OBJECTIVE

To observe the gastric mucosal injury caused by hemorrhagic shock and reperfusion and to compare the effect between Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) on it.

METHODS

A model of hemorrhage/reperfusion injury was produced by Itoh method. Wistar rats were randomly divided into three groups: 0.9% sodium chloride treatment group (NS group), SEF treatment group (SEF group), and CI treatment group (CI group). Saline, SEF and CI were injected respectively. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesion area in the gastric mucosa. The degree of gastric mucosal lesions was categorized into grades 0, 1, 2, 3. Atom absorption method was used to measure the intracellular calcium content. Radioimmunoassay was used to measure the concentrations of prostaglandins.

RESULTS

IGML (%) and grade 3 (%) were 23.18+/-6.82, 58.44+/-9.07 in NS group, 4.42+/-1.39, 20.32+/-6.95 in SEF group and 3.74+/-1.56, 23.12+/-5.09 in CI group, and the above parameters in SEF group and CI group decreased significantly (IGML: SEF vs NS, t = 6.712, P = 0.000<0.01; CI vs NS, t = 6.943, P = 0.000<0.01; grade 3: SEF vs NS, t = 8.386, P = 0.000; CI vs NS, t = 8.411, P = 0.000), but the grade 0 and grade 1 damage in SEF group (22.05+/-5.96, 34.12+/-8.12) and CI group (18.54+/-4.82, 30.15+/-7.12) were markedly higher than those in NS group (3.01+/-1.01, 8.35+/-1.95; grade 0: SEF vs NS, t = 8.434, P = 0.000<0.01; CI vs NS, t = 7.950, P = 0.000<0.01; grade 1: SEF vs NS, t = 8.422, P = 0.000<0.01; CI vs NS, t = 8.448, P = 0.000<0.01). The intracellular calcium content (microg/mg) in SEF group (0.104+/-0.015) and CI group (0.102+/-0.010) was markedly lower than that in NS group (0.131+/-0.019, SEF vs NS, t = 2.463, P = 0.038<0.05; CI vs NS, t = 3.056, P = 0.017<0.05). The levels (pg/mg) of PGE(2), 6-keto-PGF(1alpha) and 6-keto-PGF(1alpha)/TXB(2) were 540+/-183, 714+/-124, 17.38+/-5.93 in NS group and 581+/-168, 737+/-102, 19.04+/-8.03 in CI group, 760+/-192, 1 248+/-158, 33.42+/-9.24 in SEF group, and the above parameters in SEF group markedly raised (PGE(2): SEF vs NS, t = 2.282, P = 0.046<0.05; SEF vs CI, t = 2.265, P = 0.047<0.05; 6-keto-PGF(1alpha): SEF vs NS, t = 6.583, P = 0.000<0.000; SEF vs CI, t = 6.708, P = 0.000<0.01; 6-keto-PGF(1alpha)/TXB(2): SEF vs NS, t = 3.963, P = 0.003<0.001; SEF vs CI, t = 3.243, P = 0.009<0.01), whereas TXB(2) level in SEF group (45.37+/-7.54) was obviously lower than that in NS group (58.28+/-6.74, t = 3.086, P = 0.014<0.05) and CI group (54.32+/-6.89, t = 2.265, P = 0.047<0.05). No significant difference was shown between NS group and CI group (PGE(2): t = 0.414, P = 0.688>0.05; 6-keto-PGF(1alpha): t = 0.310, P = 0.763>0.05; TXB(2): t = 1.099, P = 0.298>0.05; 6-keto-PGF(1alpha)/TXB(2): t = 0.372, P = 0.718>0.05).

CONCLUSIONS

Both SEF and CI could inhibit reperfusion-induced injury in gastric mucosa, but with different mechanisms. SEF could not only enhance the protective effect of gastric mucosa, but also abate the injury factors, while CI can only abate the injury factors.

