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Childhood overweight and obesity have emerged as a public health concern in sub-Saharan Africa. We conducted a systematic review with the aim to examine the association between socio-economic status (SES) and overweight or obesity among school-age children in sub-Saharan Africa. In March 2014 we searched five electronic databases for reports which presented cross-sectional data on prevalence levels of overweight or obesity stratified by SES groups among school-age children in sub-Saharan Africa. We used a random-effect model to pool the relative indexes of inequality of the association from the individual studies. In total, 20 reports satisfied the inclusion criteria providing results of 21 datasets. The risk of overweight or obesity in children from highest SES households was 5.28 times as high as that of children from lowest SES households (95% confidence interval [CI] 2.62 to 10.66). On subgroup analysis, this association was statistically significant for household income and composite SES measures but not for parental educational attainment and occupation type. Similarly, the risk of overweight or obesity in children attending affluent (private) schools was 15.94 times as high as that of children going to either urban or rural public schools (95% CI 5.82 to 43.68). The magnitude of the association tended to be stronger for area or school-type compared with composite measures. In summary, children from higher SES households and those attending private schools tended to be overweight and obese.

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Over the past decade, the role of anatomical teaching in the undergraduate medical curriculum has changed considerably. At some medical schools, active dissection of cadaveric specimens is gradually being replaced by prosection-based methods and other resources such as e-learning. Warwick Medical School has recently obtained a large collection of plastinated prosections, which replace wet cadaveric specimens in undergraduate anatomy teaching. The aim of this study was to examine students' views on the use of plastinated prosections for their anatomical learning. A mixed method approach was employed using a questionnaire and focus group for data collection. The questionnaire was completed by 125 first-year medical students (response rate 68%). The majority of students (94%) rated plastinated prosections as a valuable resource for their anatomical learning. Various features of the specimens were highlighted, such as the detailed view of relevant anatomy, appreciation of relations between structures, and visualization of anatomy in real life. However, learning on plastinated prosections was perceived to be compromised because of limitations in terms of tactile and emotional experience. We conclude that plastinated prosections are an adequate resource for the early stages of undergraduate training, but that the learning experience may be further enhanced by providing opportunity for the study of wet cadaveric material.

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OBJECTIVE: To report outcomes for the first known cochlear implantation procedures in two patients with Brown-Vialetto-Van-Laere syndrome. PATIENTS: Two adult patients (a brother and sister) with post-lingual sensorineural deafness associated with Brown-Vialetto-Van-Laere syndrome. The female patient presented with a milder form of the syndrome. INTERVENTION: Cochlear implantation. MAIN OUTCOME MEASURE: Post-implantation speech discrimination scores. RESULTS: Auditory evoked potential testing suggested pathological changes in both patients' cochleae, auditory nerves, brainstem and (probably) central auditory pathways. In the male patient, despite implantation of the better ear, the Bamford-Kowal-Bench sentence score was zero at 21 months post-implantation. In the female patient, Bamford-Kowal-Bench sentence scores at six months post-implantation were 25 per cent in quiet and 3 per cent in noise. CONCLUSION: These poor clinical outcomes appear to be related to retrocochlear and probable central auditory pathway degeneration.

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Numerous techniques have been described for the correction of gynaecomastia, and the surgeon is faced with a wide range of excisional and liposuction procedures. There is a paucity of literature describing an integrated approach to the management of this condition and the roles of the different treatment modalities. A review of all gynaecomastia patients operated on by one surgeon over a 2-year period was undertaken. Patient satisfaction was assessed using a linear analogue scale with a maximum score of 10. In total, 48 breasts in 29 patients were treated--31 breasts by liposuction alone (19 by conventional liposuction, 12 by ultrasound-assisted liposuction), eight breasts by liposuction and open excision, and nine breasts by liposuction, open excision and skin reduction (concentric or Lejour mastopexy). There were no early postoperative complications, such as haematoma, seroma or infection, and 91% of patients were very satisfied (score: 8-10) with their cosmetic outcome. The most frequently encountered complication was a residual subareolar lump (five breasts), all in patients treated by conventional liposuction alone. In order to avoid the common complication of an uncomfortable residual subareolar nodule, the threshold for open excision in patients undergoing conventional liposuction should be low. Ultrasound-assisted liposuction extends the role of liposuction in gynaecomastia patients. Although skin excess remains a challenge, it can be satisfactorily managed without excessive scarring. A practical approach to the surgical management of gynaecomastia, which takes into account breast size, consistency, skin excess and skin quality, is proposed.

