar burst levels Inhibitors,research,lifescience,medical followed by a brief trough with noticeable levels through 15 days. Though the formulations exhibited a high initial burst, more than 98% of the cumulative AUC was contributed by drug encapsulated in the polymer matrix with initial burst amounting to a mere 1.4–1.8% of the total profile. Cumulative AUC levels for Formulations C and D, dosed at 40mg/kg, are presented in Table 2. Values of 1821 and 1522ng×mL/day were obtained for Formulations C and D, respectively. As expected,

values are higher than those observed with Formulations A and B. With Formulation C, initial burst Inhibitors,research,lifescience,medical contributed nearly 2% to the cumulative AUC whereas, with Formulation D, the value was smaller (1%). Once again, these data suggest that most of the in vivo activity was due to drug incorporated in the polymer matrix Inhibitors,research,lifescience,medical that was available for release in a sustained fashion. In contrast, the marketed formulation does not exhibit initial burst and supplementation with oral

therapy is needed to achieve pharmacologically effective levels of the drug [27], suggesting that drug encapsulated in Inhibitors,research,lifescience,medical the polymer matrix was solely responsible for in vivo activity. The following observations were noted upon analyzing the cumulative AUC values of Formulations A–D. The contribution of initial burst towards the total AUC for all formulations was minor (equal to or less than 2%). Risperidone encapsulated in the PLGA polymer was responsible for over 98% of the cumulative AUC in vivo. The cumulative AUC obtained with Formulations C and D was nearly 1.5–1.7 times greater than that observed with Formulations A and B. These Anacetrapib results suggest that proper choice of a copolymer and molecular weight will enable customization of drug release profiles from microsphere dosage forms of Risperidone. 3.2.3. Selection of Dosing Regimen The objective of the current study was to develop and evaluate PLGA microspheres of Risperidone that offered initial and maintenance levels of the drug for extended intervals. To predict the in vivo profile of Risperidone PLGA microspheres for a prolonged duration, plasma levels through 4 doses for all four formulations were simulated using the superposition principle.

Finally, an additional test was added for the interaction term.

Therefore, for a Bonferroni correction on the P-values, we used P = 0.05/(2 × (4 + 4) + 1) = 0.003 as a threshold of significance. We applied the false discovery rate (FDR) to quantify uncertainty across the citation multiple hypotheses tested in the three single marker tests and the multiple sellckchem haplotype tests. The FDR q-value was therefore calculated, which denotes the expected proportion of false negatives among multiple findings. Based on the single marker and haplotype association results, the q-value Inhibitors,research,lifescience,medical for each of these nonindependent tests was calculated using the step-up procedure (Benjamini and Hochberg 1995). The q-value calculated in this way has been shown to retain desirable properties for multiple related tests in genetic association studies and can be intuitively interpreted in terms of posterior error probability. Statistical power to detect associations was estimated using the Inhibitors,research,lifescience,medical Genetic Power Calculator (http://pngu.mgh.harvard.edu/purcell/gpc/). Thus, we determined that the SZ sample (N = 79) Inhibitors,research,lifescience,medical had 41% power to detect a risk allele with 20% frequency

using an additive genotype model at alpha of 0.003. The BD sample (N = 109) had 52% power using the same criteria. The entire sample had 67% power. Results Single markers analysis Three PIK3C3 gene variants (two SNPs: rs3813065 and rs8095411 and one microsatellite, a CA-repeat) and one BDNF gene variant (rs6265) were analyzed. Single marker Inhibitors,research,lifescience,medical association analysis detected a significant difference in genotype and allelic distributions of the PIK3C3 -432C>T (rs3813065) between BD patients and controls (P = 0.025, P = 0.028, respectively) (Table 2). This difference was mainly accounted for by lower frequencies