Recovery after stroke is closely linked to cerebral plasticity. Magnetoencephalography (MEG) is a non-invasive technique, which allows location of cerebral cells activities. In the present work, a cohort of patients has been studied with MEG. Twelve patients with a recent ischemic or hemorragic stroke were included as soon as possible after onset of stroke. Neurologic assessment, including standard neurologic examination, functional independence measure (FIM) and Orgogozo's scale was performed for 1 year in addition to a study of the somatosensory evoked field (SEF) using a 37-channel Biomagnetometer system. No response could be recorded in five patients at the first SEF exploration. In three cases, no response was ever recorded during the study. All these patients had a bad recovery. The location of the SEF sources was always in the normal non-infarcted cortex of the postcentral gyrus. Sensory recovery seemed to be linked to the reorganization of the persistent functional cortex, which was a limiting factor for recovery. These observations confirm the experimental results obtained in animal models. After stroke it can be assumed that in the case of incomplete lesion, an intensive sensory peripheral stimulation could maximize the use of residual sensory function and then contribute to improve the sensory deficit. In case of total sensory loss other techniques have to be used, such as visual monitoring of hand activity in order to improve hand function.

The supplementary eye fields (SEF) are thought to enable higher-level aspects of oculomotor control. The goal of the present experiment was to learn more about the SEF's role in orienting, specifically by examining neck muscle recruitment evoked by stimulation of the SEF. Neck muscle activity was recorded from multiple muscles in two monkeys during SEF stimulation (100 μA, 150-300 ms, 300 Hz, with the head restrained or unrestrained) delivered 200 ms into a gap period, before a visually guided saccade initiated from a central position (doing so avoids confounds between initial position and prestimulation neck muscle activity). SEF stimulation occasionally evoked overt gaze shifts and/or head movements but almost always evoked a response that invariably consisted of a contralateral head turning synergy by increasing activity on contralateral turning muscles and decreasing activity on ipsilateral turning muscles (when background activity was present). Neck muscle responses began well in advance of evoked gaze shifts (~30 ms after stimulation onset, leading gaze shifts by ~40-70 ms on average), started earlier and attained a larger magnitude when accompanied by progressively larger gaze shifts, and persisted on trials without overt gaze shifts. The patterns of evoked neck muscle responses resembled those evoked by frontal eye field (FEF) stimulation, except that response latencies from the SEF were ~10 ms longer. This basic description of the cephalomotor command evoked by SEF stimulation suggests that this structure, while further removed from the motor periphery than the FEF, accesses premotor orienting circuits in the brain stem and spinal cord in a similar manner.

The contribution of the auditory cortex to tactile information processing was studied by measuring somatosensory evoked magnetic fields (SEFs). Three kinds of vibrotactile stimuli with frequencies of 180, 280 and 380 Hz were randomly delivered on the right index finger with a probability of 40, 20 and 40%, respectively. Twenty normal subjects participated in four kinds of tasks: a control condition to ignore these stimuli, a simple task to discriminate the 280-Hz stimulus from the other two stimuli (discrimination task for the vibrotactile stimuli, Ts task), a feedback task modified from the Ts task by adding acoustic feedback of the vibratory frequency at 1300 ms poststimulus (tactile discrimination with auditory clues, TA), and an easy version of the TA task (TA-easy) to discriminate the 280-Hz stimulus (20% target) from the 180- or 380-Hz stimuli (80% nontarget). The Ts and TA tasks required accurate perception of the vibrotactile frequencies to discriminate among the three kinds of stimuli. Under such a task demand, the post hoc auditory feedback in the TA task was expected to induce acoustic imagery for the tactile sensation. The SEFs for the nontarget stimuli were analyzed. A middle-latency component (M150/200) was specifically evoked by the three discrimination tasks. In the Ts and TA-easy tasks, the M150/200 source indicated inferior parietal cortical activities (SII area). In the TA task, 11 subjects showed activity in both the SII area and the superior temporal auditory region and increased accuracy of discrimination compared with the Ts task, in contrast with other subjects who showed activity only in the SII area and small changes in task accuracy between the Ts and TA tasks. Asynchronous auditory feedback for the vibrotactile sensation induced the auditory cortex activity in the SEFs in relation to the progress in tactile discrimination, which suggested an induction of acoustic imagery to complement the tactile information processing.

Rats were tested for changes in shock-elicited fighting (SEF) following the chronic administration of saline (IP); lithium (Li+) (20 mEq./l tap water) + saline (IP); desipramine (DMI) (15 mg/kg, IP); and DMI + Li+ for 14 days. The repeated test trials indicated a significant decrease in SEF in Li+-saline group (p less than 0.05), a significant increase (p less than p.05) in the DMI group, but no difference in the DMI + Li+ group in comparison to saline controls. Combined treatment with DMI + Li+ significantly reduced (p less than 0.05) SEF in comprison to the DMI group. These results suggest that enhanced aggressivity resulting from chronic DMI administration and measured by SEF can be a useful behavioral model to study the action of lithium.

