Is implementing a post-lunch nap beneficial on evening performance, following two nights partial sleep restriction?

We have investigated the effects that partial-sleep-restriction (PSR0, 4-h sleep retiring at 02:30 and waking at 06:30 h for two consecutive nights) have on 07:30 and 17:00 h cognitive and submaximal weightlifting; and whether this performance improves at 17:00 h following a 13:00 h powernap (0, 30 or 60-min). Fifteen resistance-trained males participated in this study. Prior to the experimental protocol, one repetition max (1RM) bench press and back squat, normative habitual sleep and food intake were recorded. Participants were familiarised with the testing protocol, then completed three experimental conditions: (i) PSR with no nap (PSR0); (ii) PSR with a 30-min nap (PSR30) and (iii) PSR with a 60-min nap (PSR60). Conditions were separated by 7 days with trial order counterbalanced. Intra-aural temperature, Profile of Mood Scores, word-colour interference, alertness and tiredness values were measured at 07:30, 11:00, 14:00, 17:00 h on the day of exercise protocol. Following final temperature measurements at 07:30 h and 17:00 h, participants completed a 5-min active warm-up before performing three repetitions of left and right-hand grip strength, followed by three repetitions at each incremental load (40, 60 and 80% of 1RM) for bench press and back squat, with a 5-min recovery between each repetition. A linear encoder was attached perpendicular to the bar used for the exercises. Average power (AP), average velocity (AV), peak velocity (PV), displacement (D) and time-to-peak velocity (tPV) were measured (MuscleLab software) during the concentric phase of the movements. Data were analysed using general linear models with repeated measures. The main findings were that implementing a nap at 13:00 h had no effect on measures of strength (grip, bench press or back squat). There was a main effect for time of day with greatest performance at 17:00 h for measures of strength. In addition to a significant effect for "load" on the bar for bench press and back squat where AP, AV, PV, D values were greatest at 40% (P < 0.05) and decreased with increased load, whereas tPV and RPE values increased with load; despite this no interaction of "load and condition" were present. A post lunch nap of 30- and 60-minute durations improved mood state, with feelings of alertness, vigour and happiness highest at 17:00 h, in contrast to confusion, tiredness and fatigue (P < 0.05), which were greater in the morning (07:30 h). The word-colour interference test, used as an indicator of cognitive function, reported significant main effect for condition, with the highest total test score in PSR60 condition (P = 0.015). In summary, unlike strength measures the implementation of a 30 or 60-minute nap improved cognitive function when in a partially sleep restricted state, compared to no nap.

Lipiodol avidity of neuroendocrine liver metastases.

AIMS: Lipiodol has been shown to concentrate in most hepatocellular carcinomas as well as in some liver metastases, including those of neuroendocrine origin. Our aim was to determine the proportion of neuroendocrine liver metastases that take up lipiodol and to identify tumour characteristics that predict avidity. METHODS: Avidity was assessed in 12 patients with neuroendocrine liver metastases by performing an abdominal CT scan immediately after selective hepatic arterial injection of 5 ml of unlabelled lipiodol and this was correlated with number and size of lesions as well as angiographic and plain CT scan features. RESULTS: In seven patients the tumours displayed lipiodol avidity (four solitary, three multiple); five patients had non-avid lesions (all multiple). A large dominant liver tumour was the only predictor of avidity (mean diameter of largest lesion 9 cm vs. 3 cm for patients with non-avid tumours: P=0.01). Avidity was not related to vascularity or CT density of lesions. CONCLUSIONS: Although this is a small study, it would appear that approximately 50% of neuroendocrine liver metastases selectively concentrate lipiodol, which could have implications for targeted cancer therapy.

Pulmonary embolism in patients with intermediate probability lung scans: diagnosis with Doppler venous US and D-dimer measurement.

PURPOSE: To test the usefulness of lower limb Doppler venous compression ultrasound (US) and serum D-dimer measurements in diagnosis of pulmonary embolism in patients in whom ventilation-perfusion (V-P) scans indicate intermediate probability of pulmonary embolism. MATERIALS AND METHODS: V-P scanning, pulmonary angiography, US, and D-dimer measurements were performed in 36 patients without known deep venous thrombosis but with intermediate probability of having a pulmonary embolism. RESULTS: Pulmonary angiography demonstrated pulmonary embolism in 15 (41%) of 36 patients. US demonstrated deep venous thrombosis in only two patients, both with pulmonary embolism. Sensitivity of US was only 13%, but specificity was 100%. Five (14%) of the 36 patients had normal (< 220 micrograms/L) D-dimer levels; none of the five had pulmonary embolism. Sensitivity and specificity of D-dimer values were 100% and 16%, respectively, with a negative predictive value of 100%. CONCLUSION: Combined D-dimer measurement and US were helpful in correctly diagnosing pulmonary embolism in only seven (20%) of 36 patients. Pulmonary angiography is still required to diagnose pulmonary embolism in the majority of patients.