of CT genotype and T-allele in BD than in controls. However, this association did not hold after Bonferroni correction for multiple testing. No other association was significant either for BDNF or PI3KC3 variants (Table 2). For the microsatellite variant, genotyping analysis revealed Inhibitors,research,lifescience,medical length polymorphisms in this (CA)n repeat, with n ranging from 11 to 18. The most frequent alleles were (CA)13 (56.4%), (CA)16 (18.8%), (CA)18 (14.9%), (CA)12 (3.2%), (CA)17 (3.2%), (CA)14 (2.1%), and (CA)11 (1.4%) (Information Cilengitide not displayed), but no association was significant either for BD or SZ. Table 2 Allele and genotype distribution in SZ, BD, and control subjects for three polymorphisms of BDNF and PI3KC3 genes Haplotype analysis Omnibus tests comprising the three polymorphic markers, that is microsatellite, rs3813065, and rs8095411, from the 5′ to the 3′ end of the PIK3C3 gene, showed significant differences in the overall haplotype distribution between controls and SZ (omnibus test: P = 0.030, X2 = 13.96, df = 6), controls and BP (omnibus test: P = 0.017, X2 = 17.02, df = 7), and controls and all patients (SZ + BP) (omnibus test: P = 0.016, X2 = 18.84, df = 8).

Mice Except where otherwise indicated, all mice in the present experiments were C57BL/6J purchased from the Animal Resources Centre in Western Australia (http://www.arc.wa.gov.au/). They were housed in a temperature-controlled environment with a 12:12 h light:dark cycle and ad libitum access to standard Inhibitors,research,lifescience,medical rodent pellets and water. All

mice were >8 weeks old (i.e., sexually mature) at the beginning of experimentation and mice in each experiment were age matched and randomly assigned to different experimental groups. Mating Mated mice were housed together in pairs continuously for 7 days in standard mouse boxes. Experimental Inhibitors,research,lifescience,medical groups were male–female pair (mated), male–male pair (control males), and female–female pair (control females). No other manipulations were performed except for standard animal husbandry (daily observation and topping up food and water when necessary), which was applied equally across experimental groups. Female mice were

checked for pregnancy Inhibitors,research,lifescience,medical at the time of killing. Environment enrichment Environment-enriched mice (males only) were housed together in groups of n = 6 mice each continuously for 14 days in nonstandard boxes measuring 27 cm wide, 42 cm long, and 16 cm deep. Mice were assigned to one of three different groups: (1) standard housed (SH) comprising litter only; (2) running wheel (RW) comprising SH plus 2 RWs (per cage); and (3) environment enriched (EE) comprising RW plus toys (ropes, ladders, tunnels, and objects) with which to explore, play, climb, Inhibitors,research,lifescience,medical hide,

and nest. EE mice were also “super-enriched” for 1 h/day 5 days (Monday–Friday)/week. Super enrichment occurred at the same time each day (usually midday during the light cycle) Inhibitors,research,lifescience,medical and comprised placement into a larger cage (46 cm wide, 69 cm long, and 40 cm deep) containing novel toys. These toys were cleaned with soapy water and 80% ethanol after each session and a different set of toys was presented at each session. These mice were returned to their EE cage Multiple myeloma following super enrichment. Tissue collection, processing, Cilengitide and immunohistochemistry Immediately following the behavioral manipulations, mice were killed with sodium pentobarbitone (100 mg/kg i.p.) and perfused intracardially with 37°C heparinized phosphate-buffered saline (PBS) followed by 4% paraformaldehyde in PBS (1.15 mL/g body weight). The brain was removed and placed in PBS containing 30% sucrose for 2–3 days. Serial promotion information sections (40 μm thick) were cut through the midbrain and pons in the coronal plane using a cryostat. Every fourth section was incubated in 5% normal goat serum and 0.

1-3 Psychosocial treatment may not “work” if the term work is narrowly applied to remission of acute episodes, control of symptoms, and prevention of relapses. However, these are not the only criteria by which an intervention for this complex disease should be judged. Schizophrenia is characteristically a multiply handicapping, chronic disorder involving selleck chemicals Ganetespib marked impairments in social role functioning (eg, as a spouse or a worker), excess rates of medical illness,

and poor quality of life. Inhibitors,research,lifescience,medical Medication is generally a necessary component of treatment, but is rarely sufficient given the diffuse nature of residual neurocognitive impairment and the history of social and functional failures that mark adolescent and adult development. Psychosocial interventions can play a critical role in Inhibitors,research,lifescience,medical a comprehensive intervention program, and are probably necessary components if treatment is viewed in the context of the patient’s overall level of functioning, quality of life,