The fetal brain remains inaccessible to neurophysiological studies. Magnetoencephalography (MEG) is being assessed to fill this gap. We performed 40 fetal MEG (fMEG) recordings with gestational ages (GA) ranging from 30 to 37 weeks. The data from each recording were divided into 15 second epochs which in turn were classified as continuous (CO), discontinuous (DC), or artifact. The fetal behavioral state, quiet or active sleep, was determined using previously defined criteria based on fetal movements and heart rate variability. We studied the correlation between the fetal state, the GA and the percentage of CO and DC epochs. We also analyzed the spectral edge frequency (SEF) and studied its relation with state and GA. We found that the odds of a DC epoch decreased by 6% per week as the GA increased (P = 0.0036). This decrease was mainly generated by changes during quiet sleep, which showed 52% DC epochs before a 35 week GA versus 38% after 35 weeks (P = 0.0006). Active sleep did not show a significant change in DC epochs with GA. When both states were compared for MEG patterns within each GA group (before and after 35 weeks), the early group was found to have more DC epochs in quiet sleep (54%) compared to active sleep (42%) (P = 0.036). No significant difference in DC epochs between the two states was noted in the late GA group. Analysis of SEF showed a significant difference (P = 0.0014) before and after a 35 week GA, with higher SEF noted at late GA. However, when both quiet and active sleep states were compared within each GA group, the SEF did not show a significant difference. We conclude that fMEG shows reproducible variations in gross features and frequency content, depending on GA and behavioral state. Fetal MEG is a promising tool to investigate fetal brain physiology and maturation.

OBJECTIVE

To evaluate the effects of prone and supine sleeping positions on electrocortical activity during active (AS) and quiet (QS) sleep in low birthweight infants.

METHODS

Randomised/crossover study.

METHODS

Infant Physiology Laboratory at Children's Hospital of New York.

METHODS

Sixty three healthy, growing, low birthweight (birth weight 795-1600 g) infants, 26-37 weeks gestational age.

METHODS

Six hour continuous two channel electrocortical recordings, together with minute by minute behavioural state assignment, were performed. The infants were randomly assigned to prone or supine position during the first three hours, and positions were reversed during the second three hours.

RESULTS

Fast Fourier transforms of electroencephalograms (EEGs) were performed each minute and the total EEG power (TP), spectral edge frequency (SEF), absolute (AP) and relative (RP) powers in five frequency bands (0.01-1.0 Hz, 1-4 Hz, 4-8 Hz, 8-12 Hz, 12-24 Hz) were computed. Mean values for TP, SEF, AP, and RP in the five frequency bands in the prone and supine positions during AS and QS were then compared. In the prone sleeping position, during AS, infants showed significantly lower TP, decreased AP in frequency bands 0.01-1.0 Hz, 4-8 Hz, 8-12 Hz, 12-24 Hz, increased RP in 1-4 Hz, and a decrease in SEF. Similar trends were observed during QS, although they did not reach statistical significance.

CONCLUSIONS

The prone sleeping position promotes a shift in EEG activity towards slower frequencies. These changes in electrocortical activity may be related to mechanisms associated with decreased arousal in the prone position and, in turn, increased risk of sudden infant death syndrome.

Increased survival of extremely low birth weight infants has led to a need for new prognostic methods to predict possible future neurological impairment. We investigated the early development of the somatosensory system by recording the somatosensory evoked magnetic fields (SEFs) during natural sleep at fullterm age in 16 very prematurely born infants and 16 healthy newborns born at term. The purpose was to determine possible changes in the function of the somatosensory cortex in the prematurely born infants by comparing the latency, strength, location and morphology of the SEFs with those of healthy fullterm newborns. We recorded reliable SEFs in all patients and controls. The equivalent current dipole (ECD) strength of the first cortical response, M60, was significantly lower in the patients. Otherwise, the general morphology and latency of the SEFs were similar in the two groups of babies. The similar response latencies in the two groups indicate normally developed conduction in the somatosensory system of the prematurely born infants. The attenuated ECD strength may reflect weaker synchrony in firing or a smaller number of the cortical neurons activated by the somatosensory stimulation. At the individual level, in four of the preterm infants, a later M200 response was not present or could not be modeled: all of them had lesions of the underlying hemisphere depicted by ultrasound and magnetic resonance imaging.

