Goldmann tonometry after hyperopic laser in situ keratomileusis: comparison between retreated and nonretreated patients

PURPOSE: To identify differences in applanation tonometry between retreated and nonretreated eyes (primary LASIK eyes) 6 months after hyperopic laser in situ keratomileusis. METHODS: In a prospective study 100 eyes (100 patients) underwent conventional hyperopic laser in situ keratomileusis under a 160-microm flap. Central Goldmann applanation tonometry was determined before and 6 months after surgery in 78 (78%) primary LASIK eyes and before surgery and 6 months after the retreatment date in 22 (22%) retreated eyes. RESULTS: Preoperative mean tonometry was 14.96 +/- 1.96 mm Hg and 15.30 +/- 1.95 mm Hg in primary LASIK and retreated eyes, respectively. Six months after surgery it was 12.99 +/- 2.03 mm Hg (P < 0.001) and 12.67 +/- 2.20 mm Hg (P < 0.001), respectively. No significant differences in mean tonometry were found between retreated and primary LASIK eyes 6 months after surgery (P = 0.537). Decreased tonometric values were found in 20 retreated eyes (90.91%) and in 62 primary LASIK eyes (79.48%). Increased tonometric values higher than 1 mm Hg were found in 3 primary LASIK eyes (3.84%), but no retreated eyes showed increased values 6 months after surgery. Two retreated eyes (9.09%) and 10 primary LASIK eyes (79.49%) presented the same tonometric values before surgery and at the end of the study. CONCLUSIONS: After hyperopic laser in situ keratomileusis there was no significant difference in Goldmann applanation tonometry between retreated and primary LASIK eyes.     

Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle

Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. Received: 27 July 1998 / Accepted in revised form: 27 October 1998     

Modulation of growth and urokinase secretion by vasopressin and closely related nonapeptides in metastatic mouse mammary tumor cells

We examined the effects of the neuropeptide hormones vasopressin and oxytocin, and their respective synthetic derivatives desmopressin and isotocin, on F3II mouse mammary carcinoma cells. Vasopressin and desmopressin at concentrations ranging from 0.1 to 1 mu M were mitogenic for F3II cells and induced protein accumulation. On the contrary, oxytocin and isotocin were moderately growth inhibitory at similar doses. In confluent monolayers vasopressin stimulated the secretion of urokinase, a profibrinolytic enzyme involved in hematogenous metastasis. However, the net effect of the peptide on tumor-derived proteolytic activity was dependent on cell density. Stimulation of cell growth and urokinase production by vasopressin was strongly linked with calcium mobilization. These data suggest that vasopressin and its synthetic analog desmopressin may be important modulators of the behavior of metastatic mammary tumor cells.     

Post-traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat

The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether posttraumatic brain hypothermia (30°C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5°C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30°C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519±122 vs 952±130, mean ±SE, P=0.03, Kruskal-Wallis test) as well as contusion volume (0.50±0.14 vs 2.14±0.71 mm³, P=0.004). These data document a consistent pattern of histopathological vulnerability following normothermic TBI and demonstrate hypothermic protection in the post-traumatic setting.Supported by USPHS Grants NS30291 and NS27127     

Child and Parent Response to the 1993 World Trade Center Bombing

This study evaluated children's symptoms 3 and 9 months after the 1993 bombing of the World Trade Center, and the relationship between parent and child reactions when only the children had been in the building. Nine children who had been trapped in an elevator, 13 who had been on the observation deck, and 27 controls completed the Posttraumatic Stress Reaction Index and a Fear Inventory. Parents completed these measures about the children and comparable measures about themselves. Exposed children reported posttraumatic stress disorder (PTSD) symptoms and disaster-related fears; their parents reported experiencing PTSD symptoms. Only parents rated children's symptoms as decreasing significantly over time. Association between child symptoms and parent symptoms increased over time. Children's initial distress predicted parents' distress 9 months postdisaster.     

Verbal and nonverbal memory processing in patients with obsessive-compulsive disorder: its relationship to clinical variables

Memory deficits have been reported in several neuropsychological studies of obsessive-compulsive disorder (OCD). Dysfunction in nonverbal memory has been consistently reported, whereas findings on verbal memory are more heterogeneous. The authors studied 50 patients with OCD who were matched for sex, age, educational level, and hand dominance with 50 healthy controls (HC). Cognitive performance in both groups was assessed on verbal and nonverbal memory tasks, and several clinical variables were also assessed in the patient group. Patients with OCD showed a pattern of cognitive dysfunction with alterations in areas of nonverbal memory (recall and recognition), and verbal memory (learning and recall). Older age at onset of OCD was associated with poorer performance on verbal memory tasks. Low scores on some verbal memory tasks were associated with severity of OCD, and nonverbal memory was influenced by depressive symptoms. The study suggests the existence of dysfunction in the execution of verbal and nonverbal memory tasks in OCD; the influence of clinical variables depends on the specific neuropsychological function.     