and compliance with prescribed Inhibitors,research,lifescience,medical treatments. Current thinking suggests that, in addition to medication, effective care, and management, patients with schizophrenia require: Problem-specific psychosocial treatment Family psychoeducation Day hospital/vocational rehabilitation and educational Inhibitors,research,lifescience,medical opportunities Access to crisis counseling Easily available inpatient psychiatric care Supervised residential liging arrangements Inhibitors,research,lifescience,medical Case management to obtain entitiements and coordinate the various facets of treatment Issues to

be considered in the design and implementation of psychological treatment programs for schizophrenia overnight delivery Progress in treatment should be expected to be slow and marked by periodic disruptions and periods of regression. Consequently, it is important that treatment be long term, extending over months and years. Treatment should also be guided by concrete, short-term goals that are likely to be Carfilzomib achieved (eg, to attend day hospital at least twice a week for 1 month). While there are a number of illness characteristics that are common to most patients, there are extensive individual differences, as well as differences within the same patient over time. Thus, treatment must be tailored to the needs of each patient and adjusted as the patient changes.

29 A number of biological factors may modulate GR and add confusion to the utility of GR in observing patients with SRMs. For instance, in the prospective study by Mason and colleagues, larger tumors (> 2.45 cm) demonstrate a faster GR than smaller tumors.8 However, several retrospective analyses have failed to find a relationship between primary tumor size and GR.6,20 Kouba and colleagues Palbociclib PD 0332991 demonstrated that patients aged < 60 years Inhibitors,research,lifescience,medical had more rapidly growing tumors than those aged > 60 years.9 Finally, changes in tumor volume have been touted as more accurately reflecting

growth kinetics and the biologic aggressiveness of an SRM; however, consistent with Gompertzian growth kinetics, smaller tumors are demonstrated to grow faster volumetrically.30 A recent pooled

analysis of the AS literature demonstrated increased age, larger greatest initial tumor dimension and estimated Inhibitors,research,lifescience,medical volume, and higher linear and volumetric GR to predict metastatic progression.7 Although a number of important factors may indicate the malignant potential of an SRM, it is clear that progression to metastatic disease is exceptionally low in tumors that demonstrate slow or no GR and remain Inhibitors,research,lifescience,medical < 3 cm. Conversely, although tumors may demonstrate variable GR, the majority that progress to metastasis exceed 3 cm and often become cT1b (> 4 cm) tumors prior to or at the diagnosis of metastasis. In the retrospective literature, on average, patients undergo five to six imaging evaluations over a period of 29 to 41 months yielding an approximate average rate Inhibitors,research,lifescience,medical of imaging every 6 months.7 The majority of retrospective studies use computed tomography (CT) and magnetic resonance

imaging (MRI), with ultrasonography (US) used sparingly. The Inhibitors,research,lifescience,medical prospective study by Mason and colleagues recommended CT, MRI, or US imaging every 6 months.8 The DISSRM protocol recommends a high-quality axial image (CT or MRI with contrast) at enrollment to be followed by CT, MRI, or US every 4 to 6 months for 2 years and then every 6 to 12 months thereafter (Figure 1).10 It is our experience GSK-3 that, given conflicting reports regarding the risk of secondary malignancy,31 few patients are willing to undergo serial exposure to ionizing radiation in the form of CT scan. As GR is the main trigger for delayed intervention, we approve of serial US examination with confirmation of a change in growth with axial imaging if indicated. To better determine the aggressiveness of a new lesion, we recommend the first serial image be performed within 4 to 6 months with the caveat that GR may be exacerbated by even a small change in tumor diameter seen over a short period of time. It is known that tumor diameter measurements may vary by up to 3 mm between and among but observers.32 Consequently, wide fluctuation is seen and little prognostic value is gained by small changes in tumor diameter seen on the first surveillance image.