A brief review of previous studies is presented on ultra-fast activities>> 300 Hz (high frequency oscillations, HFOs) overlying the cortical response in the somatosensory evoked potential (SEP) or magnetic field (SEF). The characteristics of somatosensory HFOs are described in terms of reproducibility and origin (area 3b and 1) of the HFOs, changes during a wake-sleep cycle, effects of higher stimulus rate or tactile interference, etc. Also, several hypotheses on the neural mechanisms of the HFOs are introduced; the early HFO burst is probably generated from action potentials of thalamocortical fibers at the time when they arrive at the area 3b (and 1), since this component is resistant to higher stimulus rate>> 10Hz or general anesthesia: by contrast, the late HFO burst is sensitive to higher stimulus rate, reflecting activities of a postsynaptic neural network in the somatosensory cortices, area 3b and 1. As to possible mechanisms of the late HFO burst genesis, an interneuron hypothesis, a fast inhibitory postsynaptic potential (IPSP) hypothesis of the pyramidal cell and a chattering cell hypothesis will be discussed on the basis of physiological and pathological features of the somatosensory HFOs.

We investigated the relationship between electroencephalogram (EEG) activity and autonomic nervous system function using spectral analyses of EEG and heart rate variability (HRV) in healthy subjects during sleep. Eleven subjects were enrolled in this study. From EEG, the spectral edge frequencies (SEFs including SEF50, SEF90 and SEF95) were calculated. From electrocardiogram (ECG), the spectral powers of low-frequency band (LF: 0.04-0.15 Hz), high-frequency band (HF: 0.15-0.4 Hz) and the ratio of LF to HF (LF/HF) were calculated. During sleep, each set of data was obtained as the average of a 5-min measurement. We found that SEFs and LF/HF or LF decreased simultaneously and periodically, suggesting simultaneous depression of EEG activity and relative sympathetic activity, and SEFs significantly correlated with LF/HF and LF in all subjects during sleep, but not with HF. The existence of a clear correlation of SEFs with LF or LF/HF may offer a simple approach to estimate the relationship between EEG activity and autonomic nervous system function during sleep.

In order to detect on the same preparation of rat brain both 5-HT-containing elements and [3H]GABA uptake sites, immunocytochemistry (ICC) and radioautography (RAG) were combined in electron microscopy on sections of dorsal raphe nucleus (DRN) involving supraependymal fibers (SEF). At the ultrastructural level, SEF and DRN dendritic processes could be ICC positive and RAG negative, ICC positive and RAG positive, ICC negative and RAG positive, or negative for both labelings. Because of technical limitations a negative reaction should be interpreted with caution. However, the results constitute another morphological basis for intracellular relationship of endogenous 5-HT and exogenous GABA and provide additional evidence for the possible bipotentiality of some neuronal elements for both transmitters.

Both the electroencephalogram (EEG) spectral edge frequency (SEF) and lower esophageal contractility (LEC) indices have been reported to be useful indicators of anesthetic depth. We designed a prospective study to evaluate the relationship between changes in these two variables and objective measurements of physiologic responsiveness to surgical stress (i.e., changes in hemodynamic variables and plasma levels of norepinephrine, epinephrine, total catecholamines, and vasopressin). Eighty-nine consenting adult males undergoing radical prostatectomy procedures under a standardized general anesthetic technique were studied according to a randomized, single-blinded protocol. General anesthesia was induced with 30 micrograms/kg intravenous (i.v.) alfentanil, 2.5 mg/kg i.v. thiopental, and 0.1 mg/kg i.v. vecuronium, and subsequently maintained with 0.5 microgram/kg/min alfentanil, nitrous oxide (N2O) 67% in oxygen, and 0.8 microgram/kg/min vecuronium. Following retropubic dissection, 81 patients (92%) manifested acute hypertensive responses, with mean arterial pressure increasing from 90 +/- 14 to 122 +/- 14 mm Hg (mean +/- SD). This acute hypertensive response was treated with one of three different treatment modalities (20 to 60 micrograms/kg i.v. alfentanil, 0.5 to 2.0% inspired isoflurane, or 0.05 to 0.15 mg/kg i.v. trimethaphan) to return the mean arterial pressure to within 10% of the preincisional (baseline) value within 5 to 10 minutes. Although the mean arterial pressure, heart rate, and plasma levels of catecholamines and vasopressin significantly increased following the surgical stimulus, and decreased after adjunctive therapy, the EEG-SEF and LEC index (LECI) values did not significantly change during these study intervals. Furthermore, using a logistic regression analysis, we observed that preincision EEG-SEF and LECI values could not predict whether patients would manifest a hypertensive response. Therefore, the EEG-SEF and LECI were unreliable indicators of anesthetic depth.

