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This study aimed to examine the feasibility of using a frailty index (FI) based on comprehensive geriatric assessment (CGA), to assess the level of frailty in older surgical patients preoperatively and to evaluate the association of FI-CGA with poorer postoperative outcomes. Two hundred and forty-six patients aged ≥70 years undergoing intermediate- to high-risk surgery in a tertiary hospital were recruited. Frailty was assessed using a 57-item FI-CGA form, with fit, intermediate frail, and frail patients defined as FI ≤0.25, >0.25 to 0.4, and >0.4, respectively. Adverse outcomes were ascertained at 30 days and 12 months post-surgery. Logistic regression models assessed the relationship between FI and adverse outcomes, adjusting for age, gender and acuity of surgery. The mean age of the participants was 79 years (standard deviation [SD] 6.5%), 52% were female, 91% were admitted from the community, 43% underwent acute surgery, and 19% were assessed as frail. The FI-CGA form was reported as being easy to apply, with a low patient refusal rate (2.2%). The majority of items were easy to rate, although inter-rater reliability was not tested. In relation to outcomes, greater frailty was associated with increased 12-month mortality (6.4%, 15.6%, and 23% for fit, intermediate frail, and frail patients respectively, P=0.01) and 12-month hospital readmissions (33.9%, 48.9%, and 60% respectively, P=0.004). There were no statistically significant differences between fit, intermediate frail, and frail groups in perioperative adverse events (17.4%, 23.3%, and 19.1% respectively, P=0.577) or 30-day postoperative complications (35.8%, 47.8%, and 46.8% respectively, P=0.183). Our findings suggest that it is feasible to use the FI-CGA to assess frailty preoperatively, and that using the FI-CGA may identify patients at high risk of adverse long-term outcomes.

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To determine if transneuronal degeneration occurs in ventral horn motoneurons caudal to a spinal cord transection, we completely transected the spinal cord at T-9 in seven-week-old female rats. Ten, 20 or 52 weeks later, the motoneurons of the right sciatic nerve of transected and control rats were retrogradely labeled with Fluoro-Gold. There were no differences between control and transected rats in numbers or rostrocaudal distribution of labeled motoneurons at either 10, 20 or 52 weeks. At 20 weeks, there was no significant difference between control and transected rats in mean cross-sectional area of labeled neurons. We conclude that transneuronal degeneration did not occur.

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We studied the long-term effects of two retrogradely transported fluorescent dyes on survival of dorsal root ganglion neurons (DRGNs) and motoneurons (MNs). In adult female rats, we labeled DRGNs and MNs by soaking the cut sciatic nerve in Fluoro-Gold or True Blue. With True Blue, we found no difference in the number of labeled MNs or DRGNs in rats surviving 4 days or 20 weeks after nerve soak. With Fluoro-Gold, labeled DRGNs and MNs were decreased at 20 weeks compared with 4 days. Since there was no offsetting increase in unlabeled DRGNs at 20 weeks, Fluoro-Gold caused cell death.

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Integration psychophysics was used to explore the taste perception of mixtures of sucrose, fructose, and citric acid. Three levels of each stimulus were varied in a 3 x 3 x 3 factorial design. Subjects rated total intensity, sweetness, and acidity of the 27 mixtures on graphic rating scales. Consistent with earlier work, the perceived total intensity of the tertiary mixtures was found to be dictated by the intensity of the (subjectively) stronger component alone (i.e., either the integrated sweetness or the acidity, whichever was the more intense). In contrast, the sweetness and acidity of the mixture were susceptible to mutual suppression: Sweetness suppressed acidity, acidity suppressed sweetness. There was, however, a difference between sucrose and fructose in their interactions with citric acid, fructose being the more susceptible to suppression. This selectivity of suppression indicates that the two sweetnesses could not have been inextricably integrated. Implications for taste coding are discussed, and the findings are reconciled in terms of two separate coding mechanisms: one for taste intensity, another for taste quality.

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Retrograde labeling with horseradish peroxidase is greatly diminished in corticospinal and rubrospinal neurons axotomized by complete T-9 spinal cord transection. We found, 10 or 20 weeks after a complete T-9 cord transection, that the number of corticospinal and rubrospinal neurons retrogradely labeled after Fluoro-Gold insertion into a new transection at T-1 did not differ from that of controls. While transection alters uptake, transport, and/or intracellular metabolism of some transportable substances, it does not affect the ability of the neurons to be retrogradely labeled with Fluoro-Gold.

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Spinal cord transection is known to cause progressive changes in motor neurons and hind limb muscles. In the present study, regeneration of the peroneal nerve was examined in rats 25 weeks after a T9 spinal cord transection. Successful regeneration and innervation of the target muscle was observed after crush injury to the nerve in the spinal cord transected animals. It is concluded that the ability of peripheral nerve to regenerate remains preserved after spinal cord injury.