From the Armed Forces Institute of Pathology (AFIP) series, 6% of duodenal GISTs belong to patients with NF1 (14). Although NF1 patients can have GISTs elsewhere, the great majority occur in the small bowel in this population. The tumors are frequently multiple, small, and indolent with a low mitotic activity. However, NF1 patients can go on to develop malignant GISTs, which can be confused with malignant schwannomas if immunohistochemical

studies are not carried out. Interestingly, GISTs in NF1 patients likely have a different pathogenic pathway, since they rarely if ever have the c-kit and PDGFRA mutations as seen in selleck kinase inhibitor sporadic GISTs (16) (Table 2). Table 2 The Inhibitors,research,lifescience,medical incidence mutations of KIT and PDGFA in GIST The Carney triad includes gastric GIST, paraganglioma, and pulmonary chondroma. These GISTs are usually epithelioid. They often occur in children and have a strong female predominance (85%) and the Inhibitors,research,lifescience,medical majority are indolent, even in the setting of metastatic disease (14). Rare cases of familial GIST syndrome have been reported (14). Usually, they show autosomal dominant transmission of activating KIT or PDGFRA mutations. Patients with germline KIT or PDGFRA mutations have

shown Cajal cell hyperplasia and progression to discrete GISTs (17). Tumors are typically multiple with biological behavior Inhibitors,research,lifescience,medical that varies from indolent to malignant. These individuals also develop cutaneous hyperpigmentation and mastocytosis (18). A Inhibitors,research,lifescience,medical study using PCR for clonality analysis showed that diffuse Cajal cell proliferations seen in these patients are polyclonal, whereas the GIST tumors are monoclonal

(18). This suggests that additional genetic alterations are required before clonal expansion and malignant transformation can occur (14). The therapeutic drug of choice for unresectable, metastatic, or recurrent GISTs Inhibitors,research,lifescience,medical is imatinib, a competitive antagonist of the ATP binding site of tyrosine kinases such as KIT, platelet growth factor receptors alpha and beta, ABL, and ABL-related gene product. It causes interruption of the Entinostat downstream signaling process that leads to cellular proliferation. Ten to twenty percent of GISTs exhibit resistance to imatinib (10). This resistance has been associated with selection of mutations that in some cases interrupt the binding site of imatinib (19). Patients with the Kit exon 9 mutations often require a higher dose of imatinib, often double the starting dose recommended for exon 11 mutants (10). Resistance is also thought to result from secondary mutations in the KIT and/or PDGFRA kinase Veliparib domain. Several other inhibitors are being developed for resistant tumors. Surgery however, remains the only curative treatment for GISTs. Molecular pathology of gastric neuroendocrinetumors Gastric neuroendocrine tumors are being diagnosed with higher and higher frequency than previously reported (20).

However, in contrast to this cited case, our patients only withheld gabapentin for about 6 hours, not several days. Furthermore, the geriatric population is prone to abnormal

involuntary movements that gabapentin might be predicted to suppress. A noteworthy contribution of the present article is that it reports the efficacy of gabapentin when established drugs, namely benzodiazepines and a beta blocker, failed to deliver relief in treating akathisia. If this observation can be confirmed in a controlled trial, gabapentin might be a useful addition to the pharmacological Nutlin-3a Sigma armamentarium for treating akathisia. Footnotes Funding: This research received no specific grant from any funding agency in the public, Inhibitors,research,lifescience,medical commercial, or not-for-profit sectors. Conflict of interest statement: The authors have no conflicts of interest to declare. Contributor Information Maria A. Sullivan, Associate selleckchem Clinical Inhibitors,research,lifescience,medical Professor of Psychiatry, Columbia University and New York State Psychiatric Institute, New York, USA. Robert Wilbur, Robert Wilbur Associates, 125 West 96th Street, Suite 6K, New York, NY 10025, USA.
The

invention of chlorpromazine, a first-generation antipsychotic, in 1950 by Pierre Deniker and Jean Delay heralded Inhibitors,research,lifescience,medical a major revolution in the field of psychopharmacology. While the worrisome extrapyramidal side effects that are frequent with most of the first-generation antipsychotics were offset at least partially by the advent of second-generation antipsychotics, unfortunately these second-generation drugs have potentially serious side effects of their own. Risperidone, a benzoxazole derivative is a widely used second-generation Inhibitors,research,lifescience,medical antipsychotic drug which exerts its action via the blockade of dopamine (D2) and serotonin (5HT2) receptors in the limbic system. The commonly reported side effects related to risperidone include dizziness, nausea, weight gain, sleep disturbances,