Ultrastructural studies have shown that liver sinusoidal endothelial cells (LSECs) contain a cytoskeletal framework of filamentous actin, and that the presence of actin in the form of a calmodulin-actomyosin complex is responsible for regulation of the diameter of sinusoidal endothelial fenestrae (SEF). Rho has emerged as an important regulator of the actin cytoskeleton and consequently of cell morphology. We investigated actin filaments in relation to SEF in LSEC using heavy meromyosin decorated reaction and elucidated the roles of Rho and actin cytoskeleton in morphological and functional alterations of SEF. Second, according to intracytoplasmic Ca2+ concentration, plasma membrane Ca2+Mg2+-ATPase activities were clearly demonstrated on the outer surface of the labyrinth-like SEF in the isolated LSECs. Furthermore, by investigating intracytoplasmic Ca2+ concentration, we have demonstrated plasma membrane Ca2+Mg2+-ATPase activities on the outer surface of the labyrinth-like SEF in the isolated LSECs. Currently, the majority of fenestral studies are focused on finding ways to increase the liver sieve's porosity, which is reduced through pathological mechanisms.

Sclerosing epithelioid fibrosarcoma (SEF) is a distinctive variant of fibrosarcoma characterized by epithelioid tumor cells arranged in nests, cords, or sheets embedded within a sclerotic collagenous matrix. It is a relatively newly described malignant fibroblastic tumor, with only fewer than 100 cases reported in English literature. Most cases are located in the lower extremities and limb girdles. Here, we present a case of SEF of the pancreas in a 67-year-old white man and provide a review of literature to date, with emphasis on the differential diagnosis. To our knowledge, this is the first reported case of SEF involving the pancreas.

Sclerosing epithelioid fibrosarcoma (SEF) is an extremely rare soft-tissue neoplasm. Here, we describe the molecular genetic alterations and histological, immunohistochemical and ultrastructural features of a primary SEF arising in the retroperitoneum. The tumor consisted of uniform small round to ovoid epithelioid cells, arranged in nests and cords and surrounded by a prominent hyalinized collagenous matrix. The tumor cells expressed only vimentin. Ultrastructurally, the tumor cells showed features of fibroblasts, with an abundant rough endoplasmic reticulum in the cytoplasm. Neither p53 gene mutations nor p53 protein overexpression were detected, but more than 70% of all tumor cells showed strong immunoreactivity with murine double minute 2 (MDM2). Our results suggest that MDM2 overexpression is likely to play a role in tumorigenesis in this lesion in p53-dependent or p53-independent pathways. To our knowledge, the present study is the first molecular genetic study of this rare lesion. Further studies will be necessary to clarify the molecular basis of tumorigenesis of this rare lesion.

The purpose of this study was to examine whether the sonicated extract of Enterococcus faecalis (SEF) alters the cell cycle transition of lymphocytes and thus regulates the fate of the arrested cells. Human lymphocytes were activated by phytohemagglutinin in the presence or absence of SEF, and cell cycle was assessed by flow cytometry. Seventy-two hours after activation with phytohemagglutinin, cells were activated from G0/G1 to S (6.1%) and G2/M (3.8%) phases of the cell cycle. In contrast, pretreatment with SEF resulted in 90.5% of cells remaining in G0/G1, and cell cycle progression to the S and G2/M phases was consequently inhibited. Caspase assay demonstrated that SEF-treated cells exhibited significantly increased apoptosis (56.7%) compared with phytohemagglutinin alone (28.1%). We propose that if this irreversible cell cycle arrest induced by E. faecalis occurs in vivo, it may result in local immunosuppression and contribute to the pathogenesis of endodontic failure. Our findings that E. faecalis can inhibit lymphocyte responses may be of particular relevance to the pathogenesis of endodontic failure. Although the immunologic mechanism involved in the pathogenesis of persistent periapical lesion is not clearly defined, it is reasonable to predict that the altered immune reaction may be linked to the immunosuppressive potential of E. faecalis or other oral bacteria.