Percutaneous ultrasound guided cholecystostomy with double bubble catheter.

We have used a prototype double bubble cholecystostomy catheter in four very ill patients. This has been done under local anaesthetic using a Seldinger technique, ultrasound guidance, and a trans-peritoneal approach to the gallbladder. The catheter provides drainage, cholangiography, and is intended to allow instrumentation of the biliary tract at a later stage.

Cochlear morphology of the audiogenic-seizure susceptible (AGS) or genetically epilepsy prone rat (GEPR).

The organ of Corti (OC) of the genetically epilepsy prone rat (GEPR), a strain which is highly susceptible to audiogenic seizures (AGS), was examined by means of the scanning electron microscope (SEM). Ten female GEPRs (seizure intensity score of 2 or 3) and 10 female control rats (seizure intensity score of 0) were used in this study. (Seizure intensity was scored on an ascending scale of 0-9; 0 being no seizure (Jobe et al., 1973).) Each rat was perfused with buffered glutaraldehyde and the temporal bones fixed for one week in formalin. After decalcification, staining and microdissection, the entire OC was prepared for scanning electron microscopy (SEM). The GEPR organ of Corti contained several morphological differences when compared with controls. 1) In all 10 GEPRs, the headplates forming the top of the tunnel of Corti exhibited some form of structural abnormality. 2) Five animals had some form of stereocilia aberration of the inner (IHC) and/or outer (OHC) hair cells. 3) In 4 animals, significant numbers (10-15%) of IHC's were missing in large segments of all cochlear turns. 4) In 2 GEPRs, all OHC's were absent from the middle turn to the hook. In these 2 animals, IHC's were present in the upper middle turn but became less numerous and completely absent in the basal turn and hook. 5) One set of cochleas had 1000 more OHC's than had those of control rats. Since GEPRs are genetically susceptible to seizures, the preceding cochlear abnormalities are probably genetically-induced developmental defects. It is likely that the abnormally long stereocilia, mis-shaped stereocilia and deficits in hair cell populations are a consequence of the distorted headplates. The elongated stereocilia could be a compensatory attempt to contact the tectorial membrane during development. The mis-shaped stereocilia and hair cell deficits could represent a failure of compensatory mechanisms. The cochlear abnormalities may play a role in both susceptibility and intensity of audiogenic seizures.

Ototoxic drugs and noise.

Drugs that produce tinnitus can be subdivided into those which produce temporary or permanent hearing loss and those which apparently do not cause any hearing loss. The tinnitus occurring with drugs of the first group is probably secondary to the hearing loss. However, most of the drugs that produce tinnitus without an accompanying hearing loss probably do so because of their effect on biogenic amines in the central nervous system and/or as an extension of their proconvulsant side-effects. A pre-existing cochlear impairment is the underlying factor in most patients who experience tinnitus. Not only can ototoxic drugs or high levels of noise produce cochlear impairment but the interaction of the two can place humans in more jeopardy than when exposed to either agent alone. Chloramphenicol has little ototoxic potential when administered systemically in humans. However, our studies show that when chloramphenicol is combined with noise exposure in rats, considerably more cochlear damage results than from the noise alone (chloramphenicol alone does no produce any cochlear damage). We are presently conducting more detailed studies of this ototoxic interaction to determine whether it occurs with other antibiotics (such as erythromycin) which are also commonly considered to have minimal ototoxicity.

A comparison of cochlear microphonics and N1 in audiogenic-seizure-susceptible and control rats.

Although numerous studies have shown that cochlear impairment exists in audiogenic-seizure (AGS)-susceptible mice, there is only one report of cochlear potentials obtained from AGS-susceptible rats. To investigate the hypothesis that cochlear impairment also exists in AGS rats, cochlear microphonics (CM) and the primary afferent activity of the auditory division of the eighth cranial nerve (N1) were studied in AGS rats. AGS rats were obtained from the Veterans Administration Medical Center (Shreveport, La.) colony of Sprague Dawley derived animals, and control rats were obtained from Sprague Dawley, Inc. Two school bells ringing simultaneously were used to produce a sound of approximately 115 dB (AGS test stimulus). Exposure to the AGS test stimulus was once per week for three consecutive weeks. Chloramphenicol was used to treat the frequent otitis media found in the colony of AGS rats. Two categories of AGS-susceptible and control rats were studied: (1) rats exposed to the AGS test stimulus and chloramphenicol regimen; and (2) rats not receiving these treatments. All rats were anesthetized with i.p. Dial-Urethane and prepared for cochlear round window recording. Cochlear microphonics were recorded in response to a click stimulus. A significant decrease in cochlear sensitivity was seen in both groups of AGS rats when compared to appropriate controls as reflected by a 25-35 dB shift in all CM and N1 input-output functions. These results support the hypothesis that a functional cochlear impairment exists in the AGS rat.