and sexual dysfunction, which is secondary to hyperprolactinaemia. A rather rare and very much less documented [Razaq and Samma, 2004] side effect of risperidone is Inhibitors,research,lifescience,medical hypothermia: traditionally defined as a drop in core body temperature below 35°C (95°F) [Lalith et al. 2011]. Hypothermia in patients using an antipsychotic drug is a serious, unpredictable, type B adverse event frequently leading to hospital and intensive care unit (ICU) admission and sometimes even to death [van Marum et al. 2007]. While the hypothermic effects of antipsychotic drugs are less well known as opposed to the Entinostat hyperthermic effects such as malignant neuroleptic syndrome [Hägg et al. 2001], none or a few if any cases were reported with the use of risperidone in warm tropical countries in areas such as Asia. Here we report a case who has been treated for bipolar affective disorder for a considerable period of time with risperidone in a South Asian country, who went on to develop hypothermia which was reversed with the withdrawal of the offending drug.

Because of the number of patients reported in cohort series is small, we cannot estimate the true rate of treatment failures, death, and other uncommon but important adverse events in the larger population of severely envenomated patients treated with FabAV. No study reported in this series examined long-term outcomes. One prior study, reported only in abstract form, has selleck kinase inhibitor evaluated the

use of FabAV in treatment of severe crotalid envenomation[45]. In that retrospective review of poison center cases, 9.3% of crotalid envenomations were judged to be severe. Initial control was achieved in 57% of severe cases, using a mean dose of Inhibitors,research,lifescience,medical 10.5 vials of FabAV. As with any review, the conclusions of this report are limited by the available literature. To our knowledge, the largest cohort

study of Crotaline snake bite victims treated with FabAV reported 93 cases[46]. A much larger, multi-center cohort study would be extremely useful to better define the answers to unresolved management issues. Conclusion In this integrative Inhibitors,research,lifescience,medical review of the published literature, treatment of severely-envenomated crotalid snake victims with FabAV was generally associated with good short-term outcomes. Persistent, recurrent, or delayed-onset venom effects, particularly thrombocytopenia and defibrination, were observed in several patients, but no patient developed bleeding complications after receiving FabAV. FabAV therapy was well-tolerated. Inhibitors,research,lifescience,medical FabAV therapy appears to be appropriate in the management of severely envenomated crotalid snake victims. Abbreviations FabAV: Crotaline Polyvalent Immune Fab (ovine); FDA: United States Food and Drug Administration; IgG: Immunoglobulin G; INR: International normalized ratio; N/A: Not Inhibitors,research,lifescience,medical applicable; NPDS: National Poison Data System; NR: Not Reported; SSS: Snakebite selleck products Severity Score; TESS: Toxic Inhibitors,research,lifescience,medical Exposures Surveillance System; US: United States (of America). Competing interests This study was supported by a grant from Protherics, Inc, manufacturer of FabAV, to the Denver Health Hospital Authority. No author or other employee of the Denver Health Hospital Authority received direct or indirect compensation as a result of

this grant or study. Authors’ contributions All Anacetrapib authors participated in study design. SLM supervised the original library search. EJL reviewed these results and selected articles for hand review and data abstraction, which was performed by EJL and THS. SLM and JK managed the database. EJL wrote the manuscript draft. All authors read and approved the final manuscript. Pre-publication history The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1471-227X/9/13/prepub Acknowledgements This study was supported by a grant from Protherics, Inc. The study was investigator-initiated. Industry representatives did not participate in the design, execution, or writing of the study, nor did they control the decision to publish the results.

Competing interests The authors declare that they have no competing interests. Authors’ contributions AM and JS designed the study. KH and PE conducted the study. KH performed the statistical analyses and drafted the manuscript. All authors contributed substantially to the manuscript and approved its final version. Pre-publication history The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1472-684X/11/13/prepub Inhibitors,research,lifescience,medical Acknowledgements The authors wish to thank all participating patients and