We report the enhancement of the fluorescence emitted from dye-labeled DNA upon co-aggregation with silver nanoparticles. The co-aggregation process is induced by the polycationic molecule spermine, which both neutralizes the charge of the DNA backbone and aggregates the nanoparticles. This simple method generates nanoparticle aggregates with very short (1-2 nm) inter-particle distance. Even though no spacer layer was used, large enhancements of the fluorescence, in the range of 15-740× (depending on the original quantum yield of the dye used), were observed. Theoretical modeling shows that this occurs as the local enhancement of the electromagnetic field near the hotspots is sufficiently large to overcome the quenching by the surface, even at short distances of 1 nm. The predicted trend of increased SEF enhancement with a decrease in initial quantum yield is observed. The average enhancements observed in this system are on-par with the best results obtained on nanostructured surfaces to date.

Recent studies have suggested an association between tumor necrosis factor-alpha (TNF-alpha) and the development and progression of acute liver failure. To investigate the role of TNF-alpha in the mechanism of massive hepatic necrosis, we studied a mouse model of TNF-alpha and D-galactosamine (GalN) -induced hepatic necrosis by ultrastructural analysis. Administration of GalN caused edema of hepatocellular microvilli and widening of sinusoidal endothelial fenestrae (SEF); administration of TNF-alpha caused only a widening of the SEF. Massive hepatic necrosis with hemorrhage was seen 6 hr after concomitant administration of TNF-alpha and GalN. In the ultrastructural analysis, edema of the hepatocellular microvilli, widening of the SEF, and transmigration of red blood cells (RBC) and platelets to the space of Disse without exfoliation and necrosis of the sinusoidal endothelial cells were observed. Fibrin deposits were seen in areas adjacent to injured hepatocytes. The diameter of the SEF was significantly greater than in the nontreated group and the groups treated with TNF-alpha or GalN alone. These results suggest that as a consequence of the increase in diameter of the SEF, transmigration of RBCs and platelets to the space of Disse may have resulted in massive hepatic necrosis due to occlusion of the microcirculation.

We present a novel noninvasive technique for functional neurosurgical simulation combining three-dimensional magnetic resonance imaging of the brain surface with somatosensory evoked magnetic fields (SEFs) in a case of subcortical brain tumor. The preoperative analysis using this technique revealed that the central sulcus was located between the SEF source projected onto the brain surface and the tumor. At the time of surgery, the central sulcus was clearly identified by phase reversal of the cortical recordings of somatosensory evoked potentials. The actual cortical anatomy and the maximum somatosensory evoked potential location showed excellent agreement with the preoperative analysis of the brain surface magnetic resonance images and the SEF source. The subcortical tumor, which was barely identifiable without reliable functional cortical anatomy, was easily found in the motor area, just before the somatosensory evoked potential (and SEF) source. The potential clinical application of this technique is discussed.

BACKGROUND

Neuraxial anaesthesia in adults decreases the dose of i.v. or inhalational anaesthetic needed to reach a desired level of sedation. Furthermore, spinal anaesthesia alone has a sedative effect. The mechanism behind this phenomenon is presumed to be decreased afferent stimulation of the reticular activating system after sympatholysis. We hypothesized that this mechanism is equally active in infants undergoing spinal anaesthesia.

METHODS

In total, 20 unpremedicated former preterm infants underwent surgery under spinal anaesthesia with hyperbaric bupivacaine 0.5% 1 mg kg(-1) with epinephrine 10 microg kg(-1). No additional sedatives or anaesthetics were administered. Sedation was evaluated using the bispectral index (BIS) score and the 95% spectral edge frequency (SEF(95)).

RESULTS

After spinal anaesthesia, mean (SD) BIS began to decrease significantly from baseline 97.0 (1.1) to 83.9 (14.4) after 15 min (P=0.006). BIS decreased further, reaching the lowest values after 30 min [62.2 (14.0); P<0.00001]. Mean (SD) SEF(95) declined from baseline 26.1 (1.8) Hz to 24.3 (3.1) after 5 min (P=0.02) and further to 9.9 (3.8) after 30 min (P<0.00001). Mean arterial pressure also decreased significantly from 66.5 (4.7) mm Hg within 10 min to 56.1 (5.6) after spinal anaesthesia (P=0.0002), while heart rate remained stable.