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We have demonstrated previously that central noradrenergic mechanisms, especially postsynaptic alpha-1 receptors, are critically involved in the regulation of cataplexy, a pathological manifestation of rapid eye movement sleep atonia in narcolepsy. However, it has been shown recently that alpha-1 receptors constitute a heterogeneous population of binding sites, which is encoded by several distinct genes. In light of these findings, we investigated the possibility that the effect of alpha-1 compounds on cataplexy found in our previous study is mediated more specifically by certain alpha-1 receptor subtypes than by other subtypes. We therefore examined the effects of eight selective alpha-1 antagonists and five agonists on canine cataplexy and compared these with the affinities of the same compounds for the canine central alpha-1a and alpha-1b subtypes. The affinities of the compounds for the alpha-1 receptor subtypes were assessed by using [3H]prazosin receptor binding in combination with a 5-methylurapidil (an alpha-1a selective ligand) mask. Six of the eight alpha-1 antagonists tested exacerbated canine cataplexy, whereas all five agonists tested suppressed cataplexy. Furthermore, the potency (ED50 values) of the compounds on cataplexy significantly correlated with the affinity of the compounds for the alpha-1b binding site. These results are consistent with our earlier implication of the alpha-1 receptor mechanisms in the control of cataplexy and further suggest a specific involvement of the alpha-1b receptor subtype in these mechanisms.

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alpha 2-Receptors in the canine brain were pharmacologically characterized using [3H]yohimbine binding. Competition studies revealed a single class of binding sites in frontal cortex but two distinct subtypes in nucleus caudatus. The role of central alpha 2-receptors in narcolepsy was investigated in 5 normal and 5 narcoleptic Doberman pinschers. Scatchard analysis of [3H]yohimbine binding in different brain areas revealed an increase in the number of alpha 2-binding sites limited to the locus coeruleus. This suggests that altered autoinhibition of norepinephrine release may be associated with the narcoleptic symptomatology.

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The effects of intravenous administration of prostaglandins (PGs) were investigated in genetically narcoleptic Doberman pinschers. The treatment of narcoleptic dogs with PGE2 and PGE2 methyl ester, but not PGD2 and PGD2 methyl ester, induced a dose-dependent reduction of canine cataplexy, a dissociated manifestation of rapid-eye-movement sleep. The effect was specific and not associated with any change in other behavior. Furthermore, the effect was long-lasting (up to 2 hr) and could not be explained by the acute cardiovascular changes seen after intravenous PG administration. PGE2 methyl ester, a lipophilic derivative of PGE2 with more central penetration than PGE2, was 4 times more potent than PGE2. These results indicate that PGE2 modifies cataplexy through a central effect and suggest that this prostaglandin may play a role in rapid-eye-movement sleep regulation.

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This study was designed to re-examine the circadian profiles of dopamine, noradrenaline and adrenaline in the plasma and to investigate the influence of daytime noise stress on these profiles. Twelve subjects participated in two experimental series of 60 h; during one they were exposed to 85 dB(A) industrial noise from 9:00 to 21:00 h. Blood samples were taken for a period of 24 h at 20 min intervals and the plasma levels of the free and the sulfoconjugated catecholaminergic compounds were simultaneously measured. A significant (p less than 0.001) circadian rhythm was found for free noradrenaline, free adrenaline and conjugated dopamine. Noise stress significantly increased (p less than 0.001) free adrenaline levels during the first 6 h of exposure and lowered (p less than 0.001) free noradrenaline values during the whole time of exposure; dopamine did not respond. It was concluded that strong noise load has effects on the sympatho-adrenomedullary system but the actual release pattern of each catecholaminergic metabolite is controlled by separate determinants.