GPs. For data MG132 DMSO management and support in conducting the study, the input of Andreas Rölz and the student assistants at the Department of General Practice and Health Services Research, University Hospital Heidelberg is greatly appreciated. The study was supported by a grant of the German Federal Ministry Inhibitors,research,lifescience,medical of Education and Research (grant number 01GK0601).
Although there are

differences between countries, general practitioners (GPs) often play a central role in providing palliative care. Palliative care refers to the total care that is provided for a patient and his/her family when the patient has a life-threatening disease that no longer responds to curative treatment. GPs involved in palliative care need to be skilful in communicating with patients, their families, Inhibitors,research,lifescience,medical and care-givers. Communicating with palliative care patients has been acknowledged to be more difficult than communicating with patients with less serious conditions, [1] because

communication in palliative care involves a complex mix of medical, psychosocial and spiritual issues within the context of impending death. Inhibitors,research,lifescience,medical Physicians, including GPs, often fail to communicate effectively with patients about palliative care issues, [2,3] and most GPs have never received any training in communication skills with a specific focus on palliative care at all throughout their career [4,5]. KPT-330 clinical trial Moreover, there is still no Inhibitors,research,lifescience,medical evidence-based training programme available to improve the skills of GPs and GP Trainees (GPTs) in their communication with palliative care patients. In the Palliative Care Centre of Expertise at the VU University Medical Center Brefeldin_A we designed a new training programme for GP-patient communication in palliative care. The results of our recent studies yielded three categories of factors reported to be relevant for GP-patient communication in palliative care: the availability of the GP for the patient, current issues that should be raised by the GP, and the GP anticipating various scenarios [6,7]. We used the first letters of the three categories (ACA) as an acronym for the training programme. The first objective of this paper is to describe the development of this ‘ACA training programme’ to improve GP-patient communication in palliative care.

Intuitively, it would seem logical that drugs that improve attention and concentration should also promote learning and academic achievement. Inherent in terms like “cognitive enhancers,” “smart drugs,” and “neuroenhancers” is the assumption that MPH and d-AMP enhance cognition. Major magazines such as The New Yorker have reported a trend toward growing use of mean prescription stimulants by college students for “neuroenhancement”. In fact, some students

are faking ADHD to gain access to prescription stimulant medication, which has led to a shortage of ADHD drugs such as Inhibitors,research,lifescience,medical Adderall (Mitchell 2012). Unfortunately, media reports appear to condone this behavior as 95% of articles mentioned at least one possible benefit Inhibitors,research,lifescience,medical of using prescription drugs for neuroenhancement, but only 58% mentioned any risks or side effects (Partridge

et al. 2011). Duke University recently enacted a new policy prohibiting the nonmedical use of prescription stimulants for any academic purposes (McLaughlin 2012). Students received an email stating policy changes including, “The unauthorized use of prescription medication to enhance academic performance has been added to the definition of Cheating.” In the past, the use of such drugs without a prescription was only a violation under the University’s drug policy. Oddly, the assumption that prescription stimulants are truly “cognitive enhancers” Inhibitors,research,lifescience,medical is not really questioned. Stimulants reduce hyperactivity, impulsivity, and inattention in children and adults with ADHD, so it has been assumed that these drugs enhance long-term intellectual performance. However, contrary to simple implicit assumptions found in bioethics and media discourses, there are actually Inhibitors,research,lifescience,medical only a few studies on the enhancement effects of “cognitive enhancers” in individuals without ADHD. Smith and Farah (2011) reviewed data on prescription stimulants as Nutlin-3a mw neuroenhancers from over forty laboratory studies involving healthy, nonelderly

adults. Most of the Inhibitors,research,lifescience,medical studies looked at one of three types of cognition: learning, working memory, and cognitive control. Effects of d-AMP or MPH on cognition were assessed by a variety of tasks (Table 1). A typical learning task asks subjects to memorize a list of paired words; an hour, a few days, or a week later, subjects are presented with the first words in the pairs and asked to come up with the second. In general, with AV-951 single exposures of verbal material, the studies on learning showed that no benefits are seen immediately following learning, but later recall and recognition are enhanced. Of the six articles reporting on memory performance (Rapoport et al. 1978; Soetens et al. 1993; Camp-Bruno and Herting 1994; Fleming et al. 1995; Unrug et al. 1997; Zeeuws and Soetens 2007), encompassing eight separate experiments, only one of the experiments yielded significant memory enhancement on short delays (Rapoport et al. 1978).