CONCLUSIONS

These results suggest that sedation after spinal anaesthesia in infants is at least as pronounced as in adults. The sedative effect of spinal anaesthesia should be kept in mind when additional sedatives are administered, especially in former preterm infants.

The contribution of maturation and stimulation to the development of oral feeding was investigated, with two main objectives: (1) to analyze the nutritive sucking pattern of very-low-birth-weight newborns from their first oral feeding to the acquisition of independent oral feeding, and (2) to compare the nutritive sucking patterns of these babies, after feeding autonomy, with healthy term newborns.

METHODS

Two groups were considered for analysis. Group 1: N=15 Very-Low-Birth-Weight (VLBW), gestacional age (GA)=28.15+/-1.5, birth weight (BW)=1178.3+/-174.4. The intervention program began at 30.19+/-1.52 weeks GA. Group 2: N=25 term newborns, healthy, GA=39.04+/-1.2, BW=3370.42+/-310.76. Repeated measures of the following variables were taken (weekly for group 1): suction efficacy (SEF), rhythm of milk transfer (RMT), suctions, bursts and pauses. Group 2 was analysed only once between the 2nd and 5th day of life.

RESULTS

Group 1 has revealed a minimal suction number at 32 GA weeks (82+/-77.6) and maximal suction number at 36-37 GA weeks (162.7+/-60.7). The number of sucks seemed to be dependent of weight (p=0.005), duration of intervention (p=0.001) and chronological age (p=0.000). Significant statistical effects of gestational age were not observed (p=0.904). Sucks in bursts represented 77% at the beginning of oral feeding (32 weeks GA), and 96% at 33 weeks GA, remaining constant thereafter. The number of sucks and bursts increased with GA and weeks of feeding. The mean duration of the pauses decreased from first to fourth week of feeding (week1=14.1+/-9.1 and week4=6.4+/-1.4 s). The sucking efficacy (SEF) was better explained by weight (p=0.000), number of sucks in 5 min (p=0.025) and chronological age (p=0.044). Gestational age (p=0.051) and nutritive intervention duration (NDI) (p=0.110) did not contribute to explain SEF. Despite the observation of significant statistical differences between groups regarding GA (35.9/39.08; p=0.00), chronological age (53.3/2.5; p=0.00) and weight (1875/3360; p=0.00), the nutritive suction pattern was not statistically different between groups after feeding autonomy.

CONCLUSIONS

in VLBW oral feeding before 32 weeks GA allows the attainment of a mature nutritive suction pattern before term (37-40 weeks). Experience seems to be one of the influencing factors in the change of the nutritive suction pattern.

BACKGROUND

Exposure to allergens or air pollutants often leads to asthma exacerbations associated with aggravation of airway inflammation. Although, repeated allergen challenge often induces chronic allergic airway inflammation (CAAI) and airway remodelling, yet, the effects of brief exposure to air pollutants such as SO(2) on development of CAAI and airway remodelling remain to be clarified.

OBJECTIVE

The aim of the experiment was to investigate the effects of acute neutrophilic airway inflammation induced by brief exposure to SO(2) on development of CAAI and subepithelial fibrosis (SEF) in a murine model of asthma.

METHODS

Acute airway inflammation was induced by brief exposure to 50 p.p.m. SO(2) (1 h/d, 3 days). CAAI and SEF in BALB/c mice were induced by repeated challenge with ovalbumin (OVA) for 5 or 9 weeks with or without prior exposure to SO(2). Bronchoalveolar lavage fluid (BALF) eosinophilia as index of CAAI, BALF endothelin-1 (ET-1) and TGF-beta1 levels, morphometric evaluation of fibrotic area beneath subbasement membrane and lung hydroxyproline content (Hyp) as indexes of SEF were monitored.

RESULTS

Exposure to SO(2) led to acute neutrophilic inflammation and epithelial sloughing with profound elevation of BALF ET-1. Repeated OVA challenge resulted in CAAI and SEF along with elevation of Hyp, increase of fibrotic area beneath subbasement membrane and elevation of BALF TGF-beta1. Preceding SO(2) exposure exaggerated BALF eosinophilia, facilitated and enhanced SEF with more significant elevation of BALF ET-1 and TGF-beta1 levels compared with OVA-challenged mice without prior exposure to SO(2). The increase of Hyp was positively correlated with elevation of BALF TGF-beta1 during CAAI (r=0.842, P<0.01).