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This study examines the influence of daytime noise load on the spontaneous EEG activity during wakefulness and sleep. Twelve healthy male subjects participated in two experimental series, each consisting of three consecutive nights and the two days in between. EEG, EOG, EMG, ECG and respiration were continuously recorded. During one series from 9:00 to 21:00 h the subjects were exposed to 85 dB(A) industrial noise. Direct effects of the noise exposure were a slight blockade of the alpha and theta activity; towards the evening, when self-estimated tiredness was high, increased alpha and beta power were found (p less than .01). Aftereffects on subsequent undisturbed night sleep were a reduction in REM sleep (p less than .001), shortened sleep cycles (p less than .01) and an increase in slow wave sleep during the 2nd sleep cycle (p less than .05). These results are interpreted as signs of strained wakefulness and intensified fatigue, as disturbance of sleep processes and as an intensified need for recovery.

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The present study examines the effects of auditory stress on the plasma levels of pituitary hormones and cortisol. Each of twelve healthy male subjects participated in two experimental series; during one of them they were exposed to 85 dB(A) industrial noise from 9:00 to 21:00 h. Blood samples were taken by an indwelling venous catheter for 24 h at intervals of 20 min from 8:00 to 8:00 h. The plasma levels of ACTH, growth hormone, prolactin, oxytocin, vasopressin and cortisol were determined. In all subjects except one noise stress affected the profiles of the pituitary hormones but the responses were interindividually different. The oxytocin level was significantly elevated (p less than .01), ACTH also responded but less clearly, whereas the other hormones reacted only in individual cases. During the subsequent night sleep only PRL concentrations were elevated above the baseline plateau in several subjects. It was concluded that in humans the pituitary responses to noise stress are highly individual.

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The effects of strong daytime noise stress on subsequent undisturbed night sleep were studied in six male volunteers. They slept for seven consecutive nights in the laboratory, two nights being preceded by an 8 h exposure to 83 dB (A) pink noise. Continuously during all nights EEG, EOG, EMG, ECG and respiration were recorded. Additionally, during five nights, blood samples were taken every 30 min by an indwelling venous catheter for the determination of ACTH, hGH, PRL, TRP, 5-HT and 5-HIAA. After daytime noise load, increased sleep stage 4 stability, partly elevated hGH and PRL levels and decreased levels of the metabolites of the serotonergic system were found. This result may be explained by the assumption that high daytime noise stress is an additional load for the CNS which demands an intensification of recovery processes during the sleep of the subsequent night.

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The effects of daytime noise on recovery processes during subsequent undisturbed night sleep were studied in six healthy men (21-27 years), exposed to 80 dB (A) pink noise 8 h per day for 2 days. Sleep EEG, ECG, and respiration were recorded in the laboratory for five consecutive nights: two baseline nights, two nights following noise stimulation, and again one baseline night. Additionally questionnaire data were collected, reflecting a subjective impairment of the recovery function of sleep after noise exposure. EEG sleep data of the first post-noise night showed an increase in slow wave sleep with a simultaneous decrease in stage 2 sleep. During the second post-noise night these changes were less prominent. Three subjects additionally showed an instability in the sleep course coinciding with elevated heart and respiration rates. However, altogether the autonomic parameters were not clearly affected by the noise exposure. The findings support the assumption that strong daytime noise may interfere with subsequent sleep processes.

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Respiration, heart rate, cutaneous blood flow, and electroencephalogram (EEG) reactions to long-term intermittent noise exposure were recorded from 13 volunteers (20-29 yr) with normal hearing and vegetative reactivity. They received daily within 1 h 12 noise stimuli (16 s 100 dB (A) white noise) for 10 or 21 days, respectively. Most subjects reported partial subjective adaptation to the noise. Heart rate adapted within a session but did not change considerably during successive days. Vascular responses did not change during one session but diminished mainly during the first 10 days. Noise responses in the EEG remained constant, but a decrease in vigilance occurred during the whole experimental series. Respiration responses were unpredictable and showed no trend within the sessions. It was concluded that certain physiological responses adapt to loud noise but that the time course of adaptation is different. Therefore a general statement about physiological noise adaptation is not possible.

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