Neuropeptide Y-producing neurons of the arcuate nucleus regenerate axons after surgical deafferentation of the mediobasal hypothalamus

Dorsolateral and ventomedial surgical deafferentation of the hypothalamus were used to study the capacity of different types of neuropeptide Y-containing axons afferent to the dorsal hypothalamus to regenerate through surgical lesions. The kinetics of the postlesional responses of transected neuropeptide Y-axons was studied on 30–40 μm thick vibratome sections, either (i) by light or electron microscopy after peroxidase immunostaining for neuropeptide Y or (ii) by confocal microscopy after double fluorescence immunostaining for neuropeptide Y and for glial fibrillary acidic protein. The dorsolateral cut was found to sever 2 main pathways containing neuropeptide Y axons located, respectively, below the bed nucleus of the stria terminalis and in the perifornical region. In both regions transected fibers were found to abut onto the surgical lesion, but even 45 days after the lesion, they were very rarely observed to penetrate into the astroglial scar formed along the lesion. The ventromedial cut was found to sever numerous neuropeptide axons that originate in the underlying arcuate nucleus. Seven to 15 days after the lesion neuropeptide Y fibers located below this type of cut presented a dramatic increase in both their numerical density and their immunostaining intensity. With increasing post-surgery times, an increased number of neuropeptide Y fibers was observed to penetrate and to cross the lesional scar formed by densely packed astrocytic processes. Electron microscope observations further demonstrated that 45 days after the lesion, numerous neuropeptide Y-immunoreactive axonal profiles were included in the scar matrix, which appeared to be mainly composed of closely interdigitating astrocytic processes containing dense bundles of filaments. These data indicate that, in contrast to other neuropeptide Y neurons innervating the dorsal hypothalamus, neuropeptide Y neurons of the arcuate nucleus regenerate axons through the astroglial scar produced by a surgical lesion placed in the ventromedial hypothalamus. © 1993 Wiley-Liss, Inc.     

Evidence for Modulation of DoDamine-neuronal Function by Tachykinin NK3 Receptor Stimulation in Gerbil Mesencephalic Cell Cultures

Primary cultures of gerbil mesencephalon were used for studying the modulation exerted by tachykinin NK₃ receptor activation on the activity of dopamine (DA) neurons. Dopamine neurons were identified by their ability to take up [³H]DA in a nomifensine-dependent manner. Moreover, tyrosine hydroxylase immunohistochemistry revealed that these neurons accounted for 5–7% of the total cell population. The NK₃ receptor agonists, senktide (EC₅₀= 0.58 nM) and [MePhe⁷]neurokinin B (EC₅₀= 3 nM), increased spontaneous [³H]DA release in a concentration-dependent manner. In contrast, tested at a supramaximal concentration (10-⁷ M), neither septide nor substance P were found to affect [³H]DA release. The senktide-evoked [³H]DA release was not observed when extracellular Ca²⁺ was chelated, but was unaffected by nomifensine. This indicates that this increase in [³H]DA outflow resulted more from an exocytotic process than from reversal of carrier-mediated DA uptake. Moreover, the senktide effect was unaffected by the Na⁺ channel blocker tetrodotoxin, a result suggesting a direct action of senktide on DA neurons. The non-peptide NK₃ receptor antagonist, SR 142801, shifted or blocked (ICs0 = 0.89 nM) the senktide-evoked [³H]DA release, while its (-)-antipode, SR 142806, was 80-fold less potent, in agreement with binding data. Selective antagonists for NK, (SR 140333) or NK₂ (SR 48968) receptors failed to reduce the senktide effect. Light scanning microscopic analysis of mesencephalic cells loaded with the Ca²⁺ sensitive dye, fluo-3, showed that senktide induced a rise in cytosolic Ca²⁺ in 8-10% of the cell population. The senktide-induced elevation in intracellular Ca²⁺ was rapid in onset and transient (at lo⁴ M) or more sustained with no further increase in fluorescence intensity (at 10^-7 M). The proportion of senktide-responsive cells was not significantly modified when extracellular Ca²⁺ was chelated, but was reduced by 87% in the presence of SR 142801 and by 75% in cultures that were pre-treated with the DA neurotoxin l-methyl-4-phenylpyridinium. The present study shows that enhancement of spontaneous [³H]DA release and intracellular Ca²⁺ mobilization may be observed after NK₃ receptor stimulation and that both biochemical events are likely to occur in DA neurons.