CONCLUSIONS

This data demonstrated that SEF developed in parallel with severity and time course of CAAI following repeated OVA challenge. SO(2)-induced acute epithelial injury and neutrophilic inflammation could enhance CAAI and promote SEF, probably through overexpression of ET-1 and TGF-beta1.

Although we can generate movements whenever we feel like doing so, the way in which neuronal signals regulate the timing of self-initiated movements remains elusive. There is evidence that the dorsomedial frontal cortex, including the supplementary eye field (SEF), is involved in the self-triggering of movements. Because the gradual evolution of cortical activity over the dorsomedial frontal cortex is known to reflect the temporal prediction of an upcoming event, we postulated that the timing of self-initiated movements is regulated by the time course of neuronal activity in the SEF. To test the causal role, we applied electrical microstimulation to the SEF when monkeys prepared for memory-guided saccades. Stimulation delayed the initiation of saccades when animals were required to make saccades 1200 ± 300 ms following the cue (self-timed task), but not when they generated memory-guided saccades in response to the offset of the fixation point (conventional task). As well as the increment in median saccade latencies, stimulation at ∼24% of sites also increased the occurrence of early erroneous saccades. Saccades facilitated by stimulation were always directed toward the cue, even when the cue was located away from the movement field. In contrast, stimulation to the frontal eye fields during saccade preparation exerted no effects in either task. These results suggest that the preparatory signals in the SEF may play a causal role in regulating the timing rather than the direction of self-initiated saccades.

Sclerosing epithelioid fibrosarcoma (SEF) has distinctive morphology and occurs mainly in deep soft tissue of adult extremities. Approximately 59 cases of SEF have been reported, with only 12 previously described in head and neck locations. Lesions involving the oral and maxillofacial region (OMFR) and intraosseous examples are rare. We present five cases of OMFRSEF. The OMF Pathology Department Registry was searched for cases coded from 1990 to the present as "SEF," "fibrosarcoma not otherwise specified" or "neoplasm of uncertain histiogenesis." Inclusion required OMFR location, an abundantly sclerotic sarcoma with epithelioid features, and lack of other phenotype by immunohistochemistry. Five cases of SEF included 3 males and 2 females. The age of the patients were: 19, 22, 35, 47 and 47 years. Tumor location included the infra-temporal fossa, buccal mucosa (recurrence extending into bone), anterior mandible (intraosseous primary, focally extending into soft tissue), and left parotid and submandibular gland (with metaplastic bone) regions. Tumor sizes ranged from 1.0 to 5.7 cm, median 3.5 cm. Histologically, the tumors were well delineated and multinodular, separated by fibrous septae. The spindled to primarily epithelioid tumor cells formed moderately cellular sheets and cords of irregularly contoured medium to large, round to oval, occasionally overlapping nuclei, indistinct nucleoli, wispy eosinophilic (retracting) cytoplasm, and distinctive cytoplasmic borders, embedded in osteoid-like stroma. Hemangiopericytoid (HPC-like) vessels were observed. Despite numerous apoptotic cells, mitoses were generally low; necrosis was present in two cases. Three tumors were graded as 2/3 and two 1/3. Immunohistochemically, the tumor cells were positive for vimentin, 1 case focally for CD34, whereas all cases were negative for S100 protein, keratins, EMA, desmin, and SMA. Wide or radical excision was performed with no adjuvant therapy. Follow-up revealed that 4 cases recurred at a range of 12-120 months. One case had no recurrent/residual disease at 3 months. Metastatic disease was present in 2 cases, to chest wall and lumbar/thoracic spine at 12 and 21 months, respectively. One patient died of disease complications at 15 months. OMFRSEF occur in adults in various locations, but with a common propensity to involve bone; there is recurrent potential and morbidity with higher grade lesions. The differential diagnosis for these tumors in this site includes sclerosing carcinoma, Ewing/PNET, osteosarcoma, osteoblastoma, and benign and malignant myoepithelial salivary gland tumors. The collagen, focal spindle cell features, HPC-like vasculature, and weak focal CD34 reactivity in one case might have raised a possible relationship between OMFRSEF and low grade malignant solitary fibrous tumor, but the intraosseous propensity, epithelioid features and relative lack of CD34 make this a distinctive entity.