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To demonstrate definitively the fate of the somata of rubrospinal and corticospinal neurons axotomized by a complete spinal cord transection at T-9, in young adult rats we prelabeled the neurons by injection into the lumbar enlargement of a retrogradely transported fluorescent dye, Fluoro-Gold, and four days later transected the cord. We found no loss in cell number ten or 20 weeks after axotomy. The average size of the neurons in each case is slightly but significantly reduced. These findings unequivocally demonstrate that the somata of long tract neurons of the rubrospinal and corticospinal systems persist in an atrophic and presumably inactive state for at least 20 weeks, and raise the possibility that treatment of spinal cord injury may normalize cell activity and allow long tract regeneration.

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We studied Clarke's Column of the L-1 spinal cord segment of young adult female rats after first prelabeling its neurons by the intracerebellar injection of Fluoro-Gold or true blue and subsequently axotomizing the labeled cells by a complete spinal cord transection at T-9. In control rats, the number of labeled neurons at 1, 5, 10, and 20 weeks showed a progressive decrease, probably due to leakage of dye from the cells. A much greater loss of labeled neurons was found in T-9 spinal cord-transected rats than in their matched controls. At 5 weeks after transection, loss of large neurons was somewhat offset by an increase in small neurons; neuron shrinkage was a likely cause of this increase, because small, very intensely labeled neurons were found in transected rats but not in control rats. By 10 and 20 weeks post-transection, the number of all prelabeled neurons in transected rats had sharply decreased. In transected rats, but not in controls, very significant increases in labeled astroglia and microglia and other labeled small cells were found at 5 weeks. At 10 weeks, the identifiable labeled astroglia had decreased but marked increases in microglia and other labeled small cells persisted. We conclude that, following a complete T-9 spinal cord transection, axotomized Clarke's column neurons first shrink in size and then die. Labeled reactive astrocytes, which are most evident 5 weeks after injury, probably indicate phagocytosis of axotomized neurons.

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Ten weeks after complete spinal cord transection at T-9, there was a decrease in the volume of the rat corticospinal tract but no loss in the number of axons contained in the cervical (C-2) or high thoracic (T-1) corticospinal tract. The mean area of the myelinated axon profile decreased in spinal cord-transected rats, with fewer axons found in the largest size groups and more in the smaller size groups. The survival of corticospinal axons in the cervical and thoracic cord 10 weeks after cord transection at T-9 indicates that the corticospinal neurons survive at least 10 weeks after cord transection. The fate of axotomized neurons after longer survival times remains to be determined.

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Red nucleus neurons, particularly those of the caudal one-half of the nucleus, die or severely atrophy following complete spinal cord transection at T9. The size of residual horseradish peroxidase-labeled cells was smaller at 10 and 15 weeks, but those survivors which could be labeled at 25 weeks were normal in size. Hematoxylin and eosin-stained sections of the red nucleus at 52 weeks postoperative showed loss of cells from all size groups.

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The number of large neurons in Clarke's column of the L-1 segment of the spinal cord of the rat decreases five or more weeks after a T-9 spinal cord transection. Analysis of cells at 1, 2, 3, 5, 7, 9, 12, and 15 weeks (wk) postoperatively demonstrates a loss of large neurons at each time interval beyond five wk postoperatively. Comparison of cell sizes found in the anatomic region of Clarke's column at two or three wk postoperatively with the cells found at 15 wk after transection and their respective control groups, shows a decrease in total cells found in operated rats 15 wk postoperative with a profound decrease in larger neurons in these rats. We did not detect a significant offsetting increase in smaller neurons. We believe the observed changes are due to death of large neurons and can find no evidence to support the contention that axotomized cells persist in a shrunken, atrophic state.

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Five concentrations of an artificial orange drink were presented for sensory evaluation in three overlapping concentration ranges. Three sensory panels, each of 30 subjects, rated the concentrations for intensity of flavour (intensity scale), relation to ideal flavour intensity (ideal-point scale), and pleasantness (hedonic scale). Except for the two extreme concentrations, neither of which was presented in more than one range, in all three response tasks the mean rating for a given concentration varied with the concentration range in which it was presented. However, the mean ratings showed good correspondence across response tasks (e.g. the concentration perceived as "moderately sweet" on the intensity scale was perceived as "just right" on the ideal-point scale and of maximal pleasantness on the hedonic scale), suggesting a link between the intensity and hedonic dimensions of sensory experience.

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Subcutaneous injection of 6-hydroxydopamine (6-OHDA) in neonatal rats results in sprouting of collateral axons in locus coeruleus (LC) and lateral tegmental noradrenergic neurons. It has been suggested that this sprouting represents maintenance of neuronal membrane area following "pruning" of axon terminals of long projections to cortex and cord. The chemical or surgical lesions of long axons used to produce "pruning" could also result in the loss of some parent cell bodies. We tested the hypothesis that long axon damage, rather than cell loss, is sufficient to produce collateral sprouting of proximal axons in noradrenergic neurons. With neonatal injections of 6-OHDA at doses which do not produce a loss of LC neurons, there is an 85% decrease in retrograde LC labeling following horseradish peroxidase or true blue injections into the spinal cord but no significant change in the numbers of retrogradely labeled neurons in other noradrenergic cell groups which also sprout collaterals. There is no change in the number of labeled LC neurons following cerebellar injections. In experiments using the fluorescent dyes diamidino yellow and true blue, the number and distribution of LC neurons labeled from spinal cord and cerebellum injections are similar to those in the horseradish peroxidase experiments. Doubly labeled neurons are found in the caudal two-thirds of LC in control rats, but as expected, rarely observed in 6-OHDA-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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Administration of 6-hydroxydopamine to neonatal rats results in a permanent increase in the norepinephrine content in several brainstem areas. To assess the physiological effects of this hyperinnervation, we studied the noradrenergic inhibition of transmission of sensory information through the principal sensory and rostral spinal trigeminal nuclei. Unit activity produced by tactile stimulation of the face was recorded extracellularly from trigeminal sensory neurons in normal and hyperinnervated rats. The noradrenergic neurons projecting to the trigeminal sensory nuclei (locus coeruleus and the region of the lateral lemniscus) were stimulated 40 ms prior to delivery of a tactile stimulus to the face, producing complete inhibition. The interstimulus interval was then increased in 100 ms increments until the sensory response returned to control values. Compared with controls, the duration of inhibition was 30% longer in hyperinnervated rats and 25% shorter in rats depleted of catecholamines with reserpine and alpha-methyl-p-tyrosine. While the beta-adrenergic blocker, propranolol, had no effect on the duration of inhibition in normal animals, the mean latency of response to tactile stimulation was decreased from 15.3 to 10.4 ms. Propranolol given to hyperinnervated rats decreased the latency of the response to tactile stimulation from 15.1 to 9.1 ms and decreased the duration of inhibition by 40% compared with untreated hyperinnervated rats, suggesting an alteration in numbers or sensitivity of beta-receptors. Since the drug treatment never eliminated the inhibition due to locus coeruleus stimulation, there is also a non-noradrenergic component. We conclude from these observations that noradrenergic hyperinnervation is not completely counteracted by receptor down regulation.

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In 17 adult squirrel monkeys (Saimiri), horseradish peroxidase was used as a retrograde tracer substance to reveal the subcortical structures (other than the lateral geniculate nucleus and pulvinar) which project to the occipital lobe, and, in particular, to the central visual field representation in areas, 17, 18, 19, and MT. Evidence is provided that each of areas 17, 18, and MT receives a projection from locus coeruleus, nucleus dorsalis raphae, nucleus annularis, nucleus centralis superior, formation reticularis pontis oralis, nucleus basalis of Meynert, lateral hypothalamus, claustrum, and nuclei paracentralis and centralis medialis thalami. Area 19 receives a projection from all these structures except from the nucleus annularis. Only area MT was determined to be a target of a projection from the nucleus linearis. For technical reasons, only area MT was determined to receive afferent fibers from the nucleus basalis lateralis amygdalae. The results indicate that there is no topographical organization of subcortical inputs to the central visual field representation in individual cortical areas.

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The retrogradely transported horseradish peroxidase (HRP) method was used to study the areal and laminar distribution of neurons sending their axons to ipsilateral and contralateral visual cortical areas 17, 18, 19, and MT in the squirrel monkey. Further details regarding neuron type (stellate or pyramidal), size class, and spatial grouping of the cells making these corticocortical connections also were obtained. All interareal connections are reciprocal. Ipsilaterally, such connections exist between areas 17 and 18, 17 and MT, 18 and 19, 18 and MT, and 19 and MT. In addition, areas 18, 19, and MT receive association fibers from the ipsilateral frontal eye field; when combined with previous findings, these results indicate the existence of reciprocal connections between area 18 and the frontal eye field and between area MT and the frontal eye field. Each of areas 18, 19, and MT. Area 17 has only weak callosal connections. Both the ipsilateral and the contralateral connections are topographically organized such that they obey a hodological principle of visuotopic connectivity: that is, only representations of the same part of the visual field are interconnected. With regard to layers of origin, the callosal neurons of these visual areas conform to the general concept of corticocortical fibers arising from supragranular layers in that most of them are located in layer IIIb; only a few of them reside at the junction between layers V and VI. On the other hand, for all the visuocortical connections investigated, the anteriormost area of a reciprocally interconnected pair has its association neurons located predominantly in the infragranular layers while the posteriormost area has its association neurons located primarily in layer III. All callosal fibers and most association fibers arise from pyramidal cells. The callosal cells are larger and reside at a deeper level in layer III than neurons with ipsilateral corticocortical connections. However, some of the association cells at the junction of layers V and VI in area 17 which project to area MT are relatively large and may include the solitary cells of Meynert; but medium-sized pyramidal cells also participate in this projection. In area 17, some association neurons in layers IIIb and IIIc which project to area 18, as well as some in layer IIIc which project to area MT, are most likely stellate cells. Several different patterns of cell groupings were observed for the central representation interconnections. Neither ipsilateral area MT nor any of the contralateral visuocortical areas had multiple groupings of labeled neurons. The ipsilateral projections from area 17 to 18, 17 to MT, and 18 to 19 were arranged similarly according to a plan involving separate, multiple loci of origin for cells projecting to a small and isolated subregion of the central representation in the target cortical area; following larger injections, cells throughout the central representation of the projecting cortex were labeled...

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